For the first time a man has been sent to jail for not disclosing his so called 'AIDS test' result to his partner. The'test' has long been used to ban people from entry into America, frighten people into taking high toxic medications (that cost $40,000 a year and make huge profits for their manufacturers) but now it can put you behind bars.

So what are these tests really testing for? In short nothing but harmless antigens to a virus that has never even been proved to exist.

Who said you are innocent until proved guilty?

_____

UNDERSTANDING THESE USELESS TESTS

There are at least 30 tests marketed to test for HIV. None of them are approved by the FDA to diagnose the presence or absence of HIV. Not the Elisa, not viral load, not Western Blot, not the P24 antigen test. The FDA and manufacturers clearly state that the significance of testing positive on the Elisa and Western Blot test is unknown.

AIDS researchers admit that the tests contain at least 80 percent non-specific cellular material - they're, at best, 20 percent effective. But in my scientific opinion, they contain no HIV at all. The medical literature lists at least 60 different conditions that can register positive on the HIV-test. These conditions include candidas, arthritis, parasites, malaria, liver conditions, alcoholism, drug abuse, flu, herpes, syphilis, other STDs and pregnancy.


_____

Check out the ppv of these Italian figures! What happened is that they performed a confirmatory test on the 32 out of 25,562 that tested positive - only 2 remained positive.

This is data on testing the Italian armed forces. Get this.

Table II
HIV Screening in Military Blood Transfusion Centers

Number of dontations: 25,562
Number of blood donations ELISA positive: 32
Number of blood donations after confirmation test: 2

In other words, after performing a confirmation test
for the ELISA, only *2* of the 32 positive tests remained positive.


That is positive predictive value of 2/32 or 6 1/4%!!!!!!!!!!!!!

6.25%

In a country with very few other pathogens that could cause
a false positive result like in Africa (malaria, leprosy, tb, ddt, etc.).


________

DEMAND AN END TO THE AIDS MADNESS AND CRIMINAL PROFITEERING THAT FUELS THE MYTH

Join: - http://www.aidsmythexposed.com

I'm grateful that you've decided to share this information. I've known the truth about Gallo, the "inventor of the AIDS virus" for some time, now, but no-one seems to want to hear the truth. It's maddening that the truth is out there, but suppressed by all the orthodox AIDS organzations. Anyone with half a brain knows that if you have antibodies to something, you are NOT going to go on and develop an illness, especially in THIS case where the so-called virus itself hasn't ever been isolated. Even the "inventor" himself admits that in an article I read at
http://qnortheast.com/aids_debate1.htm . Thanks, Anna

BRAVO!

I have known the lies we have been told about HIV=AIDS=DEATH.
It is about time the world learns about this crime against humanity.

It's time for those people that are on "HIV/AIDS" "meds" to get off of them and take back control of their lives.

The "meds" are killing more people the AIDS ever did.

Let the truth be told!

Gregory D. Kramer

BRAVO!

I have known the lies we have been told about HIV=AIDS=DEATH.
It is about time the world learns about this crime against humanity.

It's time for those people that are on "HIV/AIDS" "meds" to get off of them and take back control of their lives.

The "meds" are killing more people the AIDS ever did.

Let the truth be told!

Gregory D. Kramer

BRAVO!

I have known the lies we have been told about HIV=AIDS=DEATH.
It is about time the world learns about this crime against humanity.

It's time for those people that are on "HIV/AIDS" "meds" to get off of them and take back control of their lives.

The "meds" are killing more people the AIDS ever did.

Let the truth be told!

Gregory D. Kramer

BRAVO!

I have known the lies we have been told about HIV=AIDS=DEATH.
It is about time the world learns about this crime against humanity.

It's time for those people that are on "HIV/AIDS" "meds" to get off of them and take back control of their lives.

The "meds" are killing more people the AIDS ever did.

Let the truth be told!

Gregory D. Kramer

attached is part 2 of Liam Scheff's seriesThe AIDS Debate Part 2

The Gay Plague

by Liam Scheff



Prologue

In 1984, Robert Gallo announced that a retrovirus called HIV was the “probable cause” of AIDS.

In Part 1 of “The AIDS Debate,” AIDS researchers gave startling evidence that retroviruses are, in fact, not toxic to cells, and are too biochemically inactive to cause any disease, let alone the 29 different diseases the Centers for Disease Control (CDC) classifies as AIDS. These researchers claim AIDS was correctly diagnosed in the early ’80s as a lifestyle disease typified by immune damage caused by massive drug use and malnutrition.

Ten years after his announcement, at a 1994 National Institute on Drug Abuse (NIDA) meeting, Robert Gallo quietly admitted that the first defining AIDS disease in gay men, Kaposi’s Sarcoma, could not be explained by HIV, but that nitrite drugs called “poppers” could be the primary cause. Poppers were a popular, legal drug heavily marketed in the gay community in the 1970s.

Gay men were indeed using poppers and other cell-damaging, mutagenic drugs in huge quantities in the 1970s, immediately prefiguring the first outbreak of AIDS diseases. But the specter of AIDS didn’t stop recreational drug use. Many gay men in the party scene continue to abuse the same drugs, including nitrite poppers.

Now they’re adding toxic AIDS pharmaceuticals to this already deadly cocktail, and it’s costing them their lives. A national study conducted by Dr. Amy Justice, an AIDS researcher at the University of Pittsburgh, revealed that liver failure is now the leading cause of death in HIV-positive individuals taking AIDS drugs. While liver failure has never been an AIDS disease, it is the primary, well-known side-effect of the new AIDS pharmaceuticals.

At the 1994 NIDA meeting, Dr. Gallo said that Dr. Peter Duesberg’s drug-based AIDS theory should be funded and investigated. Taking Gallo’s advice, I spoke with Duesberg and two other health advocates about the first AIDS patients, drug abuse and the new prescription drugs that are killing AIDS patients today.

Peter Duesberg is a professor of molecular biology at UC Berkeley. He is an expert in the field of HIV science and retrovirology.

John Lauritsen is a journalist and gay historian who’s investigated and written about AIDS for over 20 years. In 1992, he uncovered documents through the Freedom of Information Act, which revealed that the toxic AIDS drug, Azidothymidine (AZT), was approved based on fraudulent medical trials. His books include The AIDS War and The Early Homosexual Rights Movement - 1864 to 1935.

Darren Main is an author, holistic health practitioner and AIDS educator. According the CDC's 1993 redefinition, Main has AIDS, though he is not sick.

Interviews were conducted separately and integrated into a dialogue. Individual points-of-view belong only to the speaker.



The gay rights movement emerged as a powerful force in the early ’70s after decades of repression and abuse of gay men and women. What was the gay scene like in the ’70s?

John Lauritsen: There was a marvelous sense of freedom for gay men in the early ’70s. The gay liberation movement after Stonewall [a major turning point in the gay rights movement] allowed men who’d been held back by cultural taboos to come out in the growing gay centers. These were strong, healthy, young men who suddenly had this tremendous freedom offered to them. Using a lot of drugs and having a lot of sex was part of that freedom.

I lived in New York from ’63 to ’95; I was there, right in the heart of it. I lived around the corner from an extremely popular gay club called The Saint. On some nights, a couple thousand men would show up. The main activity was consuming drugs of every sort: ecstasy, poppers, marijuana, quaaludes, MDA, crystal meth, LSD, cocaine and designer drugs. Some drugs only showed up once, like the one they made specially for the club’s opening night.

At clubs like The Saint, there was a drug schedule. Someone would say, “Now it’s time for ecstasy, now it’s time for crystal, now it’s time for Special K,” and hundreds to a couple thousand guys would all do drugs at the same time. This went on all evening. They mixed this with alcohol through the course of the long, long night. A drug called “poppers” was used constantly, because it was cheap and legal.



What are poppers?

Lauritsen: Poppers are nitrite inhalants. The nitrites (amyl-, butyl- and isobutyl-) have a number of effects that made them attractive to young gay men. If used during sex, they prolong and enhance orgasm. Some men became incapable of having sex or even masturbating without them. Poppers were used to facilitate anal sex, because they deaden pain and relax the muscles in the rectum.



How were poppers used?

Lauritsen: They were used ubiquitously. They came in little vials that you’d pop open and snort. Some gay men used poppers first thing in the morning, on the dance floor and every time they had sex. At gay discothèques, men shuffled around in a daze, holding their poppers bottles under their nose. The acrid odor of poppers was synonymous with gay gathering places.



How do nitrite poppers affect health?

Lauritsen: Poppers are an extraordinarily toxic drug. They cause brain damage from strokes, severe skin burns and heart failure. They suppress the immune system and damage the lungs. They’ve caused death from a single use. They’re such an effective poison that they’ve been used to commit suicide and murder.

The nitrites are strongly mutagenic, which means they cause cellular change and genetic mutation. Nitrites produce deadly toxins when mixed with commonly used chemicals like antihistamines, artificial sweeteners and painkillers. Virtually all antibiotics are converted into potent carcinogens by nitrites.



Why were poppers legal?

Lauritsen: Poppers were originally manufactured by the Burroughs-Wellcome Corp. as a remedy for emergency heart pain, but they were replaced by nitroglycerine. In the ’60s, only a few gay men used poppers as a recreational drug.

Poppers found new life during the Vietnam War, sold on the black market to soldiers overseas. When the soldiers came home, they kept up the habit. Reports of blackouts, headaches, blood abnormalities and terrible skin burns forced a reclassification of the drug.

In the ’70s and ’80s, the FDA permitted poppers to be legally sold under the ridiculous pretext that they were "room odorizers" – at the same time that the new gay sex industry blatantly marketed them to gay men as aphrodisiacs, under such names as “Rush,” “Hard Ware” and “Ram.”

Poppers were cheap, as little as $2.99 per bottle, and they were extremely popular. Every single gay publication at the time was filled with full-page, color ads for the drug. In the ’70s, poppers were a $50 million per year business. Gay magazines like The Advocate relied heavily on ad revenue from poppers; some magazines owed their very existence to the drug. They were so popular that there was even a “Poppers” comic strip named after them.

By the end of the ’70s, some of the healthy young men weren’t looking so young and healthy. They were worn out. Their faces were gray. They looked prematurely old. I remember going to a party in the late ’70s and being shocked to see how many men were gravely ill.

In 1983, I began to work with Hank Wilson, a Bay Area gay rights activist, on researching and writing about poppers. We started writing about the dangerous medical effects of the drug and were savagely attacked for doing so. The gay press called us “homophobes” and “gay traitors” because we criticized a chemical.

In the early ’80s, medical reports on AIDS considered it a lifestyle disease. The fast-lane lifestyle of gay men was defined by incessant sex and drug use. These men had constant STD infections – concurrent cases of syphilis, gonorrhea, chlamydia, VD, bowel and parasitic infections – which they treated with increasingly strong rounds of antibiotics whenever they thought they’d caught something. Some doctors gave their gay patients open prescriptions for antibiotics and even advised them to swallow a few capsules before going to the baths. One bathhouse in New York sold black market antibiotics on the second floor, along with all kinds of street drugs.

One of the primary AIDS diseases was Kaposi’s Sarcoma, which is an overgrowth of the blood vessels that manifests as dark purple patches on the skin and face. Doctors speculated that nitrite poppers, a known mutagen, were the cause of Kaposi‘s Sarcoma (KS). Scientists wrote The Advocate with strong warnings about the dangers of poppers, but their letters were rejected or ignored.

The gay community’s reaction to the idea that chronic drug use had anything to do with illness was overt denial. In 1983, The Advocate actually ran a series of ads defending poppers. The series, called “A Blueprint for Health,” falsely claimed that government studies showed poppers were harmless and should be considered a healthy part of gay life. This was for a drug that said, “flammable, fatal if swallowed” on the label.

Peter Duesberg: AIDS was correctly diagnosed by the CDC from ’81 to ’84. They identified it as a probable lifestyle disease caused by excessive drug use and malnutrition. The New England Journal of Medicine published four articles on the drug lifestyle of what was then called GRID (Gay-Related Immune Deficiency) patients. This syndrome was typified by opportunistic infections, pneumonia and KS.

The one factor that all these people had in common was very high use of recreational drugs: amphetamines, nitrite inhalants, cocaine and heroin. The theory was simple. These men had spent a decade destroying their immune systems and were now susceptible to all sorts of infectious disease. This theory was compatible with the non-random distribution of illness.

Until ’84, this was the only credible hypothesis. But when the government supported HIV theory, the lifestyle theory was abandoned, because all the money went into retroviral research. That’s how science works; if it’s not funded, it doesn’t exist.

Lauritsen: The media immediately supported Gallo’s unproven hypothesis, and public health services followed suit. For 20 years, virtually all government funding has poured into Gallo‘s HIV-equals-AIDS theory, with nothing to show for it, while the drug and malnutrition models have been ignored.

In 1994, Robert Gallo quietly admitted that KS could not be caused by HIV. But this was never reported in the mainstream press. Gallo told the audience of scientists and activists at the ’94 NIDA meeting that HIV couldn‘t cause KS and that he‘d never even found it in T-cells, which HIV is supposed to kill. He said, “I don’t know if I made this point clear, but I think that everybody here knows – we never found HIV DNA in the tumor cells of KS. And, in fact, we’ve never found HIV DNA in T-cells. So in other words, we’ve never seen the role of HIV as transforming [cancer-causing] in any way.”

This was in complete opposition to everything Gallo had ever said about HIV or AIDS. But very few people paid attention to his retraction. The CDC ignored it, and continues to tell people KS is an AIDS disease.

When Gallo was asked what, if not HIV, caused KS, he said, “The nitrites [poppers] could be the primary factory” because “Mutagenesis” is the “most important thing.” It's a very embarrassing situation for the AIDS establishment, and they’ve kept it quiet. One of the two hallmark diseases of AIDS is now clearly understood to be totally unrelated to AIDS or HIV.

Take any AIDS diagnosis – there are good reasons why that person became sick the way they did. Take a heroin addict who develops pneumonia or a severe lung infection. This is what science has always expected as a consequence of taking opiates in excess, because opiates damage the lungs and reduce immunity.

If a gay man takes nitrite inhalants and develops KS, the best explanation is that he’s been affected by nitrite inhalants, not an infectious agent. Nitrites are mutagenic drugs that directly affect blood vessels. It’s telling that gay men who developed KS got it around the lips, nose and mouth – the same place he’d inhaled the toxic drug.

Duesberg: The defining symptoms of AIDS are chronic diarrhea, dementia, weight loss and increased incidence of viral and bacterial infection. These are the very conditions that define chronic drug abuse and malnutrition, but no one’s funding this research. Instead, billions of dollars are poured into beating AIDS with deadly drugs like AZT and protease inhibitors.

Many Americans use amphetamines, diet drugs, cocaine and designer party drugs. When you do this for years, you start getting sick. You go to the doctor, who says the first thing you need is an HIV test. You test positive because HIV tests cross-react with antibodies produced by drug use. The doctor puts you on AZT, a DNA chain terminator, which, in high doses, will finish you off in six months.

I’m not talking about a one-time use of a party drug. We’re designed to consume a lot of junk, but we’re not designed to tolerate a gram of cocaine, nitrite inhalants or heroin per day, and we’re even less capable of handling AZT.



What is AZT?

Duesberg: AZT is a DNA chain terminator. AZT kills your DNA. It kills your bone marrow, where your blood is produced; it kills the cells in your intestines so you can't eat.

AZT was designed 40 years ago as a chemotherapy drug to treat cancer. The principle of chemotherapy is simple – to kill all cells. If chemotherapy works, the cancer cells are dead before you are. But it doesn‘t work often, and there’s terrible collateral damage. Of course, chemotherapy is a short-term process. A cancer patient is only treated for a short time, because the treatment is so toxic. But AIDS patients are given AZT daily, presumably for the rest of their lives.



How was such a toxic drug approved for use on sick AIDS patients?

Lauritsen: AZT was approved on the basis of fraudulent research. The Phase 2 AZT Trials were conducted by the FDA in 1986 and monitored by Burroughs-Wellcome (now Glaxo-Wellcome), who manufacture the drug. Incidentally, Wellcome is the same corporation that first manufactured nitrite poppers for heart pain.

The Phase 2 trials were supposed to demonstrate that AZT was "safe and effective." The report on the trials, published in 1987, claimed that AZT dramatically prevented people with AIDS from dying. But these results were based on fraud.



How was fraud committed?

Lauritsen: First, the study wasn’t truly blinded. Doctors and patients knew who was taking AZT and who was taking placebos. In a medical study, one group of patients is given the test drug, the other is given harmless sugar pills. This allows doctors to observe the effects of the drug by comparing the two groups.

In a true double-blinded study, neither the doctors nor patients are supposed to know who's on the drug. This is considered the most accurate and bias-free method for approving a pharmaceutical.

In the Phase 2 trials, everybody knew who was on AZT; the information was shared among doctors and patients. Patients in the placebo group wanted to be on AZT because they thought it would help them, so they got it from other patients or their own doctors. But they were still recorded in the placebo group.

Most importantly, the case report forms were falsified. Patients taking AZT who almost died from anemia were recorded as having “no adverse reactions” to the drug. These patients had to get multiple blood transfusions to save their lives. [AZT causes anemia by destroying bone marrow, where blood cells are produced.]

One patient, who was supposed to be in the placebo group, was actually being given AZT by his doctor. He dropped out of the study but continued to take AZT, and quickly died. The investigators recorded his death in the placebo group, as if not taking the drug is what killed him. If that’s not fraud then the word has no meaning.

On the basis of these tests, AZT was approved and introduced to patients in 1987. HIV-positive men became the focus of a multimillion dollar media campaign from Wellcome. Full-page ads promoting AZT appeared in The New York Times and in lesser publications all over the world. City public health departments echoed the idea that AZT would help people live longer.

Duesberg: Doctors give HIV-positive patients drugs before they‘re even sick. As of 1993, the CDC no longer requires people to be sick to call them AIDS patients. If they have a positive antibody response to the nonspecific Elisa test and a one-time T-cell count below 200, the CDC says they have AIDS. Based on this criteria, doctors are prescribing AIDS drugs to healthy individuals.

This is what I call AIDS by prescription. Imagine that you go to your doctor and are told that you’ve tested HIV-positive. You’re perfectly healthy, but your doctor tells you that you have AIDS because your T-cell count is low, and you’d better take the drugs to stop the progression of the disease. You’re confused and alarmed, but you trust your doctor, so you take the drugs, which destroy your intestines and your immune system. Your hair falls out, you become impotent, and sooner or later you have the diseases you were trying to prevent.

The doctor says, “If you hadn’t come to me, you would’ve had the same problems six months earlier. I’ve added a half-year to your life.”

Now, because so many people died taking AZT, doctors are prescribing lower doses, which simply delays and masks the damage being done to the body.



Who’s taking AZT?

Duesberg: According to the New York Times and Time magazine, 450,000 Americans are taking AZT every single day of their life. Many patients can’t take the drugs because they’re throwing up so badly. But they try to follow their doctor’s orders.

Lauritsen: Ninety-four percent of all AIDS deaths have occurred since people started using AZT in 1987. More people died taking AZT in 1993 alone than died in the first six years of AIDS.



Did AIDS stop recreational drug use?

Lauritsen: No, by the early ’90s, gay men in San Francisco and New York had returned to the levels of drug abuse and promiscuity of the ’70s.

In ’92, several thousand gay men attended a "morning party" on Fire Island, held to benefit Gay Men's Health Crisis. At least 95 percent of them were in a state of extreme intoxication from ecstasy, poppers, cocaine and alcohol. The playwright Larry Kramer described it, saying, "There were 4,000 or 5,000 gorgeous young kids on the beach drugged out of their minds at high noon, rushing in and out of portosans to fuck. All in the name of GMHC.”

Darren Main: Drug use is very high in the gay community right now. Large circuit parties are very popular.



What’s a circuit party?

