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Help needed for HIV Education (AIDS DENIALISTS)

May 2, 2007

Hi Dr Bob, I always read this site and being a