Main: It’s an event that occurs at a specific location, like the "White Party" in Palm Springs or the "Black and Blue" in Montreal. Thousands of people attend. It’s four to five days of heavy drug use, like nothing you can imagine – crystal meth, ecstasy, special K, designer drugs, poppers.



People are still using poppers?

Main: Absolutely. It’s a real pharmacy. Guys stay up for four to five days, taking drugs and having orgy-like sex. In addition to the big circuit parties, there’s a regular party scene. A lot of guys spend their weekends going to dance clubs and getting stoned out of their minds.

These party drugs are being combined with antibiotics, because these guys are constantly exposed to syphilis, gonorrhea, herpes, amoebic infections and other STDs, which are all on the rise again in the gay community.

This sounds like the first AIDS crisis.

Main: It is. A lot of guys think that that they're protected from infections because they're taking the new AIDS drug cocktails, called HAART (highly-active anti-retroviral therapy). HAART is a combination of the older nucleoside analogues like AZT, DDI and 3TC, and the newer protease inhibitors like Saquinavir and Crixivan. [Nucleoside analogues work by stopping DNA production; protease inhibitors work by stopping protein assemblage in your cells.]



What are common side effects of protease inhibitors?

Main: Protease inhibitors cause lypodystrophy – a deformation of fat. Body fat moves out of the face, arms and legs, which become veiny sticks; the face becomes skeletal. The fat collects into a “buffalo hump” on your upper back. The belly becomes distended and bloated.

And that’s just what’s visible. The drugs cause massive cholesterol increase, which frequently leads to heart attacks. Diabetes and blood-sugar imbalances are also common. Protease inhibitors do the most damage in the liver. As a result, liver failure is now the No. 1 killer of AIDS patients in this country, though it’s not an AIDS disease.

I’ve observed that if you go on the drugs, your symptoms will start with an upset stomach and diarrhea. Within a year, it’ll begin to show in your face. The people I know who’ve been taking the drugs for a few years are visibly altered. There’s no way to know if quitting the drugs will reverse the damage. In LA, San Francisco and South Beach, there are plastic surgeons whose entire practice is based on liposucting buffalo humps and putting in cheek implants.



You consult with people diagnosed with HIV and AIDS. What do you tell them?

Main: I teach them how to rebuild and support their immune systems by doing very basic things: Developing a supportive diet, getting enough sleep, no recreational drugs, no stimulants, and adding supportive supplements. If someone’s on AIDS drugs, I encourage them take a “drug holiday.”

A lot of people are afraid to quit the drugs or challenge what doctors and pharmaceutical companies tell them. I have a client we’ll call “Jack,” whose partner died a couple years ago from drug toxicity. Jack is HIV-positive and takes the drugs. He had a very severe reaction to them – he went blind. His eyes stopped working and began to waste away due to the AIDS drugs. Jack’s doctors confirmed that the blindness was indeed caused by the drug cocktails, not by any virus or AIDS disease. When I met him, he’d just had his eyes removed. He now has prosthetic, glass eyes.



So he finally quit the drugs?

Main: No, he’s still taking them. I asked if he’d consider going off them. He said no, because he didn’t feel comfortable with his T-cell count or his viral load. He felt better losing his eyes than quitting the drugs. Protease inhibitors are slightly less toxic than AZT, but they still can be deadly. It’s a slower death.



You don’t take the drugs, even though you have an AIDS diagnosis. How’s your health?

Main: Perfect – no health problems that I know of. I’ve never had an opportunistic infection or AIDS-defining disease. I have AIDS because of a T-cell count. Mine is 120. According the CDC, that’s what AIDS is; HIV-positive plus a T-cell count below 200. Of course, in other countries, I don’t have AIDS. This is just how the CDC defines AIDS in the US, and only since ’93. But I’m quite healthy. I rock climb, go hiking and teach yoga for a living. Because of my AIDS diagnosis, I’ve been harassed by doctors to go on the drugs. “Hit hard and hit fast,” they say.



According to Dr. Amy Justice of the University of Pittsburgh, gay men are dying taking AIDS drugs. They're taking them even though HIV theory is highly debatable, and more supportive treatment options exist. Why are gay men buying into this treatment option, if it causes them so much pain and suffering?

Main: If you look at the history of the gay movement, you’ll find that HIV and AIDS have, ironically, really brought people together. In the early days, gay liberation was a bunch of guys whose main interaction was partying. When people started getting sick, these guys, who’d been rejected by mainstream society, had to support each other. They took care of each other and developed a real community. They supported each other in a way that they’d never been supported by their own families or society.

HIV and AIDS became the glue that kept people together. We’ve got a lot invested in AIDS – billions of dollars, AIDS drives, thousands of volunteer hours at community centers, full-time jobs and organizations invested in the notion that HIV is killing gay men. It’s very hard for people to let go of something they’ve put their whole lives into – their hearts, their minds and their beliefs. It’s very difficult.

It would be nice if gay men felt that they could find validation, support and community outside of HIV and AIDS. But I think that too many people are too attached to have that happen soon. Which is unfortunate, because that attachment is killing a lot of people.



Organizations dedicated to treating AIDS illnesses without toxic AIDS drugs do exist. For alternative AIDS treatments and action, go to:

HEAL – www.healaids.com

Alive and Well AIDS Alternatives – www.aliveandwell.org

Darren Main – www.darrenmain.com

Act Up San Francisco – www.actupsf.com

Articles by Peter Duesberg and John Lauritsen can be found at:

www.duesberg.com and www.virusmyth.net

In three weeks the final installment in The AIDS Debate will take a look at AIDS in Africa: Treating malaria and malnutrition with deadly AIDS drugs.

Just wanted to let everyone on this list know that Paul King is a part of what is called the Denialist movement...
They do not believe that there is such a thing called HIV..
be warned

Bitmap, you wrote "Just wanted to let everyone on this list know that Paul King is a part of what is called the Denialist movement... They do not believe that there is such a thing called HIV.. be warned ".

Did you read any of the above? There IS no such thing as HIV! Be warned! People are taking expensive medications for a disease which could be easily cured if they even HAD a disease...mostly, now, its a numbers game. If you'd put aside your fears of "HIV or no HIV" and looked into the real meaning of the tests, you might save someone's life. The most common cause of death currently called "AIDS" is liver disease, from the DRUGS not a fictitious virus! Listen to the audio file I uploaded.

If you know a naturopath or similar small drugs company there could be and infact is quite a big industry of people offering alternative therapies to aids.
If what you say is true then their remedies should be the appropriate cures and since they are easily available for a fraction of the aids drugs cost you can just get them if you want.
You could also do a clinical study on it.
Im sure they would pay you a few bucks if you could prove they wee right.

I think Bitmap needs to get out there and do the reading and research that I have done.

I don't understand why people are calling us "Denialists", we are just people LOGICALLY looking at the truth.

If a person only looks at just one side of a point of view and refuses to accept the other side, then I feel that THEY are denialists.

Science is not perfect and neither are the people that hypothesize these theories.

Humans do make mistakes.

"You could also do a clinical study on it.
Im sure they would pay you a few bucks if you could prove they wee right." ??

No one is willing to do a clinical trial for a virus that hasn't been isolated. No one CAN isolate the virus, since it doesn't exist. Once you've been mis-diagnosed, the only money being spent is by big$$pharma, and we all know they have NO interest in curing ANY disease. You can clean out your system of the flotsam and jetsum that bands at 1.16, perhaps, but you'll NEVER get rid of the antibodies to all 'germs' that your body has defeated...( which is what the test really looks at )you are not meant to. Those antibodies protect you from re-exposure. The REAL cause of "AIDS" is the test itself, invented by a corrupt and dishonest man to make money off of human suffering.

...file this thread and it's subject matter in the "crazy talkin' conspiracy theory" drawer.

And still some people wonder why this site is only home to fools and those that mock them.

Threads like this are pure spam.

Fresca,

As usual with ANYONE who discredits the "AIDS" Dissidents and supports the AID$ Industry, you have not offered ONE SINGLE scientific rebuttal to the information posted above. Might be a good idea for you to actually READ what the dissidents are saying and offer a) PROOF for the isolation of "HIV" to begin with and b) PROOF that it destroys t-cells and causes "AIDS" when Robert Gallo himself has stated:

From the second article below:

"He [Robert Gallo] said, “I don't know if I made this point clear, but I think that everybody here knows - we never found HIV DNA in the tumor cells of KS. And, in fact, we've never found HIV DNA in T-cells."

Part I: "The Most Controversial Story You've Never Heard"
http://www.weeklydig.com/dig/content/3168.aspx

Part II: "The Gay Plague"
http://www.weeklydig.com/dig/content/3499.aspx

Part III: "Africa: Treating Poverty with Toxic Drugs"
http://www.weeklydig.com/dig/content/3593.aspx

Fresca,

As usual with ANYONE who discredits the "AIDS" Dissidents and supports the AID$ Industry, you have not offered ONE SINGLE scientific rebuttal to the information posted above. Might be a good idea for you to actually READ what the dissidents are saying and offer a) PROOF for the isolation of "HIV" to begin with and b) PROOF that it destroys t-cells and causes "AIDS" when Robert Gallo himself has stated:

From the second article below:

"He [Robert Gallo] said, “I don't know if I made this point clear, but I think that everybody here knows - we never found HIV DNA in the tumor cells of KS. And, in fact, we've never found HIV DNA in T-cells."

Part I: "The Most Controversial Story You've Never Heard"
http://www.weeklydig.com/dig/content/3168.aspx

Part II: "The Gay Plague"
http://www.weeklydig.com/dig/content/3499.aspx

Part III: "Africa: Treating Poverty with Toxic Drugs"
http://www.weeklydig.com/dig/content/3593.aspx

"you have not offered ONE SINGLE scientific rebuttal to the information posted above. "

And I won't .
I won't waste any time posting proof of something that has been proven and accepted over and over beyond a shadow of a doubt globally for decades.

I won't because you, at best, only a delusional loser with internet access and obviously can't accept certain common knowledge. I suspect you believe the Earth is flat as well.

Then what the fucked killed all my friends who didn't take meds? Paul King is a moron.

Why should the whole world believe just one person (Robert C. Gallo), when there are other scientists out there disputing his theory?

I have personally lived this war, I know for a fact what is going on.

The only time I was near death, was when I was on the "Meds".
Now that I'm not on them, I am well and fully functional again.

You people need to start getting your information from more sources, getting information from only one source only leads to narrow-mindedness.

Gregory D. Kramer

And what was the time frame all your friends were killed?

early 80's? or recently?

Be a little more specific with your details if you want to argue.

I've had better debates with my cat.

"you have not offered ONE SINGLE scientific rebuttal to the information posted above. "

And I won't .

Face it Fresca, YOU CAN'T offer SCIENTIFIC PROOF. There is none.

Just answer my simple question: How does "HIV" cause "AIDS" when it has never infected one single t-cell? Shouldn't be a very difficult question to answer? Just tell me how "HIV" causes "AIDS". That's all I want to know?

This articles SAYS NOTHING about the mechanism of how "HIV" miraculously does ALL THESE THINGS. The whole article ASSUMES that "HIV" is responsible without giving ANY SCIENTIFIC PROOF. Please point out WHERE in the article the MECHANISM of "HIV" is discussed.

The article answers your question about your mistaken claim that no T-cells have shown to be affected. It appears that the conspiracy theory websites you copy and paste from have much of their content from the early days -- before PCR was used much.

In any event, to answer your questions about HIV => AIDS, spend a few hours here:

www.pubmed.com

the HIV's gp120 viral capsid protein binds to the CD4 receptor of CD4+ or so-called "helper" T lymphocytes. the HIV RNA is taken up into the cytoplasm of the lymphocyte, as is its reverse transcriptase. this reverse transcriptase catalyzes the synthesis of double stranded DNA from the HIV RNA genome, which can then integrate with the host cell genome. expression of the viral genome not only produces new virion particles, but also interferes with normal transciptional regulation in the cell, eventually resulting in cell death and systemic decrease in the number of CD4+ T lymphocytes.

now, you guys who don't believe the last bit, it is not well established exactly how the cytotoxic (cell-killing) aspect occurs, but it is a *fact* that patients with HIV experience a progressive decrease in number of circulating CD4+ T cells characteristic of "full-blown" AIDS, and that HIV infection (or more specifically, testing positive for antibodies to HIV) occurs before this decline occurs. while this is not a logical proof that HIV *causes* AIDS, it is a pretty strong correlation.

also, the recent advent of anti-retroviral "drug cocktails" which have stabilized many patients in the HIV-infected, pre-AIDS stage of the disease suggest further that the causative agent is a retrovirus such as HIV.

all this was adapted from the venerable text _basic immunology_ by abbas and lichtman, and if you don't believe them you can go to the literature: pantaleo, graziosi and fauci, NEJ med. vol 328, 327-335, 1993.

Why do I get the feeling that ol' Mike is not going to believe or even understand the above?

Dear Mike,

Here are the flaws in your argument: -


The problem is, there are thousands of unnamed cellular sub-particles -- called "retroviral-like" and "viral-like" particles.

None of them have been shown to be infectious -- that is - disease causing -- in humans.

There is significant doubt as to whether RTV's actually act as infectious agents at all, or simply arise in the presence of Oxidizing Agents --

Agents which bring destructive free-radicals into the cell and do damage, stimulate breakdown, carcinogenisis, arthritis and more.

Everybody should know this one little secret --

Both Robert Gallo and Luc Montagnier, the co-creators of the HIV paradigm clearly and loudly admit that none of the surrogate markers they used as a stand-in for HIV* show up unless the cells are artificially chemically stimulated with compounds which cause oxidation, mitosis (cellular division), and hyperstimulation of Tcells.


*(they didn't actually isolate a virus, they used non-specific markers like an enzyme called reverse transcriptase)
No HIV in people, and none in the cell culture -- only markers which turn out to be non-specific, and only in artificially stimulated cultures.

By the way, if you artificially stimulate non "HIV" pos cell cultures, you get the Exact Same Result.
Reverse Transcriptase activity and normal cellular proteins which AIDS researchers use to tell you that you're HIV positive.

EVERYBODY REACTS POSITIVE
ON THE ELISA TEST FOR HIV

By Roberto Giraldo

Continuum Midwinter 1998/9


For the last 6 years I have been working at the laboratory of clinical immunology in one of the most prestigious University
Hospitals in the
City of New York. Here I have had the opportunity to personally run and get to know in detail the current tests used for the
diagnosis of HIV
status, namely, the ELISA, Western Blott and Viral Load tests.

1. Diluting the serum for the ELISA test.

The ELISA test is a test for antibodies against what is supposed to be the Human Immunodeficiency Virus or HIV. To run
this test, an
individual's serum has to be diluted to a ratio of 1:400 with a special specimen diluent. According to the test kit manufacturer
this diluent
contains

0,1% triton X-100, Bovine and Goat Sera (minimum concentration of 5%) and Human T-Lymphocyte Lysate (minimum
titer 1:7500). Preservative: 0.1% Sodium Azide (1).

This extraordinary high dilution of the person's serum [400 times] took me by surprise. Most serologic tests that look for the
presence of
antibodies against germs uses neat serum [undiluted]. For example, the tests that look for antibodies to hepatitis A and B
viruses, rubella virus,
syphillis, hystoplasma and cryptococus, to mention a few of them, use straight serum [undiluted]. However, to try to prevent
false positive
reactions some serologic tests use diluted serum; for example this is the case with tests that look for antibodies to measles,
varicelia and mumps
viruses which use a dilution of 1:16, to cytomegalovirus [CMV] 1:20 and to Epstein-Barr Virus [EBV] 1:10.

The obvious questions are: What makes HIV so unique that the test serum nedds to be diluted 400 times?. And what would
happen if the
individual's serum is not diluted?.

2. Testing the ELISA test without diluting the serum.

To answer these questions I ran an experiment in a medical laboratory in Yorktown Heights, New York. I ran it using the same
test kit reagents
that are usually used to run the ELISA test in most clinical laboratories worldwide (1).

I first took samples of blood that, at 1:400 dilution, tested negative for antibodies to HIV. I then ran the exact same serum
samples through the
test again, but this time without diluting them. Tested straight, they all came positive.

Since that time I have run about 100 specimens and have always gotten the same result. I even ran my own blood which, at
1:400 reacts
negative. At 1:1 [undiluted] it reacted positive. I should mention that with the exception of my own blood, the patient samples
all came from
doctors who requested HIV tests. It is therefore likely that most of the blood samples that I tested belonged to individuals at
risk for AIDS.

According to Abbott Laboratories, the absorbance value [yellow color intensity]

develops in proportion to the amount of antibodies to HIV-1 which is bound to the bead (1).

What I noticied is that the absorbance values of the specimens that tested negative when diluted [1:400], but positive when
undiluted [1:1], had
lower values than the samples that, diluted, react positive on both the ELISA and Western Blott tests. This would probably
mean that the blood
that is negative when diluted but positive when undiluted has a lower level of antibodies than the diluted blood that is doubly
positive and,
therefore, may probably test negative on the Western Blott test. However, I have not had the opportunity to check this
hypothesis.

The graphic below ilustrates how blood that reacts negative for HIV at 1:400 ratio always turn positive when run at 1:1
[undiluted].

Run of ELISA test for HIV with two different concentrations of the person's serum.
(a) Results at 1:400
(b) Results at 1:1
9112324b G5 0.076 ---
9112324b G5 0.262 reactive
9112325b H1 0.081 ---
9112325b H1 0.259 reactive
9112326b H2 0.071 ---
9112326b H2 0.329 reactive
9112327b H3 0.060 ---
9112327b H3 0.401 reactive
9112328b H4 0.073 ---
9112328b H4 0.345 reactive
9112329b H5 0.062 ---
9112329b H5 0.343 reactive
9112330b J1 0.060 ---
9112330b J1 0.234 reactive
9112331b J2 0.077 ---
9112331b J2 0.306 reactive
9112332b J3 0.067 ---
9112332b J3 0.248 reactive
9112333b J4 0.086 ---
9112333b J4 0.222 reactive


Column (a) shows 10 specimens reacting negative at 1:400 dilution.
Column (b) shows the same specimens reacting positive at 1:1 dilution.

It is important to note that the Western Blott antibody test for «HIV» also needs serum to diluted. Although it too has an
usually high dilution,
here the individual serum is only diluted at the ratio of 1:50 (2). I have not yet had the opportunity to run this test with
undiluted [1:1]
specimens.

3. Discussion.

The following are three possible explanations for why undiluted specimens of blood always react positive at the ELISA test:

3.1. Everybody has HIV antibodies.

It is accepted worldwide that the ELISA test for HIV detects antibodies against what is known as the Human
Immunodeficiency Virus
(3-4-5-6). And the pharmaceutical company that commercialises the ELISA kits states that

Abbott HIVAB HIV-1 EIA is an vitro qualitative Enzyme Immunoassay for the Detection of Antibody to Human
Immunodeficiency Virus Type 1 (HIV-1) in Human Serum and Plasma (1).

Since all undiluted blood specimens react positive on the ELISA test, a test that supposedly tests for antibodies to HIV, the
results presented
here suggest that every single human being has HIV antibodies. And this suggests that everybody has been exposed to HIV
antigens.

This would mean that all of us have been exposed to the virus that is believed to be the cause of AIDS. The people that react
positive even at a
dilution of 1:400, would be the ones that have had the highest level of exposure to HIV antigens. The rest of the people -the
ones that only react
positive with undiluted serum [1:1]- would have had a lower level of exposure to HIV.

3.2. Everybody has different levels of HIV infection.

It is also believed worldwide that a person that reacts positive for antibodies against HIV has not only been exposed to but is
infected with a
deadly virus that causes immunodeficiency (3-4-5-6). Therefore, the positive reactions of all undiluted sera would mean that
everybody, or at
least all the blood samples that I have tested, including my own, infected with this «deadly» virus. The ones that react positive
at a ratio of 1:400
would simply have a higher level of «deadly» infection than the «deadly» infection has by the ones that reacts positive only
with undiluted
serum.

3.3. The test is not specific for HIV.

The results presented here could also mean that the tests used for detecting antibodies to HIV are not specific for HIV, as has
been explained
previously (7-8-9-10-11-12-13-14). In this case, there would be reasons other than HIV infection, past or present, to explain
why a person
reacts positive to it. The test also reacts positive in the absence of HIV (7-8-9-10-11-12-13-14).

The scientific literature has documented more than 70 different reasons for getting a positive reaction other than past or present
infection with
HIV (7,10,11,14,15). All these conditions have in common a history of polyantigenic stimulations (15,16).

Even Abbott Laboratories is well aware of the specificity problems with the ELISA tesst. This is why they state:

EIA testing alone cannot be used to diagnose AIDS, even if the recommended investigation of the reactive specimens
suggests a high probability that the antibody to HIV-1 is present

and

Although for all clinical and public health applications of the EIA both the degree of risk for HIV-1 infection of the
person
studied and the degree of reactivity of the serum may be of value in interpreting the test, these correlations are impefect.
Therefore, in most settings it is appropiate to investigate repeatably reactive specimens by additional more specific or
supplemental tests (1).

Interestingly, there are countries like Great Britain where the diagnosis of HIV status is based on the ELISA test alone. No
Western Blott or
any other test is needed there.

The only proper way for establishing the sensitivity and specificity of a given test is with a gold standard. However, since HIV
has never been
isolated as an independent purified viral entity (17-18-19), there cannot be a gold standard for HIV. The sensitivity and
specificity of the
antibody tests for HIV have instead been defined based on the assumption that HIV is the cause of AIDS. In this way,

The Abbot studies show that: Sensitivity based on an assumed 100% prevalence of HIV-1 antibody in AIDS patients is
estimated to be 100% (144 patients tested).

and

Specificity based on the assumed zero prevalence of HIV-1 in random donors is estimated to be 99.9/o (4.777 random
donors tested (1)).

At present there is no recognized standard for establishing the presence and absence of HIV-1 antibody in human blood.
Therefore sensitivity was computed based on the clinical diagnosis of AIDS and specificity based on random donors (1).
[Emphasis is mine].

Since there is no scientific evidence that the ELISA test is specific for HIV antibodies, a reactive ELISA test at any
concentration of the serum
would mean presence of nonspecific or polyspecific antibodies (20). These antibodies could be present in all blood samples.
They are most
likely a result of the stress response, having no relation to any retrovirus, let alone HIV (21,22). In this case, a reactive test
could be a measure
of the degree of one's exposure to stressor or oxidizing agents (15,16).

The inevitable conclusion is that all positive reactions for antibodies to HIV are simply false positives. If nobody is positive for
HIV, then
people who react positive on the ELISA test do so due to something other than HIV.

4. Proposal to find out the real meaning of the «HIV antibody» tests.

To uncover the meaning of these tests I propose a simple experiment: Take blood from three groups of a people and run the
tests highly
diluted, undiluted and at a wide spectrum of dilutions in between. The first group would be a group of healthy people of many
age groups; the
second group would be a group of people from the conventional AIDS «risk groups»; the third group would be a group of
people with clinical
conditions both related and unrelated to AIDS. All groups would be subjected to both the ELISA and Western Blott tests.

Additionally, all blood samples could be subjected to «the viral load test for HIV».

The results of such an experiment could determine whether these test measurements bear any relationship to an individual's
level of exposure to
stressor or oxidizing agents. If so, the tests could be salvaged as a measure of an individual's level of intoxication.

Let us find the economic support necessary to run this experiment. In the mean time, since people are reacting positive on tests
that are not
specific for HIV, let's please stop labeling them as «HIV positive».

Acknowledgments.

I want to thank Mr. Albert Padovani, Director of Yorktown Medical Laboratory for permitting me to run the experiments
reported here in his laboratory and for
providing the reagents for the tests. Also I thank Tom Di Ferdinando Executive Director of Health Education AIDS Liaison
(HEAL) in New York City for editing the
manuscript for this article and for his valuable suggestions.

Roberto A. Giraldo, MD. Physician, specialist in internal medicine, infectious and tropical diseases. Member of the Boards od
Directors of
The Group for the Scientific Reappraisal of the HIV-AIDS Hypothesis and Health Education AIDS Liaison (HEAL).
Independent AIDS
Researcher. Author of the book AIDS and Stressors, New York City. E-mail: rgiraldo@cdiusa.com.

References.

(1) ABBOT LABORATORIES. Human Immunodeficiency Virus Type 1. FUVAB FffVI EIA. Abbott Laboratories,
66-8805/R5, january 1997:5.
(2) EPITOPE ORGANON TEKNIKA. Human Immunodeficiency Virus Type 1 (fuV-1) . I-UV-1 Western Blott Kit.
PN201-3039 revision number 6.
(3) FEINBERG MA & VOLBERDING PA. Testing for Human Immunodeficiency Virus. In: COHEN PT, SANDE MA and
VOLBERDING PA. The AIDS
Knowledge Base. Boston: Little, Brown and Company, 1994: section 2.
(4) PINS MR. TERUYA and STOWELL CP. Human Immunodeficiency Virus Testing and Case Definition: Pragmatic and
Technical Issues. In: COTTON D and
WATTS DH. The Medical Management of AIDS in Women. New York. John Wiley & Sons, 1997: 163-176.
(5) METCALF JA, DAVEY RT and LANE HC. Acquired Immunodeficiency Syndrome: Serologic and Virologic Tests. In
DEVITA VT, CURRAN J, HELLMAN S,
et al. AIDS: Etiology, Diagnosis, Treatment and Prevention. 4th Edition. Philadelphia: Lippincott-Raven, 1997: 177-196.
(6) WEISS SH. Laboratory Detection of Human Retroviral Infections. In: WORMSER GP. AIDS and Other Manifestations
of FUV Infection. New York:
Lippincott-Raven, 1998:175-200.
(7) PAPADOPULOS-ELEOPULOS, E., TURNER V. & PAPADIMITROU JM. Is a Positive Western Blott Proof of HIV
Infection?. Bio/Technology 1993;
11:696-707.
(8) PAPADOPULOS-ELEOPULOS, E., TURNER, V., PAPADIMITROU JM. & CAUSER D. HIV Antibodies: Further
Questions and a Plea for Clarification. Curr
Med Res Opin 1997; 13:627-634.
(9) HODGKINSON N. Science Falls the «AIDS Test» In: AIDS: The Failure of Contemporary Science. How a Virus that
Never Was Deceived the World. London:
Fourth Estate, 1996:232-262.
(10) JOHNSON C. Factors Known to Cause False-Positive HIV Antibody Test Results; Zenger's, San Diego, California,
september 1996a:8-9.
(11) JOHNSON C. Whose Anitbodies Are There Anyway?. Continuum (London) . September/october 1996b; 4(3) :4-5.
(12) TURNER VF. Do Antibody Tests Prove HIV Infection?. Interview by Huw Christie Editor of Continuum. Continuum
(London) Winter 1997/1998; 5(2) :10-19.
(13) SHENTON J. Positively False: Wrong Tests and Long-Term Survivors. In: Positively False: Exposing the Myths
around HIV and AIDS. London: I.B. Tauris,
1998: 238-239.
(14) GIRALDO RA. Milking the Market. Will Mothers Dish Out the W.H.O. Formula?. Continuum (London) 1998; 5(4)
:8-10.
(15) PAPADOPULOS-ELEOPULOS E. Reappraisal of AIDS - Is the Oxidation Induced by the Risk Factors the Primary
Cause?. Medical Hyphotesis 1988;
25:151-162.
(16) GIRALDO RA. AIDS ans Stressors U: A Proposal for the Pathogenesis of AIDS. In: AIDS and Stressors. Medellín,
Colombia: Impresos Begón, 1997: 57-96.
(17) PAPADOPULOS-ELEOPULOS, E., TURNER, V., PAPADIMITROU JM. & CAUSER D. The Isolation of HIV: Has
it Really Been Achieved?. The Case
Against. Continuum (London) 1996; 4(3) :S1-S24.
(18) LANKA S. No Viral Identification: No Cloning as Proof of Isolation. Continuum (London) 1997; 4(5) :31-33.
(19) DE HARVEN E. Remarks on Methods for Retroviral Isolation. Continuum (London) 1998; 5(3) :20-21.
(20) WING MG. The Molecular Basis for a Polyspecific Antibody. Clin Exp Immunol 1995; 99:313-315.
(21) SNYDER HW and FLEISSNER E. Specificity of Human Antibodies to Oncovirus Glycoproteins: Recognition of
Antigen by Natural Antibodies Directed Against
Carbohydrate Structures. Proc Nat Acad Sci USA 1980; 77:1622-1626.
(22) BARBACID K., BOLOGNESI D. & AARONSON SA. Humans Have Antibodies Capable of Recognizing Oncoviral
Glycoproteins: Demonstration that These
Antibodies are Formed in Response to Cellular Modification of Glycoproteins Rather than as Consequence of Exposure to
Virus. Proc Nat Acad Sci USA 1980;
77:1627-1621.

I personally know to people who had tests that later turned out to be FALSE POSITIVES.

The information above makes it clear the scientific reasons why these test are quite, quite useless and a potential death sentence.


I agree. DO NOT TEST. NEVER, NEVER, NEVER!!!!!!!!!!!!!

Aletta Lo--------

HERE ARE SOME OF THE CAUSES OF FALSE POSITIVES
(Remember even a 'true' positive is only proof of completely harmles antigens).


Factors Known to Cause
False Positive HIV Antibody Test Results

1.Anti-carbohydrate antibodies 52,19,13
2.Naturally-occurring antibodies 5,19
3.Passive immunization: receipt of gamma globulin or immune (as prophylaxis against infection which contains antibodies) 18, 26, 60, 4,
22, 42, 43, 13
4.Leprosy 2, 25
5.Tuberculosis 25
6.Mycobacterium avium 25
7.Systemic lupus erythematosus 15, 23
8.Renal (kidney) failure 48, 23, 13
9.Hemodialysis/renal failure 56, 16, 41, 10, 49
10.Alpha interferon therapy in hemodialysis patients 54
11.Flu 36
12.Flu vaccination 30, 11, 3, 20, 13, 43
13.Herpes simplex I 27
14.Herpes simplex II 11
15.Upper respiratory tract infection (cold or flu) 11
16.Recent viral infection or exposure to viral vaccines 11
17.Pregnancy in multiparous women 58, 53, 13, 43, 36
18.Malaria 6, 12
19.High levels of circulating immune complexes 6, 33
20.Hypergammaglobulinemia (high levels of antibodies) 40, 33
21.False positives on other tests, including RPR (rapid plasma
reagent) test for syphilis 17, 48, 33, 10, 49
22.Rheumatoid arthritis 36
23.Hepatitis B vaccination 28, 21, 40, 43
24.Tetanus vaccination 40
25.Organ transplantation 1, 36
26.Renal transplantation 35, 9, 48, 13, 56
27.Anti-lymphocyte antibodies 56, 31
28.Anti-collagen antibodies (found in gay men, haemophiliacs, Africans of both sexes and people with leprosy) 31
29.Serum-positive for rheumatoid factor, antinuclear antibody (both found in rheumatoid arthritis and other autoantibodies) 14, 62, 53
30.Autoimmune diseases 44, 29, 1O, 40, 49, 43
31.Systemic lupus erythematosus, scleroderma, connective tissue disease, dermatomyositis Acute viral infections, DNA viral infections 59,
48, 43, 53, 40, 13
32.Malignant neoplasms (cancers) 40
33.Alcoholic hepatitis/alcoholic liver disease 32, 48, 40, 10, 13, 49, 43, 53
34.Primary sclerosing cholangitis 48, 53
35.Hepatitis 54
36."Sticky" blood (in Africans) 38, 34, 40
37.Antibodies with a high affinity for polystyrene (used in the test kits) 62, 40, 3
38.Blood transfusions, multiple blood transfusions 63, 36, 13, 49, 43, 41
39.Multiple myeloma 10, 43, 53
40.HLA antibodies (to Class I and II leukocyte antigens) 7, 46, 63, 48, 10, 13, 49, 43, 53
41.Anti-smooth muscle antibody 48
42.Anti-parietal cell antibody 48
43.Anti-hepatitis A IgM (antibody) 48
44.Anti-Hbc IgM 48
45.Administration of human immunoglobulin preparations pooled before 1985 10
46.Haemophilia 10, 49
47.Haematologic malignant disorders/lymphoma 43, 53, 9, 48, 13
48.Primary biliary cirrhosis 43, 53, 13, 48
49.Stevens-Johnson syndrome 9, 48, 13
50.Q-fever with associated hepatitis 61
51.Heat-treated specimens 51, 57, 24, 49, 48
52.Lipemic serum (blood with high levels of fat or lipids) 49
53.Haemolyzed serum (blood where haemoglobin is separated from red cells) 49
54.Hyperbilirubinemia 10, 13
55.Globulins produced during polyclonal gammopathies (which are seen in AIDS risk groups) 10, 13, 48 cross-reactions 10
57.Normal human ribonucleoproteins 48, 13
58.Other retroviruses 8, 55, 14, 48, 13
59.Anti-mitochondrial antibodies 48, 13
60.Anti-nuclear antibodies 48, 13, 53
61.Anti-microsomal antibodies 34
62.T-cell leukocyte antigen antibodies 48, 13
63.Proteins on the filter paper 13
64.Epstein-Barr virus 37
65.Visceral leishmaniasis 45
66.Receptive anal sex 39, 64

Christine Johnson, a researcher and author, compiled this list of conditions documented in the scientific literature to cause positives on HIV
tests, and provides references for each condition.

Christine notes:

"Just because something is on this list doesn't mean that it will definitely, or even probably, cause a false-positive. It depends on what
antibodies the individual carries as well as the characteristics of each particular test kit.

For instance, some, but not all people who have had blood transfusions,
prior pregnancies or an organ transplant will make HLA antibodies. And some, but not all test kits (both ELISA and Western blot) will be
contaminated with HLA antigens to which these antibodies can react. Only if these two conditions coincide might you get a false-positive
due to HLA cross-reactivity.

There are conditions that are more likely than others to cause false-positives. And there are some conditions that we aren't aware of yet which
may be documented in the future to cause false-positives. Some of the factors on the list have been documented only for ELISA, while some
have been documented for both ELISA and Western blot (WB) tests.

People may be eager to argue that if a factor is only known to cause false-positives on ELISA, this problem won't be carried over to the
WB. But remember, a WB is positive by virtue of accumulating enough individual positive bands to add up to the total required by whatever
criteria is used to interpret it 39. So the more exposure a person has had
to foreign antigens, proteins and infectious agents, the more various antibodies he or she will have in their system, and the more likely it is
that there will be several cross-reacting antibodies, enough to make the WB positive.

It is to be noted that all AIDS risk groups (and Africans as well), but not the general US or Western European population, have this problem
in common: they have been exposed to a plethora of foreign antigens and proteins. This is why people in the AIDS "risk groups" tend to
have positive WBs (i.e., to be considered "HIV-infected") and people in the
population don't. However, even people in low-risk populations have false-positive Western blots for poorly understood reasons 47.

Since false-positives to every single HIV protein have been documented 36, how do we know if the positive WB bands represent the various
proteins to HIV, or a collection of false-positive bands reacting to several different non-HIV antibodies?"

GREAT INFO. SO TRUE.

Answering the AIDS Denialists: CD4 (T-Cell) Counts, and Viral Load

AIDS TREATMENT NEWS Issue #341, April 21, 2000
Bruce Mirken


--------------------------------------------------------------------------------
The self-styled "AIDS dissidents," groups and individuals advocating the view that HIV does not cause AIDS, and often urging people with HIV to reject medical care, have raised their profile in recent months, ratcheting up their advocacy in the U.S. and attempting to influence the health policies of foreign governments. Although these forces sometimes accept the need to treat opportunistic infections, most reject the vast majority of conventional HIV/AIDS treatment, especially use of drugs to combat HIV. This article is part of a series in which AIDS TREATMENT NEWS examines key arguments put forth by the "dissidents"--perhaps more accurately termed "AIDS denialists," because most deny that AIDS is a genuine epidemic and many deny that the term "AIDS" even describes a real medical condition.
The AIDS denialist movement is not unified (for example, some groups say that HIV is a harmless virus, while others say HIV does not exist), so the summary here of some of their arguments is necessarily only a sketch. More detailed descriptions can be found in the references listed below.

Answering Denialist Views on CD4 (T-Cell) Tests

One consistent thread running through the denialist literature is the assertion that AIDS medicine has made a serious mistake by relying on laboratory markers such as CD4 cell counts, and viral load as measured by techniques such as polymerase chain reaction (PCR). These markers are criticized as unreliable at best and a devious effort to hide the failure of HIV/AIDS science at worst. One recently-formed group, ACT UP Hollywood (not connected with long-standing ACT UP chapters in New York, Philadelphia and elsewhere), argues that "all HIV and viral load tests as well as T-cell counts need to be banned immediately because they are useless indicators of a person's health."(1)

The arguments against use of CD4 center around two broad issues. One is the natural variability in CD4 counts, which can be lower than average for reasons not related to AIDS.(2,3) The other is whether or not CD4 numbers actually correlate with clinical prognosis. In her book WHAT IF EVERYTHING YOU THOUGHT YOU KNEW ABOUT AIDS WAS WRONG?, Christine Maggiore, founder of Los Angeles-based Alive and Well AIDS Alternatives, writes, "A number of studies found in the biomedical literature show that low T cell counts do not correlate with compromised immunity, and that normal ranges for T cells in HIV negative persons can vary from 300 to 2,000."(3) Some denialists cite the famous Concorde study of early versus deferred use of AZT monotherapy--in which an AZT-induced boost in CD4 counts did not translate to improved survival--as proof that, as one writer put it, "there was absolutely no correlation between CD4 T-cell counts and clinical health."(4)

The denialist argument appears to be built upon a narrow and highly selective reading of the data. For example one of the sources Maggiore cites as proof for the above statement that low CD4 counts can occur without HIV, a Transfusion Safety Study Group report at the 9th International AIDS Conference, specifically notes that HIV-negative individuals with two or more CD4 counts below 300 were rare, and that both those with known and unknown causes of immune suppression "differ from the retrovirus immunodeficiency pattern" in a number of key parameters, including CD4 percentage and CD4/CD8 ratio.(5)

In other words, transient low CD4 counts seen in other circumstances do not equal AIDS and bear little resemblance to what is typically seen in HIV-infected individuals. What the denialists regularly ignore is that while unusually low CD4 counts can occur for a variety of reasons, numerous large, long-term cohort studies have demonstrated a distinct pattern associated with HIV infection: A statistically significant CD4 decline commonly begins around the time of seroconversion and gradually becomes more severe over time, eventually leading to increased susceptibility to opportunistic infections. This has been observed in cohorts of gay men, transfusion recipients and hemophiliacs. In these cohorts a decline in CD4 count has been consistently and strongly associated with the development of AIDS-defining illnesses.(6)

Also neglected in denialist discussions of CD4 is the large body of evidence associating specific opportunistic infections with lowered CD4 counts. For example, in the Pulmonary Complications of HIV Study, an 1,182-person cohort, 79 percent of cases of pneumocystis carinii pneumonia (PCP) occurred in individuals with CD4 counts below 100 and 95 percent occurred in patients whose CD4 count was below 200.(7) The Multicenter AIDS Cohort Study (MACS) has also reported a "greatly increased risk" of PCP when CD4 counts drop below 200.(8) Numerous other studies have found similar associations between lowered CD4 counts and increased risk of PCP and other opportunistic infections.(6,9,10) Such findings formed the basis for long-standing recommendations regarding opportunistic infection prophylaxis (using drugs to prevent these infections). Other research relevant to this discussion is covered in the section on viral load, below.

Regarding the effect of treatment-induced increases in CD4 on clinical prognosis, the small increases seen in Concorde indeed did not correlate with improved long-term outcome. But numerous other studies do show a strong correlation with lowered risk of AIDS-defining opportunistic infections or death, particularly with larger, HAART-induced CD4 increases. In the U.S.-government trial ACTG 320 (which compared AZT plus 3TC vs. AZT plus 3TC plus indinavir [Crixivan(R)]), the indinavir group had a mean CD4 increase roughly three times that of the AZT/3TC only group, and half as many AIDS- defining events.(11) In a meta-analysis (combined analysis) of seven (mostly pre-HAART) antiretroviral studies, researchers found that "having either a reduction in HIV-1 RNA level or an increase in CD4+ lymphocyte count, or both, was associated with a delay in clinical disease progression."(12) Overall, a large body of evidence involving both treated and untreated patients shows a clear correlation between low or declining CD4 counts and increased risk of opportunistic infections or death.(13,14)

The denialist view of CD4 counts is used to call into question the 1993 revision of the CDC's AIDS case definition, which added a CD4 count of 200 or lower as an AIDS-defining condition. In Maggiore's words, it "allows HIV-positives with no symptoms or illness to be diagnosed with AIDS. Since 1993, more than half of all newly diagnosed AIDS cases are counted among people who are not sick."(3) The mass of evidence showing that HIV-infected individuals with CD4 counts below 200 are at overwhelmingly increased risk for life-threatening infections is simply ignored.

And on Viral Load

Maggiore states in her book that "low levels of viral load have not been correlated with good health, with absence of illness or high T-cell counts, while high viral loads do not correspond with low T-cells or sickness."(3) In a recent newspaper column she also complains that viral load tests are not FDA-approved for diagnosis of HIV infection, and notes, "Viral loads are found in people who test HIV-negative."(15) Denialist objection to viral load testing is bolstered by the fact that Kary Mullis, who won a Nobel prize for developing the basic technique of PCR, is a supporter of their cause and has questioned the use of his technique to quantify virus.(3)

In a 1996 article published in the denialist journal REAPPRAISING AIDS, authors Christine Johnson and Paul Philpott demonstrate their scorn for viral load measurements in the title of their discussion, "Viral Load of Crap." Focusing on the 1995 Ho and Shaw NATURE papers on viral dynamics, they write:

"Ho and Shaw's technique looks for HIV RNA, the genetic material found in the viral core. They assume that since each HIV contains two HIV RNAs, there must be one HIV for every two HIV RNAs they count. But the large amount of HIV RNA they report is found only after sending blood samples through polymerase chain reactions (PCR). PCR is the 'DNA fingerprinting' technology which takes tiny numbers of genetic molecules (RNA or DNA) and turns them into huge quantities." What these tests find, they argue, is meaningless: "Some of these are HIVs that have been neutralized by antibodies, some are defective HIVs (those that did not form correctly) and some are free-floating HIV RNA. Though none of these entities has any pathological capacity, the viral load technique confuses them with whole, infectious virus, the only kind that has any biological significance."(16)

This essay is typical of the denialist analysis of viral load, illustrating both its strengths and weaknesses. Like much of the movement's literature, they discuss only PCR and not the other technologies used to quantify viral load, mistakenly stating that Ho used PCR when in fact he used bDNA (branched DNA)--a different process marketed by a different company.(17,18)

Philpott and Johnson effectively lay out the theoretical reasons why PCR-based viral load tests might produce a misleading result. Indeed, company researchers and the FDA have acknowledged potential causes of error and variation in viral load results, and a potential margin of error in these assays of roughly threefold.(18,19) Thus, when the FDA approved the Roche Amplicor HIV-1 Monitor (a PCR-based assay), it required the labeling to indicate that the test can accurately detect a three-fold or greater change in HIV RNA for patients with a viral load of 1000 copies or greater and a six-fold or greater change for patients whose viral load is below 1000.(19) (Although Maggiore is correct in saying that the FDA has not approved PCR for diagnosing HIV infection, she neglects to mention that the agency did approve it "to assess patient prognosis... or to monitor the effect of antiviral therapy").

Strikingly, Philpott and Johnson stick entirely to theory and do not address the key question of whether or not viral load measurements predict the likelihood of disease progression or death in the real world. A very large body of evidence indicates they do, some of which was available prior to their dismissal of the tests as a "Viral Load of Crap." The mass of confirming data--from ongoing cohort studies as well as antiretroviral trials--that has accumulated since then is rarely acknowledged in denialist writings.

Beginning in 1995 John Mellors and colleagues published a series of articles detailing MACS cohort data showing a strong correlation between baseline viral load and subsequent disease progression.20,21,22 Using stored blood samples from patients' early study visits, Mellors examined the rates of AIDS-defining events and deaths in relation to viral load levels measured using bDNA. In a 1604-patient sample, only 0.9 percent of those whose baseline viral load was 500 copies or lower died of AIDS within six years, while 69.5 percent of those whose viral load was greater than 30,000 copies died. "Plasma viral load was the single best predictor of outcome," Mellors wrote, "followed by CD4+ lymphocyte counts [T-cell counts] and neopterin levels, beta2-microglobulin levels, and thrush or fever. We observed a strong association between viral load and the subsequent rate of decline in CD4+ lymphocyte counts."(22)

Similarly strong associations between viral load levels and clinical outcome have been reported in numerous other cohort studies, including the 1170-patient EuroSIDA cohort(23) and the Multicenter Hemophilia Cohort Study,(24) among others. In the hemophilia cohort, "each log(10) increase in baseline viral load was associated with a five-fold increase in risk for AIDS-related illness during the first six months of follow-up." The predictive value of viral load was independent of that of CD4 count.

One particularly interesting study looked at viral load in gay men in the Baltimore MACS cohort and injection drug users in the Baltimore "AIDS Link to Intravenous Experiences" (ALIVE) cohort. Rather than measuring plasma HIV-RNA in the usual way, using PCR or bDNA, this study looked at cell- associated infectious viral load using the quantitative microculture assay. This method "quantifies the biologically functional and infectious cell-associated HIV-1 by measuring the amount of HIV infected cells capable of infecting donor cells from an uninfected person in culture."(25) Looking at the risk of AIDS-defining infections, non-AIDS-defining bacterial infections, and death, the researchers found that "higher levels of infectious viral load were significantly related to increased hazards for all three outcomes," with little difference between the gay men and the intravenous drug users. After adjusting for CD4 level and numerous other factors, viral load was strongly predictive of risk of progression to AIDS.

The association between viral load (measured using bDNA or PCR) and clinical progression has been seen consistently in HIV treatment trials, including the meta-analysis of seven studies discussed above,(12) in which "each 10-fold decrease in HIV-1 RNA was associated with a 51 percent reduction in progression risk." In both the pivotal trial of ritonavir(26) and ACTG 320,(11) patients randomly assigned to the protease inhibitor arm showed significantly better suppression of viral load and significantly reduced AIDS-defining events.

After reviewing the available data, including numerous studies not listed here, the expert panel convened by the Department of Health and Human Services to determine HIV treatment guidelines recommended using both CD4 and viral load in conjunction with the clinical condition of the patient to guide therapeutic decision-making. The panel noted, "Multiple analyses in over 5,000 patients who participated in approximately 18 trials with viral load monitoring showed a statistically significant dose-response type association between decreases in plasma viremia and improved clinical outcome."(27)

Discussion of this data is notably absent even in current denialist literature. Maggiore's recent column,(15) for example, cites one article from 1993(28)--very early in the development of these assays--as "studies showing that viral load test results do not correlate with illness, with wellness, with T-cell counts or even the finding of virus by co-culture." This is at best a dubious interpretation of this study, and Maggiore fails to discuss any of the more recent evidence showing precisely the opposite. Evidence cited of viral loads found in HIV-negative people turns out to be a handful of anomalous cases, several of which involve false- negative antibody tests in people who clearly had AIDS.(29)

Evaluating the Evidence

No lab test or surrogate marker is perfect. All have innate limitations, natural variation, and a chance of error, and as a result HIV/AIDS researchers and treatment activists alike have cautioned that physicians must always remember they are treating patients, not lab values.

The limitations of CD4 and viral load tests, both real and theoretical, have been exhaustively described by the denialists. But their declarations that these tests are meaningless are based on a skewed, highly selective reading of the data that simply omits anything which might contradict their views. The overwhelming preponderance of evidence strongly indicates that both CD4 and viral load measurements can provide useful and important information that doctors and patients can use to evaluate progress and make treatment decisions.

For More Information

Many of the denialist Web sites and books are accessible through the references below.

Unfortunately, the medical mainstream has usually not bothered to answer these views--so persons with sincere questions have heard only one side. This is changing. Meanwhile, the U.S. National Institute of Allergy and Infectious Diseases has prepared a page of links to publications with evidence that HIV causes AIDS, http://www.niaid.nih.gov/spotlight/hiv00/default.htm . Also, see http://www.aegis.org/topics/aids_debate.html .

References

1. ACT UP Hollywood home page, http://www.outspoken.org/actuphollywood/index.html

2. Strausberg, John. THE AIDS HERETICS. New York Press. March 9, 2000; 13: 10.

3. Maggiore, Christine. WHAT IF EVERYTHING YOU THOUGHT YOU KNEW ABOUT AIDS WAS WRONG (4th Edition, 2000). American Foundation for AIDS Alternatives, Studio City, California.

4. Conlan, Mark Gabrish. Interview: John Lauritsen. ZENGER'S. April 1997.

5. Mosley, James. Idiopathic CD4+ Lymphocytopenia: Other Lymphocyte Changes. IX International Conference on AIDS, Berlin, 1993, abstract #WS-A25-5.

6. Stein, Daniel S, Korvick, Joyce A. and Vermund, Sten H. CD4+ Lymphocyte Cell Enumeration for Prediction of Clinical Course of Human Immunodeficiency Virus Disease, a Review. JOURNAL OF INFECTIOUS DISEASES, 1992; 165: 352-363.

7. Stansell, J.D., and others. Predictors of Pneumocystis carinii pneumonia in HIV-infected persons. Pulmonary Complications of AIDS Study Group. AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE. January 1997; 155:1, 60-66.

8. Phair, J., and others. The risk of Pneumocystis carinii pneumonia among men infected with human immunodeficiency virus type 1. Multicenter AIDS Cohort Study Group. NEW ENGLAND JOURNAL OF MEDICINE. January 1990; 322:3, 161-165.

9. Nightingale, SD, and others. Incidence of Mycobacterium avium-intracellulare complex bacteremia in human immunodeficiency virus-positive patients. JOURNAL OF INFECTIOUS DISEASES. June 1992; 165: 6, 1082-1085.

10. Spaide, R.F., Gaissinger, A., and Podhorzer, J.R. Risk factors for cotton-wool spots and for cytomegalovirus retinitis in patients with human immunodeficiency virus infection OPHTHALMOLOGY. December 1995; 102:12, 1860-1864.

11. Hammer, S., and others. A controlled trial of two nucleoside analogues plus indinavir in persons with human immunodeficiency virus infection and CD4 cell counts of 200 per cubic milliliter or less. NEW ENGLAND JOURNAL OF MEDICINE. 1997; 337: 725-733.

12. Marschner, I. C., and others. Use of Changes in Plasma Levels of Human Immunodeficiency Virus Type 1 RNA to Assess the Clinical Benefit of Antiretroviral Therapy. JOURNAL OF INFECTIOUS DISEASES. 1998; 177: 40-47.

13. Smith, D.K., and others. Causes and rates of death among HIV-infected women 1993-1998: The contribution of illicit drug use and suboptimal HAART use. 7th Conference on Retroviruses and Opportunistic Infections, San Francisco, January 30-February 2, 2000, abstract #682.

14. O'Brien, William A., and others. Changes in plasma HIV RNA level and CD4+ lymphocyte counts predict both response to antiretroviral therapy and therapeutic failure. ANNALS OF INTERNAL MEDICINE. 1997; 126: 939-945.

15. Maggiore, Christine, Questioning AIDS, Q & A. MAGNUS. March/April, 2000.

16. Johnson, Christine and Philpott, Paul. Viral Load of Crap. REAPPRAISING AIDS. October, 1996.

17. Ho, D.D., and others. Rapid turnover of plasma virions and CD4 lymphocytes in HIV-1 infection. NATURE. January 12, 1995; 373: 123-126.

18. Todd, J. Performance Characteristics for the quantitation of plasma HIV-1 RNA using the branched DNA signal amplification technology. JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY. 1995; 10: supplement 2, S35-44.

19. Food and Drug Administration, letter to Roche Molecular Systems, March 2, 1999.

20. Mellors, J., and others. Quantitation of HIV-1 RNA in plasma predicts outcome after seroconversion. ANNALS OF INTERNAL MEDICINE. 1995; 122: 573-579.

21. Mellors, J., and others. Prognosis in HIV-1 infection predicted by the quantity of virus in plasma. SCIENCE. May 24, 1996; 272: 1167-1170.

22. Mellors, J., and others. Plasma viral load and CD4+ lymphocytes as prognostic markers in HIV-1 infection. ANNALS OF INTERNAL MEDICINE. 1997; 126: 946-954.

23. Miller, V., and others. Association of viral load, CD4 cell count, and treatment with clinical progression in HIV patients with very low CD4 cell counts: The EuroSIDA cohort. 7th Conference on Retroviruses and Opportunistic Infections, San Francisco, January 30-February 2, 2000, abstract #454.

24. Engels, E., and others. Plasma HIV-1 viral load in patients with hemophilia and late-stage HIV disease: A measure of current immune suppression. ANNALS OF INTERNAL MEDICINE. 1999; 131:256-264.

25. Lyles, C.M., and others. Cell-associated infectious HIV-1 load as a predictor of clinical progression and survival among HIV-1 infected injection drug users and homosexual men. EUROPEAN JOURNAL OF EPIDEMIOLOGY. 1999, 15:99-108.

26. Cameron, D.W., and others. Randomized placebo-controlled trial of ritonavir in advanced HIV-1 disease. THE LANCET. February 21, 1998; 321: 543-549.

27. Panel on Clinical Practices for Treatment of HIV Infection. GUIDELINES FOR THE USE OF ANTIRETROVIRAL AGENTS IN HIV-INFECTED ADULTS AND ADOLESCENTS. January 28, 2000. (This document is available at http://www.hivatis.org .)

28. Piatak, M, and others. High levels of HIV-1 in plasma during all stages of infection determined by competitive PCR. SCIENCE. March 1993; 259: 1749-1753.

29. Sullivan, P.S., and others. Persistently negative HIV-1 antibody enzyme immunoassay results for patients with HIV-1 infection and AIDS: serologic, clinical and virologic results. Seronegative AIDS Clinical Study Group. AIDS. January 1999; 12:1, 89-96.

Answering the AIDS Denialists: CD4 (T-Cell) Counts, and Viral Load

AIDS TREATMENT NEWS Issue #341, April 21, 2000
Bruce Mirken


--------------------------------------------------------------------------------
The self-styled "AIDS dissidents," groups and individuals advocating the view that HIV does not cause AIDS, and often urging people with HIV to reject medical care, have raised their profile in recent months, ratcheting up their advocacy in the U.S. and attempting to influence the health policies of foreign governments. Although these forces sometimes accept the need to treat opportunistic infections, most reject the vast majority of conventional HIV/AIDS treatment, especially use of drugs to combat HIV. This article is part of a series in which AIDS TREATMENT NEWS examines key arguments put forth by the "dissidents"--perhaps more accurately termed "AIDS denialists," because most deny that AIDS is a genuine epidemic and many deny that the term "AIDS" even describes a real medical condition.
The AIDS denialist movement is not unified (for example, some groups say that HIV is a harmless virus, while others say HIV does not exist), so the summary here of some of their arguments is necessarily only a sketch. More detailed descriptions can be found in the references listed below.

Answering Denialist Views on CD4 (T-Cell) Tests

One consistent thread running through the denialist literature is the assertion that AIDS medicine has made a serious mistake by relying on laboratory markers such as CD4 cell counts, and viral load as measured by techniques such as polymerase chain reaction (PCR). These markers are criticized as unreliable at best and a devious effort to hide the failure of HIV/AIDS science at worst. One recently-formed group, ACT UP Hollywood (not connected with long-standing ACT UP chapters in New York, Philadelphia and elsewhere), argues that "all HIV and viral load tests as well as T-cell counts need to be banned immediately because they are useless indicators of a person's health."(1)

The arguments against use of CD4 center around two broad issues. One is the natural variability in CD4 counts, which can be lower than average for reasons not related to AIDS.(2,3) The other is whether or not CD4 numbers actually correlate with clinical prognosis. In her book WHAT IF EVERYTHING YOU THOUGHT YOU KNEW ABOUT AIDS WAS WRONG?, Christine Maggiore, founder of Los Angeles-based Alive and Well AIDS Alternatives, writes, "A number of studies found in the biomedical literature show that low T cell counts do not correlate with compromised immunity, and that normal ranges for T cells in HIV negative persons can vary from 300 to 2,000."(3) Some denialists cite the famous Concorde study of early versus deferred use of AZT monotherapy--in which an AZT-induced boost in CD4 counts did not translate to improved survival--as proof that, as one writer put it, "there was absolutely no correlation between CD4 T-cell counts and clinical health."(4)

The denialist argument appears to be built upon a narrow and highly selective reading of the data. For example one of the sources Maggiore cites as proof for the above statement that low CD4 counts can occur without HIV, a Transfusion Safety Study Group report at the 9th International AIDS Conference, specifically notes that HIV-negative individuals with two or more CD4 counts below 300 were rare, and that both those with known and unknown causes of immune suppression "differ from the retrovirus immunodeficiency pattern" in a number of key parameters, including CD4 percentage and CD4/CD8 ratio.(5)

In other words, transient low CD4 counts seen in other circumstances do not equal AIDS and bear little resemblance to what is typically seen in HIV-infected individuals. What the denialists regularly ignore is that while unusually low CD4 counts can occur for a variety of reasons, numerous large, long-term cohort studies have demonstrated a distinct pattern associated with HIV infection: A statistically significant CD4 decline commonly begins around the time of seroconversion and gradually becomes more severe over time, eventually leading to increased susceptibility to opportunistic infections. This has been observed in cohorts of gay men, transfusion recipients and hemophiliacs. In these cohorts a decline in CD4 count has been consistently and strongly associated with the development of AIDS-defining illnesses.(6)

Also neglected in denialist discussions of CD4 is the large body of evidence associating specific opportunistic infections with lowered CD4 counts. For example, in the Pulmonary Complications of HIV Study, an 1,182-person cohort, 79 percent of cases of pneumocystis carinii pneumonia (PCP) occurred in individuals with CD4 counts below 100 and 95 percent occurred in patients whose CD4 count was below 200.(7) The Multicenter AIDS Cohort Study (MACS) has also reported a "greatly increased risk" of PCP when CD4 counts drop below 200.(8) Numerous other studies have found similar associations between lowered CD4 counts and increased risk of PCP and other opportunistic infections.(6,9,10) Such findings formed the basis for long-standing recommendations regarding opportunistic infection prophylaxis (using drugs to prevent these infections). Other research relevant to this discussion is covered in the section on viral load, below.

Regarding the effect of treatment-induced increases in CD4 on clinical prognosis, the small increases seen in Concorde indeed did not correlate with improved long-term outcome. But numerous other studies do show a strong correlation with lowered risk of AIDS-defining opportunistic infections or death, particularly with larger, HAART-induced CD4 increases. In the U.S.-government trial ACTG 320 (which compared AZT plus 3TC vs. AZT plus 3TC plus indinavir [Crixivan(R)]), the indinavir group had a mean CD4 increase roughly three times that of the AZT/3TC only group, and half as many AIDS- defining events.(11) In a meta-analysis (combined analysis) of seven (mostly pre-HAART) antiretroviral studies, researchers found that "having either a reduction in HIV-1 RNA level or an increase in CD4+ lymphocyte count, or both, was associated with a delay in clinical disease progression."(12) Overall, a large body of evidence involving both treated and untreated patients shows a clear correlation between low or declining CD4 counts and increased risk of opportunistic infections or death.(13,14)

The denialist view of CD4 counts is used to call into question the 1993 revision of the CDC's AIDS case definition, which added a CD4 count of 200 or lower as an AIDS-defining condition. In Maggiore's words, it "allows HIV-positives with no symptoms or illness to be diagnosed with AIDS. Since 1993, more than half of all newly diagnosed AIDS cases are counted among people who are not sick."(3) The mass of evidence showing that HIV-infected individuals with CD4 counts below 200 are at overwhelmingly increased risk for life-threatening infections is simply ignored.

And on Viral Load

Maggiore states in her book that "low levels of viral load have not been correlated with good health, with absence of illness or high T-cell counts, while high viral loads do not correspond with low T-cells or sickness."(3) In a recent newspaper column she also complains that viral load tests are not FDA-approved for diagnosis of HIV infection, and notes, "Viral loads are found in people who test HIV-negative."(15) Denialist objection to viral load testing is bolstered by the fact that Kary Mullis, who won a Nobel prize for developing the basic technique of PCR, is a supporter of their cause and has questioned the use of his technique to quantify virus.(3)

In a 1996 article published in the denialist journal REAPPRAISING AIDS, authors Christine Johnson and Paul Philpott demonstrate their scorn for viral load measurements in the title of their discussion, "Viral Load of Crap." Focusing on the 1995 Ho and Shaw NATURE papers on viral dynamics, they write:

"Ho and Shaw's technique looks for HIV RNA, the genetic material found in the viral core. They assume that since each HIV contains two HIV RNAs, there must be one HIV for every two HIV RNAs they count. But the large amount of HIV RNA they report is found only after sending blood samples through polymerase chain reactions (PCR). PCR is the 'DNA fingerprinting' technology which takes tiny numbers of genetic molecules (RNA or DNA) and turns them into huge quantities." What these tests find, they argue, is meaningless: "Some of these are HIVs that have been neutralized by antibodies, some are defective HIVs (those that did not form correctly) and some are free-floating HIV RNA. Though none of these entities has any pathological capacity, the viral load technique confuses them with whole, infectious virus, the only kind that has any biological significance."(16)

This essay is typical of the denialist analysis of viral load, illustrating both its strengths and weaknesses. Like much of the movement's literature, they discuss only PCR and not the other technologies used to quantify viral load, mistakenly stating that Ho used PCR when in fact he used bDNA (branched DNA)--a different process marketed by a different company.(17,18)

Philpott and Johnson effectively lay out the theoretical reasons why PCR-based viral load tests might produce a misleading result. Indeed, company researchers and the FDA have acknowledged potential causes of error and variation in viral load results, and a potential margin of error in these assays of roughly threefold.(18,19) Thus, when the FDA approved the Roche Amplicor HIV-1 Monitor (a PCR-based assay), it required the labeling to indicate that the test can accurately detect a three-fold or greater change in HIV RNA for patients with a viral load of 1000 copies or greater and a six-fold or greater change for patients whose viral load is below 1000.(19) (Although Maggiore is correct in saying that the FDA has not approved PCR for diagnosing HIV infection, she neglects to mention that the agency did approve it "to assess patient prognosis... or to monitor the effect of antiviral therapy").

Strikingly, Philpott and Johnson stick entirely to theory and do not address the key question of whether or not viral load measurements predict the likelihood of disease progression or death in the real world. A very large body of evidence indicates they do, some of which was available prior to their dismissal of the tests as a "Viral Load of Crap." The mass of confirming data--from ongoing cohort studies as well as antiretroviral trials--that has accumulated since then is rarely acknowledged in denialist writings.

Beginning in 1995 John Mellors and colleagues published a series of articles detailing MACS cohort data showing a strong correlation between baseline viral load and subsequent disease progression.20,21,22 Using stored blood samples from patients' early study visits, Mellors examined the rates of AIDS-defining events and deaths in relation to viral load levels measured using bDNA. In a 1604-patient sample, only 0.9 percent of those whose baseline viral load was 500 copies or lower died of AIDS within six years, while 69.5 percent of those whose viral load was greater than 30,000 copies died. "Plasma viral load was the single best predictor of outcome," Mellors wrote, "followed by CD4+ lymphocyte counts [T-cell counts] and neopterin levels, beta2-microglobulin levels, and thrush or fever. We observed a strong association between viral load and the subsequent rate of decline in CD4+ lymphocyte counts."(22)

Similarly strong associations between viral load levels and clinical outcome have been reported in numerous other cohort studies, including the 1170-patient EuroSIDA cohort(23) and the Multicenter Hemophilia Cohort Study,(24) among others. In the hemophilia cohort, "each log(10) increase in baseline viral load was associated with a five-fold increase in risk for AIDS-related illness during the first six months of follow-up." The predictive value of viral load was independent of that of CD4 count.

One particularly interesting study looked at viral load in gay men in the Baltimore MACS cohort and injection drug users in the Baltimore "AIDS Link to Intravenous Experiences" (ALIVE) cohort. Rather than measuring plasma HIV-RNA in the usual way, using PCR or bDNA, this study looked at cell- associated infectious viral load using the quantitative microculture assay. This method "quantifies the biologically functional and infectious cell-associated HIV-1 by measuring the amount of HIV infected cells capable of infecting donor cells from an uninfected person in culture."(25) Looking at the risk of AIDS-defining infections, non-AIDS-defining bacterial infections, and death, the researchers found that "higher levels of infectious viral load were significantly related to increased hazards for all three outcomes," with little difference between the gay men and the intravenous drug users. After adjusting for CD4 level and numerous other factors, viral load was strongly predictive of risk of progression to AIDS.

The association between viral load (measured using bDNA or PCR) and clinical progression has been seen consistently in HIV treatment trials, including the meta-analysis of seven studies discussed above,(12) in which "each 10-fold decrease in HIV-1 RNA was associated with a 51 percent reduction in progression risk." In both the pivotal trial of ritonavir(26) and ACTG 320,(11) patients randomly assigned to the protease inhibitor arm showed significantly better suppression of viral load and significantly reduced AIDS-defining events.

After reviewing the available data, including numerous studies not listed here, the expert panel convened by the Department of Health and Human Services to determine HIV treatment guidelines recommended using both CD4 and viral load in conjunction with the clinical condition of the patient to guide therapeutic decision-making. The panel noted, "Multiple analyses in over 5,000 patients who participated in approximately 18 trials with viral load monitoring showed a statistically significant dose-response type association between decreases in plasma viremia and improved clinical outcome."(27)

Discussion of this data is notably absent even in current denialist literature. Maggiore's recent column,(15) for example, cites one article from 1993(28)--very early in the development of these assays--as "studies showing that viral load test results do not correlate with illness, with wellness, with T-cell counts or even the finding of virus by co-culture." This is at best a dubious interpretation of this study, and Maggiore fails to discuss any of the more recent evidence showing precisely the opposite. Evidence cited of viral loads found in HIV-negative people turns out to be a handful of anomalous cases, several of which involve false- negative antibody tests in people who clearly had AIDS.(29)

Evaluating the Evidence

No lab test or surrogate marker is perfect. All have innate limitations, natural variation, and a chance of error, and as a result HIV/AIDS researchers and treatment activists alike have cautioned that physicians must always remember they are treating patients, not lab values.

The limitations of CD4 and viral load tests, both real and theoretical, have been exhaustively described by the denialists. But their declarations that these tests are meaningless are based on a skewed, highly selective reading of the data that simply omits anything which might contradict their views. The overwhelming preponderance of evidence strongly indicates that both CD4 and viral load measurements can provide useful and important information that doctors and patients can use to evaluate progress and make treatment decisions.

For More Information

Many of the denialist Web sites and books are accessible through the references below.

Unfortunately, the medical mainstream has usually not bothered to answer these views--so persons with sincere questions have heard only one side. This is changing. Meanwhile, the U.S. National Institute of Allergy and Infectious Diseases has prepared a page of links to publications with evidence that HIV causes AIDS, http://www.niaid.nih.gov/spotlight/hiv00/default.htm . Also, see http://www.aegis.org/topics/aids_debate.html .

References

1. ACT UP Hollywood home page, http://www.outspoken.org/actuphollywood/index.html

2. Strausberg, John. THE AIDS HERETICS. New York Press. March 9, 2000; 13: 10.

3. Maggiore, Christine. WHAT IF EVERYTHING YOU THOUGHT YOU KNEW ABOUT AIDS WAS WRONG (4th Edition, 2000). American Foundation for AIDS Alternatives, Studio City, California.

4. Conlan, Mark Gabrish. Interview: John Lauritsen. ZENGER'S. April 1997.

5. Mosley, James. Idiopathic CD4+ Lymphocytopenia: Other Lymphocyte Changes. IX International Conference on AIDS, Berlin, 1993, abstract #WS-A25-5.

6. Stein, Daniel S, Korvick, Joyce A. and Vermund, Sten H. CD4+ Lymphocyte Cell Enumeration for Prediction of Clinical Course of Human Immunodeficiency Virus Disease, a Review. JOURNAL OF INFECTIOUS DISEASES, 1992; 165: 352-363.

7. Stansell, J.D., and others. Predictors of Pneumocystis carinii pneumonia in HIV-infected persons. Pulmonary Complications of AIDS Study Group. AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE. January 1997; 155:1, 60-66.

8. Phair, J., and others. The risk of Pneumocystis carinii pneumonia among men infected with human immunodeficiency virus type 1. Multicenter AIDS Cohort Study Group. NEW ENGLAND JOURNAL OF MEDICINE. January 1990; 322:3, 161-165.

9. Nightingale, SD, and others. Incidence of Mycobacterium avium-intracellulare complex bacteremia in human immunodeficiency virus-positive patients. JOURNAL OF INFECTIOUS DISEASES. June 1992; 165: 6, 1082-1085.

10. Spaide, R.F., Gaissinger, A., and Podhorzer, J.R. Risk factors for cotton-wool spots and for cytomegalovirus retinitis in patients with human immunodeficiency virus infection OPHTHALMOLOGY. December 1995; 102:12, 1860-1864.

11. Hammer, S., and others. A controlled trial of two nucleoside analogues plus indinavir in persons with human immunodeficiency virus infection and CD4 cell counts of 200 per cubic milliliter or less. NEW ENGLAND JOURNAL OF MEDICINE. 1997; 337: 725-733.

12. Marschner, I. C., and others. Use of Changes in Plasma Levels of Human Immunodeficiency Virus Type 1 RNA to Assess the Clinical Benefit of Antiretroviral Therapy. JOURNAL OF INFECTIOUS DISEASES. 1998; 177: 40-47.

13. Smith, D.K., and others. Causes and rates of death among HIV-infected women 1993-1998: The contribution of illicit drug use and suboptimal HAART use. 7th Conference on Retroviruses and Opportunistic Infections, San Francisco, January 30-February 2, 2000, abstract #682.

14. O'Brien, William A., and others. Changes in plasma HIV RNA level and CD4+ lymphocyte counts predict both response to antiretroviral therapy and therapeutic failure. ANNALS OF INTERNAL MEDICINE. 1997; 126: 939-945.

15. Maggiore, Christine, Questioning AIDS, Q & A. MAGNUS. March/April, 2000.

16. Johnson, Christine and Philpott, Paul. Viral Load of Crap. REAPPRAISING AIDS. October, 1996.

17. Ho, D.D., and others. Rapid turnover of plasma virions and CD4 lymphocytes in HIV-1 infection. NATURE. January 12, 1995; 373: 123-126.

18. Todd, J. Performance Characteristics for the quantitation of plasma HIV-1 RNA using the branched DNA signal amplification technology. JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY. 1995; 10: supplement 2, S35-44.

19. Food and Drug Administration, letter to Roche Molecular Systems, March 2, 1999.

20. Mellors, J., and others. Quantitation of HIV-1 RNA in plasma predicts outcome after seroconversion. ANNALS OF INTERNAL MEDICINE. 1995; 122: 573-579.

21. Mellors, J., and others. Prognosis in HIV-1 infection predicted by the quantity of virus in plasma. SCIENCE. May 24, 1996; 272: 1167-1170.

22. Mellors, J., and others. Plasma viral load and CD4+ lymphocytes as prognostic markers in HIV-1 infection. ANNALS OF INTERNAL MEDICINE. 1997; 126: 946-954.

23. Miller, V., and others. Association of viral load, CD4 cell count, and treatment with clinical progression in HIV patients with very low CD4 cell counts: The EuroSIDA cohort. 7th Conference on Retroviruses and Opportunistic Infections, San Francisco, January 30-February 2, 2000, abstract #454.

24. Engels, E., and others. Plasma HIV-1 viral load in patients with hemophilia and late-stage HIV disease: A measure of current immune suppression. ANNALS OF INTERNAL MEDICINE. 1999; 131:256-264.

25. Lyles, C.M., and others. Cell-associated infectious HIV-1 load as a predictor of clinical progression and survival among HIV-1 infected injection drug users and homosexual men. EUROPEAN JOURNAL OF EPIDEMIOLOGY. 1999, 15:99-108.

26. Cameron, D.W., and others. Randomized placebo-controlled trial of ritonavir in advanced HIV-1 disease. THE LANCET. February 21, 1998; 321: 543-549.

27. Panel on Clinical Practices for Treatment of HIV Infection. GUIDELINES FOR THE USE OF ANTIRETROVIRAL AGENTS IN HIV-INFECTED ADULTS AND ADOLESCENTS. January 28, 2000. (This document is available at http://www.hivatis.org .)

28. Piatak, M, and others. High levels of HIV-1 in plasma during all stages of infection determined by competitive PCR. SCIENCE. March 1993; 259: 1749-1753.

29. Sullivan, P.S., and others. Persistently negative HIV-1 antibody enzyme immunoassay results for patients with HIV-1 infection and AIDS: serologic, clinical and virologic results. Seronegative AIDS Clinical Study Group. AIDS. January 1999; 12:1, 89-96.

modern HIV treatment on improved survival. Some cautions:

(1) Almost all doctors today agree that not everyone infected with HIV needs to take antiretroviral or other drugs. But everyone with HIV does need medical monitoring and care -- and access to treatment when and if it is appropriate for them.

(2) Just because studies described below found that those with treatment had a fraction of the death rate of those without does not necessarily mean that your chance of survival will be correspondingly increased by antiretrovirals. The reduced death rates reflect the benefit of treatment for those who needed it most.

This article is part of our series to counter misinformation about AIDS treatment and prevention. Fringe groups are aggressively promoting such ideas as that HIV is harmless (or does not exist) in ways that encourage people to ignore medical and infection-control advice, risking their own health and the health of others. They are telling people that AIDS drugs are worthless poisons, prescribed because of a vast mistake or corruption, and suggesting that people with HIV or AIDS reject most or all medical care for that condition.

These bizarre theories -- sometimes presented with dozens of hundreds of misused references or snippets from legitimate scientific articles -- have led some people with HIV to stop all medical care based on one-size-fits-all conspiracy theories, regardless of their individual medical condition. Some of the believers are highly intelligent, and properly skeptical of mainstream authority; some have sincerely tried to investigate both sides of the controversy. Often they have found mainstream professionals too busy to talk with them, and not interested in explaining their work to the public -- while medical cultists, flush with mystery money but with no responsibilities for actual AIDS research or patient care, have spent years learning how to slickly package their arguments, complete with celebrity endorsements.

The following article, and others in this series, focus on bringing together findings of recognized scientists and explaining them for those who are not medical specialists. All of the articles will be available on our Web site (http://www.aidsnews.org).


John S. James, AIDS Treatment News


* * * * * *

A sharp decline in AIDS deaths in the United States, Canada, Europe, and Australia began in 1996, coinciding with the widespread adoption of what has become known as "highly active antiretroviral therapy" (sometimes abbreviated "HAART"). These combination treatments have received much of the credit for the plunging death rate.

But AIDS denialist have disputed this claim, branding it a "myth." The denialists -- who prefer to call themselves "AIDS dissidents" -- not only reject the evidence that HIV causes AIDS, most even reject the idea that the term "AIDS" describes a unique medical condition. The denialists include a handful of scientists who had substantial credentials but have done little or no research with actual AIDS patients. Although members of this movement don't agree completely, most reject virtually all accepted HIV/AIDS medical treatment, as well as the use of condoms and safer sex to prevent AIDS.

Debate about the impact of anti-HIV drugs long precedes the advent of HAART. In 1992 this writer asked the late Michael Callen, an early AIDS activist and persistent skeptic about HIV, what would convince him that HIV caused AIDS. His immediate answer: "If antiretroviral drugs actually made people better." Callen, who unequivocally accepted the fact that AIDS was something new and deadly even as he doubted HIV's role in it, saw the minimal impact of the drugs available at the time -- AZT, ddI and ddC, generally used as monotherapy (single drug treatment) -- as corroborating his belief that HIV was not the cause.

While factions in the denialist camp disagree about what actually makes people with AIDS sick, there is nearly universal agreement in the movement that anti-HIV drugs are useless or worse. HIV is irrelevant, they argue, so the drugs provide nothing but toxicity.


"Die Offs" and "Shocking Statistics"

When a steady stream of reports of improved health and decreasing death rates started to flood the media in 1996 and 1997, denialists like AZT: Poison by Prescription author John Lauritsen dismissed them as so much smoke and mirrors. In a March 1997 talk he attributed the apparent good news to the "psychological effect" of people with AIDS being "expected to have a Lazarus recovery" and to "the selective reporting of anecdotes."1 He predicted that this house of cards would soon collapse, declaring, "I expect within the next half year or year we'll see a perfectly hideous crash, a die-off."
But the die-off failed to materialize. The Centers for Disease Control and Prevention continued to log declines in AIDS deaths in 1997, 1998 and -- tentatively, as reporting may still be incomplete -- 1999.2,3


As it has become indisputable that the drop in AIDS deaths is real, other explanations have been put forth. In her book, What If Everything You Thought You Knew About AIDS Was Wrong?, Christine Maggiore suggests that "a more likely explanation for decreased deaths would be the change in the official AIDS definition adopted in 1993, which allows HIV positives with no symptoms or illness to be diagnosed with AIDS. Since 1993, more than half of all newly diagnosed AIDS cases are counted among people who are not sick."

The logic behind this statement is unclear. If, as Maggiore argues, CD4 cell counts do not correlate with health or illness, then the 1993 addition of a CD4 count below 200 as an AIDS-defining condition has qualified some perfectly healthy people for an AIDS diagnosis. But giving otherwise healthy people an AIDS diagnosis would not necessarily affect either the number of people who had AIDS based on the old criteria or their survival prospects. If, as some charge, the drugs actually cause AIDS, it might even increase the number of AIDS deaths by encouraging healthy people to go on toxic regimens.

In her book and on the Web site of Alive and Well AIDS Alternatives, Maggiore makes a second argument: "AIDS deaths began to decline in 1994, two years before the new 'AIDS cocktails' were made available for general use," and so shouldn't be credited with a trend that had already started.4,5

In fact, according to the U.S. Centers for Disease Control and Prevention (CDC), U.S. AIDS deaths rose from 45,271 in 1993 to 49,677 in 1994 and 49,992 in 1995. AIDS deaths dropped to 36,930 in 1996, 20,945 in 1997 and 16,432 in 1998, the lowest number since 1986.3

A variation on this argument -- that the decline in AIDS deaths began well before the advent of HAART -- was put forth by Celia Farber in the March, 2000 issue of Gear. She quotes David Pasquarelli, of the group that calls itself ACT UP San Francisco, writing that his organization "recently unearthed a 1997 study by San Francisco Health Department director Dr. Mitch Katz which exposes a shocking statistic which would appear to dispel the claim that the cocktails have caused AIDS deaths to plummet. Using stored blood samples and computer analyses, the study, published in the Journal of AIDS and Human Retrovirology, concluded that new HIV-antibody positive diagnoses peaked in 1982 in San Francisco -- two years before AIDS even had a name." She notes that the study estimated new HIV infections in San Francisco at 500 per year from 1987 on, adding that "Katz has since confirmed the group interpreted his data correctly."6


The study projected that reduced rates of HIV transmission would lead to fewer AIDS cases a decade later. But in announcing this "shocking" fact Farber never explains why she and Pasquarelli seem to fully accept estimates based on an assumption both have emphatically rejected: that HIV causes AIDS.7 This also may be the only time ACT UP San Francisco has agreed with Katz, whom it accused of "genocide" in 1997 for studying post-exposure prophylaxis,8 and more recently branded "a lying AIDS industry clown who pulls bogus HIV increases out of a hat in order to secure funding." 9

Farber's claim that Katz accepts ACT UP San Francisco's interpretation of his data is mistaken. The key conclusion, that reduced HIV transmission in the 1980s foreshadowed fewer AIDS cases in the 1990s, is stated explicitly in the article and requires no interpretation. Katz firmly disputes the claim that HAART has had no effect.

The numbers of actual and projected AIDS cases -- not mentioned in Farber's article -- appear to back him up. Katz and colleagues, assuming that treatment would only be as effective as AZT monotherapy and adjusting for distortions caused by the 1993 change in the CDC AIDS definition, projected that the drop would level out beginning in 1995 with 1,283 new AIDS cases that year, 1,200 in 1996, 1,122 in 1997 and 1,115 in 1998.7 But 1995 saw 1,743 AIDS cases, 40 percent above the projection. In 1996, the year protease-based combinations became the standard of care, new cases plunged to 1,178. They kept dropping to 899 in 1997 and 713 in 1998 -- more than a third below projected levels. "That," says Katz, "is the treatment effect."10


What the Cohort Studies Say

Still, the basic issue put forth by Farber, Pasquarelli and Maggiore needs to be answered: If some unknown factor or factors unrelated to treatment reduced the number of AIDS patients, HAART could be receiving undeserved credit for the drop in deaths. On the other hand, if it can be shown that HAART has substantially improved patients' survival it is at least partly responsible for the good news.

The critical question, then, is: Is there evidence that HAART has improved the survival of HIV/AIDS patients? According to a leading denialist, University of California chemist David Rasnick, "It may come as a surprise that there is not even one study in the vast scientific, medical literature that shows that... a group of HIV-positive adults or children who take the anti-HIV drugs live longer or better quality lives than a similar group of adults or children who are HIV-positive and do not take the drugs.'11

In fact there is an abundance of such evidence. Some, from clinical trials, has been discussed in detail in medical articles and at conferences. But clinical trials, conducted on limited numbers of patients for a relatively short time, with care often provided by physicians with more HIV expertise than average doctors, might not reflect what happens to most patients.

Real-world information on the impact of HAART in daily practice comes from what are known as cohort studies, which follow the experiences of specific groups of patients over extended periods of time. A number of large, prospective cohorts, specifically set up to track both the natural course of HIV infection and the effects of treatment and behavioral factors, have now reported results covering the pre and post-HAART eras. Additionally, a number of individual hospitals and clinics have reported on the impact of HAART on their patients.

The results from these cohorts, covering tens of thousands of patients from a wide range of locations and backgrounds, have been astonishingly consistent despite differing methodologies: When HAART is introduced, opportunistic infections and deaths drop. Patients on anti-HIV therapy do better than those on no therapy, and those on regimens involving more drugs do better than those on fewer. Most of these analyses, by focusing on deaths among patients already diagnosed with AIDS, are not affected by any overall reduction in the number of AIDS cases, whether due to reduced HIV transmission or some unknown factor.

One of the world's largest AIDS cohorts is the CDC's Adult/Adolescent Spectrum of Disease Project. The ASD project began in 1990 and has enrolled over 49,000 participants at 93 hospitals and clinics in nine cities. As of January 1998, 19,565 had an AIDS diagnosis by the 1993 definition.


During that period 9,280 deaths were recorded, and researcher Amy McNaughten and colleagues included in their analysis all except 188 deaths caused by murder, suicide or drug overdose. Average survival time after diagnosis increased in the later years of the study, coinciding with a shift from monotherapy (a single antiretroviral, such as AZT alone, or ddI alone) to two-drug regimens, and later to three-drug HAART combinations. All anti-HIV regimens improved survival compared to no treatment, with more intensive regimens producing greater improvement. Patients on three-drug combinations had a 1.6 times lower risk of death than those on dual therapy and a 2.5 times lower risk of death than those on monotherapy.12

The ASD researchers later reported that incidence of AIDS-defining opportunistic infections in the whole study population of over 49,000 patients plummeted when HAART came into common use in 1996. Strikingly, 46 percent of PCP cases after 1996 occurred in people who had never been in HIV/AIDS care.13

One of the most-cited reports came from the HIV Outpatient Study, which has followed over 3,500 patients in eight U.S. cities since 1992. Researchers analyzed data for all who had ever had a CD4 count below 100 (considered most vulnerable for opportunistic infections or death) from 1994 through June, 1997. Use of protease-inhibitor-containing regimens among these 1255 patients went from two percent in mid-1995 to 82 percent by June, 1997.

Mortality (deaths per 100 person-years) remained roughly constant in 1994 and 1995, then dropped abruptly in the second quarter of 1996 and continued dropping. To determine the effect of treatment, investigators classified patients by type of therapy: no antiretrovirals, nucleoside analogue monotherapy, nucleoside combination therapy, and combination therapy including a protease inhibitor. Patients on no anti-HIV treatment were 1.5 times as likely to die as those on monotherapy, 2.9 times as likely to die as those taking combination nucleosides and 4.5 times as likely to die as those on protease inhibitor combinations. The risk of serious opportunistic infections was reduced in a nearly identical pattern.14

Strikingly similar results were reported by the EuroSIDA cohort, a prospective observational cohort that began recruiting patients from across Europe in May 1994. In November 1998 researchers reported on all 4,270 patients enrolled who were over age 16 and had a CD4 count below 500. Through March 1998, 1,215 had died.


As in the HIV Outpatient Study, the death rate was analyzed by treatment category. The results, published in The Lancet, are broken down into six-month periods, and the correlation between more intensive regimens and fewer deaths is consistent and dramatic.


The lowest death rate recorded in any period for patients on no treatment was 50.3 per 100 person-years, while for those on one antiretroviral the death rate never rose above 22.3 per 100 person-years. On two drugs deaths never rose above 7.9 per 100 person years and on three or more drugs the highest rate recorded was 3.9 per 100 person-years. In other words, the lowest death rate for patients on no anti-HIV drugs was 13 times the highest death rate recorded for those on three or more. The researchers further noted that "in any given 6-month period, the death rate among patients taking protease inhibitors was much lower than among those not taking protease inhibitors.'15

The EuroSIDA researchers also examined opportunistic infection incidence for HAART and non-HAART patients. Patients with CD4 counts below 200 were over three times as likely to have an opportunistic infection if they weren't on HAART.16

Several other large European cohorts have reported similar results, including the Swiss HIV Cohort,17 the Italian HIV Seroconverter Study18 and the Italian Register for HIV Infection in Children.19


Local Studies with All HIV/AIDS Patients

Certain localities have been able to assemble cohorts that reach essentially the entire population seeking care for HIV or AIDS-related illness. For example, since 1986 the Canadian province of British Columbia has distributed anti-HIV drugs at no cost through a centralized system under specific guidelines, making tracking and analysis relatively simple.
In order to compare the real-world results of dual-nucleoside combinations vs. three-drug regimens including either a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor, researchers at the British Columbia Centre for Excellence in HIV/AIDS studied all HIV-positive patients in the system who began anti-HIV treatment from Oct. 1, 1994 through Dec. 31, 1996. In a multivariate analysis (using statistical methods to adjust for a variety of differences between patients), those on two drugs were over three times as likely to die as those on three.20


San Francisco has an AIDS surveillance system which captures basic data for approximately 95 percent of the city's AIDS patients, and this data is particularly interesting in light of Farber's allegations. Unlike the study Farber cites, which used a complex collection of computer models and projections to estimate HIV infection rates and AIDS cases, this "active surveillance" system assembles data on actual patients from health care facilities, death certificates and other sources. An analysis of this information was published earlier this year in the American Journal of Epidemiology, with a year's worth of additional follow-up presented at the International AIDS Conference in Durban, South Africa (July 9-14, 2000).

The first report found that survival after an AIDS diagnosis improved dramatically for those diagnosed in 1995 and 1996 compared to earlier periods. Researchers then analyzed all deaths among San Franciscans diagnosed with AIDS from 1993 through 1996 for whom treatment and CD4 data was available, finding that any antiretroviral treatment, before or after an AIDS diagnosis, significantly reduced the risk of death. When protease inhibitors were included the risk of death was cut by 75 percent compared to no treatment. The analysis included deaths from all causes, so any deaths from drug toxicities were included.21 The research team's Durban presentation extended the findings through 1997 and again found that "antiretroviral therapy, especially combined with a protease inhibitor, strongly predicts improved survival."22

A number of other presentations at Durban reported a similar association between HAART and reduced rates of death and illness. Dr. Gary Reiter of the River Valley HIV Clinic in Holyoke, Massachusetts presented an analysis of HIV patients seen at his clinic and another Holyoke facility from March. 31, 1997 to Dec. 31, 1999.

177 of 300 patients were on HAART, defined as any regimen that maintained HIV suppression below 25 copies. According to Reiter, baseline characteristics of HAART and non-HAART patients were similar, except that those not on therapy generally went untreated because of psychosocial instability, mental illness and/or substance abuse. 20 of 23 deaths were in the 123 non-HAART patients. None of the three HAART deaths were due to AIDS-related infections, but one was from a drug side effect: ddI-related pancreatitis.22,23


Reiter, who began his career in San Francisco at the start of the AIDS epidemic, commented, "Those of us who've been involved with the epidemic since '81 know that antiretroviral therapy works. I had hundreds and hundreds of patients die in San Francisco (1981 to 1985) and then western Massachusetts (1987 to 1995) until we got effective therapy. We are coming up on four years now of no AIDS deaths in treated individuals."23

Even early skeptics about some of the mainstream ideas have seen the value of anti-HIV treatment. Joseph Sonnabend, M.D., who treated some of the first AIDS patients about 20 years ago and whose early articles are still quoted on some denialist Web sites, now says, "the antiviral therapies available since about 1996 can be life saving in people with more advanced disease, and HIV clearly plays a central role in this disease."


The "Drug-AIDS" Hypothesis

It is worth noting that some in the denialist camp not only claim that anti-HIV treatment is worthless, but that it actually causes AIDS. The most well known of such theorists is University of California Berkeley molecular biologist Peter Duesberg, who has proposed that AIDS in the U.S. and Europe is caused entirely by recreational drugs and antiretroviral medications, especially AZT.25,26 Many in the denialist movement who do not fully embrace Duesberg's hypothesis agree that anti-HIV drugs play a role in causing AIDS. Maggiore, for example, accuses AZT of killing HIV patients and suggests that all of the nucleoside analogues may constitute "AIDS by prescription."27 Pasquarelli recently asserted that "the ONLY people dying are those who take poisonous AIDS drugs."28 (emphasis in original)
Such theories are difficult to sustain in light of the data cited above, and the broader picture backs up the studies. During the period in which AIDS deaths dropped by two thirds, sales of the drugs condemned as "toxic DNA chain terminators" skyrocketed. Sales of Glaxo's antiretrovirals, led by AZT and 3TC, quadrupled between 1995 and 1999.29 Bristol-Myers Squibb, the other leading maker of nucleoside drugs, also reported large sales increases.30


Since Duesberg's "drug-AIDS hypothesis" pins much of the blame on recreational drugs, it is plausible that a massive decline in recreational drug use might have overcome the exponential growth in use of allegedly murderous antiretrovirals, but the opposite appears to have happened. The government's major instrument for measuring rates of drug use, the National Household Survey on Drug Abuse, charted an almost unbroken rise in the use of illegal drugs during the 1990s. The survey noted substantial increases in use of many of the specific drugs Duesberg implicates in AIDS, including heroin, cocaine and inhalants.31 While information on drug use by gay men, still disproportionately affected by AIDS, is less complete, there has been much discussion in the gay press and in popular books about increasingly heavy drug use in certain segments of the gay community, particularly the so-called "party circuit." At least one study has reported significant increases in both numbers of drug users and severity of drug use among young gay men from 1994 to 1997.32

Might it be that this increase in use of anti-HIV and recreational drugs hasn't had enough time to do damage? While theoretically possible, such a proposition would directly contradict the arguments Duesberg made throughout the 1990s. In making an epidemiological case for drugs as the cause of AIDS, he cited evidence that drug use -- as indicated by increases in drug-related arrests and hospital emergency room admissions -- had risen in tandem with AIDS cases during the 1980s.25,26 He has also argued that Kimberly Bergalis, famous for allegedly being infected with HIV by her dentist, was killed by AZT in just two years.33

The arguments that once seemed to bolster the drug - AIDS hypothesis now severely undercut it. And the evidence overwhelming demonstrates that HAART has played a large role in reducing AIDS deaths in the last several years.

This does not mean that antiretroviral drugs are benign or that their toxicities are not serious. Indeed, this and other HIV/AIDS publications have noted a growing movement away from the so-called "hit early and hard" approach precisely because the drugs now in use may well be too toxic for most patients to use indefinitely. There is much work to be done, both to develop new, safer treatments and to make better use of the ones we have.

Indeed, one of the tragedies of the denialist movement is that it has distracted attention from these issues. By forcing researchers and activists to take time and energy defending what has already been proven, it has diverted effort from critical questions regarding what sort of research is needed and how to speed the development of better, less toxic therapies.


References

1) Lauritsen, John, lecture at San Francisco HEAL meeting, Park Branch Public Library, March 14, 1997.
2) Crumbley, Dorcus, CDC spokeswoman, personal communication, 8/10/00.

3) Centers for Disease Control and Prevention, U.S. HIV and AIDS Cases Reported Through December, 1999 Year-End Edition, Vol. 11, No. 2., table 22.

4) Alive and Well AIDS Alternatives, "AIDS Myth Busters," http://www.aliveandwell.org, undated (viewed 8/14/00).

5) Maggiore, Christine, What if Everything You Thought You Knew About AIDS Was Wrong? 4th edition, American Foundation for AIDS Alternatives, 2000, p.21.

6) Farber, Celia, "Science Fiction," Gear, March, 2000.

7) Lemp, G., et al. "Projected incidence of AIDS in San Francisco: The Peak and Decline of an Epidemic." Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology, 1997, 16:3, 182-89.

8) ACT UP San Francisco flyer, "Genocide From the AIDS Office,"1997.

9) "Antigay AIDS scare sparks silly string scandal," ACT UP San Francisco press release, 8/9/00.

10) Katz, Mitchell, personal communication, 8/11/00.

11) Rasnick, David, "The AIDS blunder, how could it happen?" Rethinking AIDS, 8:8, 1-2, July 2000.

12) McNaghten, A.D., et al, "Effects of antiretroviral therapy and opportunistic illness primary chemoprophylaxis on survival after AIDS Diagnosis," AIDS 1999 13:13, 1687-95.

13) Kaplan, J., et al, "Epidemiology of Human Immuno-deficiency Virus-associated opportunistic infections in the United States in the era of highly active antiretroviral therapy," Clinical Infectious Diseases, 2000; 30 (Supplement 1), S5-14.

14) Palella, F., et al, "Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection," New England Journal of Medicine, 338:13, 853-60, 1998, March 26.

15) Mocroft, A., et al, "Changing patterns of mortality across Europe in patients infected with HIV-1," The Lancet, 352: 1725-30, Nov. 28, 1998.

16) Mocroft, A., and others, "AIDS across Europe, 1994-98: the EuroSIDA study," The Lancet, 356: 291-96, July 22, 2000.


17) Egger, M. and others, "Impact of new antiretroviral combination therapies in HIV infected patients in Switzerland: Prospective multicentre study," British Medical Journal, 315: 1194-9, Nov. 8, 1997.

18) Dorrucci, Maria and others, "Temporal changes in the rate of progression to death among Italians with known date of HIV seroconversion: Estimates of the population effect of treatment," Journal of Acquired Immune Deficiency Syndromes, 22:1, 65-70, Sept. 1, 1999.

19) DeMartino, M. and others, "Reduction in mortality with availability of antiretroviral therapy for children with perinatal HIV-1 infection," Journal of the American Medical Association, 284:190-7, July 12, 2000.

20) Hogg, R.S., et al, "Improved survival among HIV-infected patients after initiation of triple-drug antiretroviral regimens," CMAJ, 1999: 160:659-65.

21) Schwarcz, S. and others, "Impact of protease inhibitors and other antiretroviral treatments on acquired immunodeficiency syndrome survival in San Francisco, CA 1987-1996," American Journal of Epidemiology. 152:2. 178-85, 2000.

22) Schwarcz, S. and others, "Trends in AIDS survival in San Francisco: Does treatment continue to be effective?" 13th International AIDS Conference, abstract # ThOrC722.

23) Reiter, G., and Wojnarowski, C., "Steep declines in mortality and no AIDS deaths in HAART treated patients," 13th International AIDS Conference, abstract # MoPe2491

24) Reiter, G., personal communication, Aug. 13., 2000.

25) Duesberg, P., "The role of drugs in the origin of AIDS," Biomedicine and Pharmacotherapy, 46:3-15, 1992.

26) Duesberg, P. and Rasnick, D., "The AIDS dilemma: Drug diseases blamed on a passenger virus," Genetica, 104:85-132, 1998.

27) Maggiore, p. 30.

28) Pasquarelli, D., "Dynamic duo ready for trial!" Aug. 13, 2000.

29) Glaxo Wellcome, annual reports: 1996, 1997, 1998, 1999.

30) Bristol-Myers Squibb, annual reports: 1996, 1997, 1998, 1999.

31) Substance Abuse and Mental Health Services Administration, National Household Survey on Drug Abuse, 1999.

32) McNall, M. and Remafedi, G., "Relationship of amphetamine and other substance use to unprotected intercourse among young men who have sex with men," Archives of Pediatric and Adolescent Medicine, 153:1130-6, Nov., 1999.

33) Duesberg, P. Inventing the AIDS Virus, Chapter 9, Regnery, 1995.

Well, It all boils down to one thing. Money. Somebody is making a bag of money on this, and that somebody doesn't want the gravey train to end. Censorship, pure and simple in order to line the pockets of the government and big drug companies.

PCR was invented by Dr. Kary Mullis, who won the Nobel Prize for it in 1993. He has called quantitative PCR an "oxymoron." I'm going to take the inventor's opinion about PCR over yours. If you're looking for something with PCR, you're looking for something which is there in such miniscule amounts it could never cause any disease whatsoever.

Why don't you debate Kary Mullis on the topic, in a public forum?

"now, you guys who don't believe the last bit, it is not well established exactly how the cytotoxic (cell-killing) aspect occurs,"

After $118 billion dollars and millions of death sentences passed out, it should be established beyond any doubt how this happens.

"but it is a *fact* that patients with HIV experience a progressive decrease in number of circulating CD4+ T cells characteristic of "full-blown" AIDS, and that HIV infection (or more specifically, testing positive for antibodies to HIV) occurs before this decline occurs. while this is not a logical proof that HIV *causes* AIDS, it is a pretty strong correlation. "

Well, when you get the "logical proof" (that's how science works, right?) please let us know, and please stop terrorizing and killing people before you get that "logical proof".

Correlation is not causation.

You all take care now.

Join: www.AIDSMythExposed.com End the mass medical terror and genocide.

"...it should be established beyond any doubt how this happens."

The disease-causing mechanisms of many diseases, including many diseases, including tuberculosis and hepatitis B, are poorly understood. Therefore, your reasoning would lead to the conclusion that M. tuberculosis is not the cause of tuberculosis or that hepatitis B virus is not a cause of liver disease.

Foolishness.

The main thing about the 'AIDS' hypothesis is that nothing adds up. We have had twenty years to see this theory of a common cause of immune suppression is just plain nonsense.

THIS IS ONE OF MANY EXAMPLES: -

If 'AIDS really is a sexually transmitted syndrome (common cause -'HIV'- for old existing diseases) then why is there almost no 'AIDS' in Japan. Total cases in twenty years amount to only 7,500 or 375 a year.

The Japanese are the number one sex tourists to Thailand (Source: TAT - Tourist Authority of Thailand).

The Japanese are the largest overseas tourists visiting Nevada Brothels and even have regular bus trips to them (Sourse: Penthouse Magazine)

The Japanese travel MORE then almost any other nation.

The Japanese have a past culture that accepted homosexuality (even Samari 'swung' both ways) and have a larger than average gay community.

Japan has a booming sex trade (estimated at $13 billion annually (Source: - 17/03/03 -- San Francisco Chronicle)

Numerous surveys demonstrate that 'most men and women in their 20s do not use condoms'. (Source: 17/03/03 -- San Francisco Chronicle)

The Japanese are only different from other Asian cultures in that they have NO real poverty.

Have you considered that poverty NOT sex is the real cause of immune suppression?


NOTE: - By comparison, Cambodia, whose population is less than a tenth of Japan's, had 170,000 people living with HIV or AIDS as of the end of 2001, according to United Nations estimates. SOURCE. Reuters 19 Sept 2003 (http://www.alertnet.org/thenews/newsdesk/T130295.htm).

* 'Living with HIV/AIDS' simply means that they meet the WHO/CDC Bengui definition which also fits EVERY epidemic disease in poor countries.

Sex And HIV: Behaviour-Change Trial Shows No Link
The East African (Nairobi)
March 17, 2003
Posted to the web March 19, 2003
By Paul Redfern, Special Correspondent
Nairobi

A UK funded trial aimed at reducing the spread of Aids in Uganda by
modifying sexual behaviour appears to have had little discernible
effect.

The trial, carried out on around 15,000 people in the Masaka region,
involved distributing condoms, treating around 12,000 victims of
sexually transmitted diseases and counselling.

However, while the trial led to a marked change in sexual behavioural
patterns, with the proportion reporting causal sexual partners falling
from around 35 per cent to 15 per cent, there was no noticeable fall
in the number of new cases of HIV infection, although there was a
significant reduction in sexually transmitted diseases such as
syphilis and gonorrhoea.

The trial results, which were reported in the British medical journal
The Lancet, have already aroused some controversy.

The team leader of the trial, Dr Anatoli Kamalai, acknowledged that
there was "no measurable reduction" in HIV incidence with "no hint of
even a small effect."

But the research team's view is that the spread of HIV was already
declining in the area and the trial might not have been big enough to
detect any additional change.

There is, however, another view which has recently been put forward
which claims that inadequately sterilised needles across Africa have
led to a greater rate of HIV infection than sexual contact.

It is a view put forward by a mainly American group of scientists,
including Dr David Gisselquist, who told the Times of London that
"Results from the Masaka study add to the already long list of
findings from other studies that don't fit the hypothesis that most
HIV in African adults is from sexual transmission.

"These results from Masaka are similar to results published earlier
from a similar study in Rakai, Uganda, where interventions that
reduced STD prevalence had no impact on HIV incidence." However, such
a view is by no means mainstream in the latest thinking on the spread
of HIV in Africa.

Most scientific research still believes that HIV is mainly spread by
sexual transmission and that people suffering from STDs are
particularly prone.

The trial was the first systematic attempt on a large scale to assess
whether modifying sexual behaviour and better management of other
sexual diseases could cut the transmission of HIV in Africa.

In a commentary in The Lancet, Judith Stephenson and Frances Cowan of
the Royal Free and University College Medical School in London
acknowledged that "many people will be disappointed by the lack of
reduction in HIV incidence, despite an apparently appropriate
intervention that reduced other STDs and was implemented on a huge
scale with great care and commitment."

The two researchers suggest that it might have been "the right trial
and the wrong time" - when HIV incidence was falling and when there
were already substantial reductions in risk behaviour.

Copyright © 2003 The East African. All rights reserved. Distributed
by AllAfrica Global Media (allAfrica.com).
http://allafrica.com/stories/200303190482.html
http://allafrica.com/stories/printable/200303190482.html

It took me about 5 minutes to find TWO SITES that explain how M. Tuberculosis causes disease.

Mycobacterium avium.
Mycobacterium avium is an opportunistic pathogen, and comes in two forms, the bacillary and spheroplast form. Both of these forms can cause disease in animals. The spheroplast form also causes disease in humans. The people who most often contract disease from Mycobacterium avium are sufferers from AIDS, whose immune systems have been suppressed by the HIV virus. In immunocompromised people, Mycobacterium avium invades the white blood cells of the infected person, and uses them as sites to multiply.

Tuberculosis. See CDC fact sheet.
M. tuberculosis is a strictly aerobic bacterium, with a very slow doubling time (12-18 hours)
View electron micrograph of M. tuberculosis
Mycobacteria have very waxy coats (made of mycolic acid compounds). They resist destaining with acid and alcohol, and are called the acid-fast bacteria. Their waxy coats resist uptake of many antibiotics.
TB has a long latent period; first detectable signs of antibody response are 8-12 weeks after infection.
TB is usually asymptomatic; only 10-20% of infected persons become diseased.
How does M. tuberculosis cause disease? Almost any tissue can become infected, but lung is common focus of infection, so consider TB in lung:
Bacterium is taken up inside phagosome by macrophage (first stage of phagocytosis)
Bacterium secretes proteins that block fusion of phagosome with lysosome
Bacterium slowly grows and replicates inside macrophage host cell, gradually turning cell into a bacterial replicator.
Macrophages migrate to regional lymph nodes
Other macrophages are attracted by chemotaxis to the site of infection, forming an early tubercule. Activated macrophages kill M. tuberculosis, stop spread. Host develops cell-mediated immunity, delayed hypersensitivity to tuberculin, a protein secreted by M. tuberculosis.
In some cases, mature tubercules are formed as firm outer layer of macrophages "wall off" inner mass of infected macrophages. Center of tubercule liquiefies, forms air-filled cavity that promotes growth of bacteria, liquefaction of tubercule contents.
Rupture of tubercule can allow bacteria to enter bronchioles, spread throug respiratory system and other tissues
Patients with pulmonary TB have respiratory problems, cough up mucus secretions frequently. TB can attack many other sites in body as well as lungs.
View cross-section of normal lung
View cross-section of lung with TB
View cross-section of lung with "miliary" TB (so called because of extensive white abcesses resembling grains of millet)
TB is one of the most common diseases world-wide. The following annual estimates are probably too low:
Worldwide annual deaths from TB: 3 million (98% in developing countries)
Worldwide annual reported disease cases: 8 million
Worldwide incidence of infection: somewhere between 1 in 10 to 1 in 3 people
U.S. incidence in 1995: 22,860 cases (8.7 cases per 100,000 population)
View world map showing incidence of new cases
View further information about TB
Want to play doctor? Practice your diagnostic skill with a Web-based case study of a patient with TB.
Since you started reading this page

You are outright lying to this board as ALL "AIDS" Apologists do.

I'm goint to take this man's word, Nobel Laureate and Japan Prize winner, who hasn't earned a cent off the "HIV/AIDS" mass terror and genocide over a "Biologist's".

THE MEDICAL ESTABLISHMENT VS. THE TRUTH
Book Excerpt
By Kary Mullis

Penthouse Sept. 1998


Dr. Mullis was awarded the 1993 Nobel Prize in Chemistry. This article is excerpted from his forthcoming book, Dancing Naked in the Mind Field, to be published by Pantheon.

When I first heard in 1984 that Luc Montagnier of France's Pasteur Institute and Robert Gallo of America's National Institutes of Health had independently discovered that the retrovirus H.I.V. -- human immunodeficiency virus -- caused AIDS, I accepted it as just another scientific fact. It was a little out of my field of biochemistry, and these men were specialists in retroviruses.

Four years later I was working as a consultant at Specialty Labs in Santa Monica. Specialty was trying to develop a means of using P.C.R. [polymerase chain reaction, a D.N.A.-amplification method conceived by Mullis] to detect retroviruses in the thousands of blood donations received per day by the Red Cross. I was writing a report on our progress for the project sponsor, and I began by stating, "H.I.V. is the probable cause of AIDS."

I asked a virologist at Specialty where I could find the reference for H.I.V. being the cause of AIDS.

"You don't need a reference," he told me. "Everybody knows it."

"I'd like to quote a reference." I felt a little funny about not knowing the source of such an important discovery. Everyone else seemed to.

"Why don't you cite the C.D.C. report?" he suggested, giving me a copy of the Centers for Disease Control's periodic report on morbidity and mortality. I read it. It wasn't a scientific article. It simply said that an organism had been identified -- it did not say how. It requested that doctors report any patients showing certain symptoms and test them for antibodies to this organism. The report did not identify the original scientific work, but that didn't surprise me. It was intended for physicians, who didn't need to know the source of the information. Physicians assumed that if the C.D.C. was convinced, there must exist real proof somewhere that H.I.V. was the cause of AIDS.

A proper scientific reference is usually a published article in a reliable scientific magazine. These days the magazines are on slick glossy paper with pictures on the front and lots of advertisements, a lot of editorial material by people who are professional journalists, and a few pictures of girls selling you things you might want to buy for your lab. The advertisers are the companies that make things for scientists to buy and the companies that make drugs for doctors to sell. Therefore there are no major journals without corporate connections.

Scientists submit the articles in order to report their work. Preparing articles describing their work and having them published is crucial to a scientist's career, and without articles in major journals they will lose their rank. The articles may not be submitted until experiments supporting the conclusions drawn are finished and analyzed. In primary journals every single experimental detail has to be there either directly or by reference, so that somebody else can repeat exactly what was done and find out whether it comes out the same way in their hands. If it doesn't, somebody will report that, and the conflict eventually has to be resolved so that when we go on from here we know where "here" is. The most reliable primary journals are refereed. After you send in your article, the editors send copies of it to several of your colleagues for review. They become the referees.The editors are paid for their work on the journal; the colleagues are not. But what they do gives them power, which most of them like.

I did computer searches. Neither Montagnier, Gallo, nor anyone else had published papers describing experiments which led to the conclusion that H.I.V. probably caused AIDS. I read the papers in Science for which they had become well known as AIDS doctors, but all they had said there was that they had found evidence of a past infection by something which was probably H.I.V. in some AIDS patients. They found antibodies. Antibodies to viruses had always been considered evidence of past disease, not present disease. Antibodies signaled that the virus had been defeated. The patient had saved himself. There was no indication in these papers that this virus caused a disease. They didn't show that everybody with the antibodies had the disease. In fact they found some healthy people with antibodies.

If Montagnier and Gallo hadn't really found this evidence, why was their work published, and why had they been fighting so hard to get credit for the discovery? There had been an international incident wherein Robert Gallo of the N.I.H. had claimed that his own lab had not been able to grow the virus from the sample sent to him by Luc Montagnier in Paris. The virus he was able to grow, he said, came from samples collected at his end from putatuive AIDS patients. Gallo had patented the AIDS test based on these samples, and the Pasteur Institute had sued. The Pasteur eventually won, but back in 1989 it was a standoff, and they were sharing the profits.

I was hesitant to write "H.I.V. is the probable cause of AIDS" until I found published evidence that would support it. Mine was the most minimal statement possible. In my progress report I wasn't trying to say that it absolutely did cause AIDS, I was just trying to say that it was likely to cause it for some known reasons. Tens of thousands of scientists and researchers were spending billions of dollars a year doing research based on this idea. The reason had to be there somewhere; otherwise these people would not have allowed their research to settle into one narrow channel of investigation.

I lectured about P.C.R. at innumerable meetings. Always there were people there talking about H.I.V. I asked them how it was that we knew H.I.V. was the cause of AIDS. Everyone said something. Everyone had the answer at home, in the office, in some drawer. They all knew, and they would send me the papers as soon as they got back. But I never got any papers. Nobody ever sent me the news about how AIDS was caused by H.I.V.

I finally had the opportunity to ask Dr. Montagnier about the reference when he lectured in San Diego at the grand opening of the U.C.S.D. AIDS Research Center, which is still run by Bob Gallo's former consort, Dr. Flossie Wong-Staal. This would be the last time I would ask my question without showing anger. In response Dr. Montagnier suggested, "Why don't you reference the C.D.C. report?"

"I read it," I said. "That doesn't really address the issue of whether or not H.I.V. is the probable cause of AIDS, does it?"

He agreed with me. It was damned irritating. If Montagnier didn't know the answer, who the hell did?

One night I was driving from Berkeley to La Jolla and I heard an interview on National Public Radio with Peter Duesberg, a prominent virologist at Berkeley. I finally understood why I was having so much trouble finding the references that linked H.I.V. to AIDS. There weren't any, Duesberg said. No one had ever proved that H.I.V. causes AIDS. The interview lasted about an hour. I pulled over so as not to miss any of it.

I had known of Peter when I was a graduate student at Berkeley. He had been described as a truly brilliant scientist who had mapped a particular mutation to a single nucleotide in what was to become known eventually as an oncogene. In the 1960s that was a real feat. Peter went on to develop the theory that oncogenes might be introduced by viruses into humans and cause cancer. The idea caught on and became a serious theoretical driving force behind the research that was funded under the unfortunate name "War on Cancer." Peter was named California Scientist of the Year.

Not satisfied resting on his laurels, Peter torched them. He found flaws in his own theory and announced to his surprised colleagues who were working on demonstrating it that it was highly unlikely. If they wanted to cure cancer, their research should be directed elsewhere. Whether it was because they were more interested in curing their own poverty than cancer or that they just couldn't come to grips with their mistake, they continued to work fruitlessly on the viral-oncogene hypothesis for ten years. And they didn't seem to notice the irony: The more frustrated they got, the more they chastised Peter Duesberg for questioning his own theory and their folly. Most of them had been trained to obtain grants from the government, hire people to do research, and write papers that usually ended with the notion that further research should be done along these same lines -- preferably by them and paid for by someone else. One of them was Bob Gallo.

Gallo had been a friend of Peter's. They had worked in the same department at the National Cancer Institute. Of the thousands of scientists who had worked fruitlessly to assign a causal role in cancer to a virus, Bob was the only one who had been overzealous enough to announce that he had. No one paid any attention because all he had demonstrated was an anecdotal and very weak correlation between antibodies to a harmless retrovirus, which he called H.T.L.V. I, and an unusual type of cancer found mainly on two of the southern islands of Japan.

In spite of his lack of luster as a scientist, Gallo worked his way up in the power structure. Peter Duesberg, despite his brilliance, worked his way down. By the time AIDS came along, it was Bob Gallo whom Margaret Heckler approached when President Reagan decided that enough homosexuals picketing the White House was enough. Margaret was the Secretary of Health, Education, and Welfare, and thereby the top dog at the N.I.H. Bob Gallo had a sample of a virus that Luc Montagnier had found in the lymph node of a gay decorator in Paris with AIDS. Montagnier had sent it to Gallo for evaluation, and Bob had appropriated it in the pursuit of his own career.

Margaret called a press conference and introduced Dr. Robert Gallo, who suavely pulled off his wraparound sunglasses and announced to the world press, "Gentlemen, we have found the cause of AIDS!" And that was it. Gallo and Heckler predicted that a vaccine and a cure would be available within a couple of years. That was 1984.

All the old virus hunters from the National Cancer Institute put new signs on their doors and became AIDS researchers. Reagan sent up about a billion dollars just for starters, and suddenly everybody who could claim to be any kind of medical scientist and who hadn't had anything much to do lately was fully employed. They still are.

It was named human immunodeficiency virus by an international committee in an attempt to settle the ownership dispute between Gallo and Montagnier, who had given it different names. To call it H.I.V. was a shortsighted mistake that preempted any thought of investigation into the causal relationship between acquired-immune-deficiency syndrome and the human immunodeficiency virus.

Duesberg pointed out wisely from the sidelines in the Proceedings of the National Academy of Sciences that there was no good evidence implicating the new virus. He was ignored. Editors rejected his manuscripts, and committees of his colleagues began to question his need for having his research funds continued. Finally, in what must rank as one of the great acts of arrogant disregard for scientific propriety, a committee including Flossie Wong-Staal, who was feuding openly with Duesberg, voted not to renew Peter's Distinguished Investigator Award. He was cut off from research funds. Thus disarmed, he was less of a threat to the growing AIDS establishment. He would not be invited back to speak at meetings of his former colleagues.

We live with an uncountable number of retroviruses. They're everywhere -- and they probably have been here as long as the human race. We have them in our genome. We get some of them from our mothers in the form of new viruses -- infectious viral particles that can move from mother to fetus. We get others from both parents along with our genes. We have resident sequences in our genome that are retroviral. That means that we can and do make our own retroviral particles some of the time. Some of them may look like H.I.V. No one has shown that they've ever killed anyone before.

There's got to be a purpose for them; a sizable fraction of our genome is comprised of human endogenous retroviral sequences. There are those who claim that we carry useless D.N.A., but they're wrong. If there is something in our genes, there's a reason for it. We don't let things grow on us. I have tried to put irrelevant gene sequences into things as simple as bacteria. If it doesn't serve some purpose, the bacteria get rid of it right away. I assume that my body is at least as smart as bacteria when it comes to things like D.N.A.

H.I.V. didn't suddenly pop out of the rain forest or Haiti. It just popped into Bob Gallo's hands at a time when he needed a new career. It has been here all along. Once you stop looking for it only on the streets of big cities, you notice that it is thinly distributed everywhere.

If H.I.V. has been here all along and it can be passed from mother to child, wouldn't it make sense to test for the antibodies in the mothers of anyone who is positive for H.I.V., especially if that individual is not showing any signs of disease?

Picture a kid in the heartland of America. His lifelong goal has been to join the Air Force when he graduates and become a jet pilot. He's never used drugs and he's had the same sweet girlfriend, whom he plans to marry, all through high school. Unbeknownst to him, or anyone else, he also has antibodies to H.I.V., which he inherited from his mother, who is still alive, when he was in her womb. He's a healthy kid, it doesn't bother him in any way, but when he is routinely tested for H.I.V. by the Air Force, his hopes and dreams are destroyed. Not only is he barred from the Air Force, but he has a death sentence over his head.

The C.D.C. has defined AIDS as one of more than 30 diseases accompanied by a positive result on a test that detects antibodies to H.I.V. But those same diseases are not defined as AIDS cases when the antibodies are not detected. If an H.I.V.-positive woman develops uterine cancer, for example, she is considered to have AIDS. If she is not H.I.V.-positive, she simply has uterine cancer. An H.I.V.-positive man with tuberculosis has AIDS; if he tests negative he simply has tuberculosis. If he lives in Kenya or Colombia, where the test for H.I.V. antibodies is too expensive, he is simply presumed to have the antibodies and therefore AIDS, and therefore he can be treated in the World Health Organization's clinic. It's the only medical help available in some places. And it's free, because the countries that support WHO are worried about AIDS. From the point of view of spreading medical facilities into areas where poor people live, AIDS has been a boon. We don't poison them with A.Z.T. like we do our own people because it's too expensive. We supply dressing for the machete cut on their left knee and call it AIDS.

The C.D.C. continues to add new diseases to the grand AIDS definition. The C.D.C. has virtually doctored the books to make it appear as if the disease continues to spread. In 1993, for example, the C.D.C. enormously broadened its AIDS definition. This was happily accepted by county health authorities, who receive $2,500 from the feds per year under the Ryan White Act for every reported AIDS case.

In 1634 Galileo was sentenced to house arrest for the last eight years of his life for writing that the Earth is not the center of the universe but rather moves around the sun. Because he insisted that scientific statements should not be a matter of religious faith, he was accused of heresy. Years from now, people looking back at us will find our acceptance of the H.I.V. theory of AIDS as silly as we find the leaders who excommunicated Galileo. Science as it is practiced today is largely not science at all. What people call science is probably very similar to what was called science in 1634. Galileo was told to recant his beliefs or be excommunicated. People who refuse to accept the commandments of the AIDS establishment are basically told the same thing: "If you don't accept what we say, you're out."

It has been disappointing that so many scientists have absolutely refused to examine the available evidence in a neutral, dispassionate way. Several respected scientific journals have refused to print a statement issued by the Group for the Scientific Reappraisal of the H.I.V./AIDS Hypothesis simply requesting "a thorough reappraisal of the existing evidence for and against this hypothesis."

I spoke publicly about this issue for the first time at a meeting of the American Association for Clinical Chemists in San Diego. I knew I would be among friends there. It was a small part of a much longer speech—at most I spoke for 15 minutes about AIDS. I told the audience how my inability to find a simple reference had sparked my curiosity.

The more I learned, the more outspoken I became. As a responsible scientist convinced that people were being killed by useless drugs, I could not remain silent.

The responses I received from my colleagues ranged from moderate acceptance to outright venom. When I was invited to speak about P.C.R. at the European Federation of Clinical Investigation in Toledo, Spain, I told them that I would like to speak about H.I.V. and AIDS instead. I don't think they understood exactly what they were getting into when they agreed. Halfway through my speech, the president of the society cut me off. He suggested I answer some questions from the audience. I thought it was incredibly rude and totally out of line that he cut me off, but what the hell, I would answer questions. He opened the floor to questions, and then decided that he would ask the first one. Did I understand that I was being irresponsible? That people who listened to me might stop using condoms? I replied that fairly reliable statistics from the C.D.C. showed that in the United States, at least, the number of reported cases of every known venereal disease was increasing, meaning people were not using condoms, while using the initial definition of AIDS, the number of reported cases of AIDS was decreasing. So, no, I didn't understand that I was being irresponsible. He decided that that was enough questions and ended the meeting abruptly.

Whenever I speak on this issue the question always comes up, "If H.I.V. isn't the cause of AIDS, then what is?" The answer to that is that I don't know the answer to that, any more than Gallo or Montagnier knows. Knowing that there is no evidence that H.I.V. causes AIDS does not make me an authority on what does. It is indisputable that if an individual has extremely close contacts with a lot of people, the number of infectious organisms that this individual's immune system is going to have to deal with will be high. If a person has 300 sexual contacts a year - with people who them selves are each having 300 contacts a year - that's 90,000 times more opportunity for infections than a person involved in an exclusive relationship.

Think of the immune system as a camel. If the camel is overloaded, it collapses. In the 1970s we had a significant number of highly mobile, promiscuous men sharing bodily fluids and fast lifestyles and drugs. It was probable that a metropolitan homosexual would be exposed to damn near every infectious organism that has lived on humans. In fact if you had to devise a strategy to collect every infectious agent on the planet, you would build bathhouses and encourage very gregarious people to populate them. The immune system will fight, but the numbers will wear it down.

The scientific issue gets tangled up with morality. What I'm describing has nothing at all to do with morality. This is not "God's wrath" or any other absurdity. A segment of our society was experimenting with a lifestyle, and it didn't work. They got sick. Another segment of our pluralistic society, call them doctor/scientist refugees from the failed War on Cancer, or just call them professional jackals, discovered that it did work. It worked for them. They are still making payments on their new BMWs out of your pocket.

I was invited by the Glaxo Pharmaceutical Company to speak at a conference. They sent me a letter in December of 1993 asking me to be the November 1994 symposium banquet speaker. If that time was not convenient for me, they wanted me to speak at the November 1995 banquet. Dr. John Partridge, who was the director of the Chemical Development Division, had not met me personally but had heard about a lecture I had given in 1991 at the Gordon Research Conference that, in his words, was "the most highly praised lecture that I have ever heard about from my academic and industrial colleagues."

He was looking for "particularly articulate scientists who bridge the biochemical and medical disciplines and routinely engage in 'out of the box' thinking."

Well, that certainly was me.

Dr. Partridge wrote that he would be pleased to pay all my travel and accommodations, as well as an honorarium of $1,500.

I thought this sounded all right, but I figured Glaxo could pay me a little more. What made this invitation particularly interesting to me was the fact that Glaxo was the largest drug company in the world, and one of their profitable drugs was the cellular poison being used against AIDS, A.Z.T. It kills cells like a cancer chemotherapeutic does. It keeps them from reproducing by preventing them from making new D.N.A. It also kills. In cancer, there is a rationale at least for using them, although I personally would never use chemotherapeutics on myself, cancer or not. But here's the way the explanation goes.

I think it stinks of an old therapy they used to use against syphilis: arsenic. The syphilis was surely going to kill you, the arsenic might kill you, but maybe it would kill the syphilis first and you would live to fraternize again. The use of poisonous chemotherapeutics in cancer follows the same line. The cancer is surely going to kill you. The chemotherapeutic surely will also, but maybe it will kill the cancer cells before it kills you. It's a gamble. We will give you almost enough to kill you and hope it's sufficient to kill the cancer. I wouldn't go for it myself. I don't need to take drugs that make my hair fall out. But what the hell, if somebody wants to take this kind of gamble, it does have a sort of logic to it. Nothing fun. Nothing you would do for a headache. But it's a chance somebody might want to take when the alternative is to die too young to watch their kids grow up. And some people do recover from cancer even after they have taken chemotherapeutics.

In the case of AIDS, the same strategy took a diabolic trurn. AIDS might kill you, A.Z.T. might also. It will surely make you sick. It will prevent the proliferation of any rapidly growing cells in your body, including the CD-4 immune cells that your doctor thinks you need now more that anything. It may kill the H.I.V. It kills it in petri dishes. But that may not cure you. The damage to you may have already been done, whatever it is. The complete absence of all H.I.V. from your body, even if it is accomplished, may not cure you of AIDS. No one has ever recovered from AIDS, even though they have recovered from H.I.V. And we are not going to give it to you in a limited dose as we do in the case of cancer chemotherapy, where we are gambling that although we are hurting you, we are hurting the cancer more and maybe you will survive longer. Here we are not gambling. No one has ever recovered from AIDS. We cannot expect that you might recover. We are going to ask you to swallow this poison until you die.

About half a million people went for it. No one has been cured. Most of them are dead. The ones who are not are also taking another drug now, a protease inhibitor. Who knows what it will do? The manufacturers didn't know when they started selling it. The FD.A. didn't require them to show that it would cure AIDS and not kill the patient, any more than they required them to show that about A.Z.T. They only required that a surrogate goal be met. A surrogate goal means that something that we think may be related to the disease in question may be improved by the drug, like the level of CD-4 cells, whatever the fuck they are. It's a way to get around the notion that a drug ought to be effective in curing the disease that it is sold for before it can be sold. The surrogate-goal bullshit is an indication that our F.D.A. no longer serves our needs. Or at least it does not serve our needs unless we own stock in the pharmaceutical industry and don't give a shit about health care.

I was interested in giving a seminar about things like this to the scientists assembled in North Carolina by Glaxo, formerly Burroughs Wellcome, and by the University of North Carolina in the name of Frontiers in Chemistry and Medicine. I was thinking that this technique of killing people with a drug that was going to kill them in a way hardly distinguishable from the disease they were already dying from, just faster, was really out there on the edge of the frontiers of medicine. In previous interviews and seminars I had said that I thought A.Z.T. was not only useless against AIDS, but in fact it was poisoning people. There were large-scale medical studies done in Europe, called the Concorde Study, that indicated just this. A.Z.T was worthless against AIDS and harmful even to healthy people. This conclusion was reached despite the fact that the study was heavily funded by Glaxo.

I wondered if these people knew how I felt about their product when they issued the invitation. I notified Dr. Partridge that I was pleased to accept if they would raise the ante a little. On January 26, 1994, I received a letter from M. Ross Johnson, the vice president of the division of chemistry They were very happy that I had accepted, and wrote that they would send me firstclass airfare for two, accommodation expenses, and an honorarium of $3,000. In closing, he asked me for the title of my banquet presentation.

So far, so good. I responded as requested, explaining that I intended to speak to this audience about a subject that should be of tremendous concern to the entire scientific community. I would speak about the fact that there is no scientific evidence that H.I.V. is the probable cause of AIDS and that I believed people taking A.Z.T. were being poisoned.

On October 14, 1994, a month before the meeting, I received another letter from Glaxo—this time from Gardiner F. H. Smith. No title. He was sincerely regretting having to inform me that they could no longer accommodate my presentation. He said that they would send me a check for $1,000 to compensate me for any inconvenience.

I responded with the following letter:

Dear Mr. Johnson:

Enclosed please find a copy of a fairly uninformative letter from a Mr Gardiner Smith, with whom I have not been in contact or correspondence previously.

As you know, my overall schedule is compact and very difficult to rearrange on short notice. I have declined, as a result of my commitment to Glaxo, income from other potential engagements. With Mr. Smith, I sincerely regret that your company had been forced into the "changing of the structuring," whatever that means to Mr. Smith, of "the abovereferenced event."

Unfortunately, I have made arrangements to attend several nonprofit institutional functions in the Southeast in connection with this trip, appearances which I will not cancel. Therefore, your company's reluctance, as related perfunctorily by Mr. Smith, to abide by the terms of your (previous) correspondence represents a considerable loss of income as well as an unanticipated expense to me personally.

Mr. Smith's unexplained offer of $1,000 compensation for my "time and trouble" adds a bit of mystery here as to who Mr. Smith is and what he must misconceive to be the value of my time and trouble.

I do not understand what Mr. Smith is exactly apologizing for in his letter, but I will be kindly expecting immediately, with or without an explanation from some more cordial and informed representative of Glaxo, a check for $6,048.00.

For Mr. Smith's information, round-trip airfare between San Diego and RaleighDurham first class for two is $3,048. Addition of our agreed-on honorarium of $3,000 results in the above figure.

One more thing you might consider, Dr. Johnson. A number of attendees at your meeting will likely have something to say to me about my failure to appear. You should be careful to explain there publicly precisely why Mr. Smith felt the need to inform me that your company has taken the liberty of "restructuring" in such a way as to be unable to "accommodate" my presentation. I am not in the habit of canceling public appearances at such short notice, and would not care to gain such a reputation on your account. I hope you understand that this is not' for me or for Glaxo, a trivial matter.

Cordially,
Dr. Kary B. Mullis

On November 30, 1994, I received another letter from Mr. Smith. It was quite brief, saying that he had received a copy of my letter to Dr. Johnson. Enclosed was a check from Glaxo in the amount of $6,048.

This was the most money I had ever made specifically for not doing something. And it occurred to me that, with my growing reputation for creating controversy, there might be many groups or individuals who did not want to hear me speak. Certainly that was their right, but if people did not want to hear ideas that would make them uncomfortable, they ought to be willing to pay not to hear them. With that thought in mind, I drafted the following offer:

HAVE SLIDES, WILL STAY HOME

Dr. Kary B. Mullis wants to talk to you and your associates, your friends, your sons and daughters. Is there anything you can do about it?

YES ... BUT YOU MUST ACT NOW ... SPECIAL OFFER

Dr Mullis won the Nobel Prize in Chemistry in 1993 and promptly launched a worldwide lecture tour Universities, research institutes, conventions, high schools, businesses, community groups, he even addressed "Connect"—a joint project of U.C.S.D. and the San Diego biotech industry—right on the beach in front of his very own apartment, which has been described in the national press as "rented rooms filled with his tools of seduction. "

He is usually invited to lecture on the Polymerase Chain Reaction, but when the lights go down and the slides come on, well...

John Martin, President of the European Society for Clinical Investigation, said in Nature, "His [Dr. Mullis's] only slides (or what he has called his art) were photographs he had taken of naked women with colored lights projected upon their bodies. He accused science of being universally corrupt with widespread falsification of data to obtain grants. Finally he impugned the personal honesty of several named scientists working in the H.I.V field.... The council of the European Society for Clinical Investigation will not be inviting Dr Mullis to further meetings. "

Really do you need this in your community? Of course not.

And now, for a limited time only you can be assured that Dr. Mullis will not ever lecture at your society, school, research lab, etc.

You personally ... and confidentially ... can assure it.

Call now at (my phone number) and ask for (my beautiful assistant). Have your Visa or MasterCard ready. Prevention rates begin at $500 per year guaranteed, and are progressive with the size and sensitivity of your organization. You may request personal anonymity or for $79.95 plus shipping we will send you a Special Service Award embossed with your name and a special inscription commending your judgment, foresight, and unselfish devotion to your community. Custom inscriptions are a little extra but can be especially commemorative.

Think about honoring your boss or one of your associates by taking advantage of our special "Help a Friend Stop Mullis" offer Call for details. Don't delay Only one offer of complete protection per year can be extended to any single organization. Be first Be smart. Be safe.

Recently, Glaxo Pharmaceuticals found it necessary to send Dr Mullis a check for $6,048.00 simply to prevent him from speaking at their annual Chemistry and Medicine at the Frontiers Conference in Chapel Hill, MC. No one at Glaxo had seen fit to acquire protection from a Mullis seminar, and, haplessly Dr. Ross Johnson, now no longer with Glaxo, had invited him.

I must report that the response to this offer has been underwhelming. NeimanMarcus has not chosen to include it in their famed Christmas catalog. So I have continued to speak out to any forum when I have been given the opportunity.

It is not too late, however If you would like to give the gift of my silence to an individual or an organization, all reasonable offers will be accepted.

NOTE: This offer is not open to family members or employees of Kary Mullis, who are doomed to have to listen to what I say. *

I never read that article before. Great stuff.

Thanks Mike.

HIV = PROFIT not AIDS

Challenge to the Denialists:

Assume I can get my hands on a fresh, sealed batch of HIV from the CDC.

Will you agree to meet me next weekend so I can witness you injecting a solution of HIV into your bloodstream? Don't worry, the needle will be brand new.

What do you say?

Hi,

Why would you, a biologist, want to inject people who you disagree with -- over a scientific issue -- to inject themselves with a Tcell leukemia culture, which has been chronically agitated with IL-2, PHA, HTGF and antiserum to interferon?

What would be the health benefit of that?

It's well known that the injection of any foreign material presents risks to health.

Your point, I suppose, is that if people really believe that these hyper-stimulated cell cultures don't, in proveable fact, contain that tricky devil of a reluctant microbe, HIV, that critics of the theory ought to be willing to inject themselves with a blood sample known to contain the non-specific surrogate markers that are meant, somehow, through some suspension of critical thinking, to represent said deadly, infectious but reluctant microbe?

How about this, you go and find any two AIDS patients, and we'll draw blood from them, and look at that blood under a microscope, and take peripheral T-cell counts, and see if we can find a single causative agent that these two people have in common that can be shown within a reasonable doubt to cause -- really understand that word "Cause" -- to cause whatever AIDS-defining diseases they might have. These diseases include salmonella, yeast infections, TB, and of course, cerival cancer in women.

Well, that's just not the protocol. If I want to, according to you, find HIV in a patient, first I have to draw blood and culture it in a mass of leukemia cells. Then I have to stimulate those cells into dividing by adding various mitogenic agents.
Then I spin the supernatant (liquid) in a density gradient (testube) and look for --- no, not a virus, not a single virion -- but for an enzyme -- at the 1.16 ml/gm level of the tube.

How do I prove this enzyme is there?

By adding pieces of RNA with radioactive tags -- if these pieces are copied into a longer strand of DNA, I assume I've found an enzyme capable of copying RNA into DNA.

But we know that I have not found any specific enzyme, because we know that there are a multiplicity of enzymatic processes carried on in healthy tissue - as well as mitogenicaly stimulated tissue -- that copy RNA to DNA.

Once upon a time, researchers imagined that this process was unique to RTVs,, now we know better.

So, have we found a virus?

No.

Clearly not.

We can look for protein/antibody response --

We take proteins from the cell culture and match them with antibody proteins from a patients blood -- which proves that some of the proteins in the stimulated cell culture which contained the patients blood match proteins from the patients blood.

Which proves... nothing.

Come on ladies and germs,

Let's not be dense.

I don't care if you believe HIV causes AIDS or Rickets or the Common Cold.

It's well understood that we still do not know how this might happen.

So why are we treating people who have yeast infections with AZT and Viramune?

Why are we trying to defend the body by destroying its ability to thrive?

We can do better than this.

AIDS Denial Kills

If you want to lowdown on these posts about AIDS, read this article, linked.

http://lists.indymedia.org/pipermail/imc-nyc-editorial/2003-October/003110.html

from the article:

"AIDS is not a myth. That is the plain fact. From looking at what happened in San Francisco with this issue a couple of years back back, we can see that the folks who aggressively promote the "don't use condoms" and "stop taking your medicine" schools of thought are not principled. In fact, there was one well-publicized case where some of these "activists" required restraining orders for stalking and harrassing individuals with whom they disagreed. We can also see this behavior in recent spam on the wire calling non-denialists "Jacobin Pharma-Fags." This is in reference to their theory that the ENTIRE AIDS movement (and medical establishment and governments of third world countries who are creating generic versions of life-saving drugs) have been bought out by pharmaceutical companies. Fascinating theory. Great delivery."

AIDS Apologists VS AIDS Dissidents - Truths About AIDS Denialists

©AIDS-Dissidents.tk
**Dear webmaster, we see your group/forum is being attacked by AIDS dissidents (we have had the same problem from sites like dissidentaction and virusmyth or from paulking, so we are warning you). Please make sure you block domain names listed on http://www.medchecker.com/dissident/aids-dissidents.htm . You must do what you can to stop these web terroists/trolls before they take over your web site and any rational conversations! It may be a good idea to remove this entire thread...

AIDS apologists are those who know HIV leads to AIDS (proven by science, so much scientific proof) and we are defending the scientifically known fact that viral pathogenesis and progression of 'HIV to AIDS' causes the eventual need for combination therapies to prolong life. Mixed "AIDS Apologist" links here or find comments here from both sides (dissidents and the scientific community), but still about AIDS Apologist activities...

AIDS dissidents (better known as AIDS Denialists who are AIDS dissidence, dissidence is anti-establishment like, against science and progression, argumentative) deny HIV causes AIDS and claim the medications kill the patients (AZT "over use" alone started this myth in the late 80s, but medicine combo/therapies are working today in the year 2000+). Basically a group of non doctors and non scientists who challenge the conventional HIV/AIDS model or hypothesis and do not accept the proven evidence. These dissident groups seem almost fanatical by them posting the same message multiple times to a targeted list of internet websites (non dissident sites of course, clogging up the normal flow of reading material with intentions of shutting the sites down) and insulting/bashing anyone who may not agree.

What are AIDS dissidents? Find out who, what, where, when and why:
http://www.hivforum.com/?dissident=dissident+site:aegis.com

What are AIDS denialists all about? See the myths exposed:
http://www.hivforum.com/?dissident=dissident+site:thebody.com

Learn about how they are murdering HIV positive people:
http://www.medchecker.com/dissident/aids-dissidents.htm

Thanks.
http://www.HIVforum.com

AIDS DissiDUNCE Exposed Blogs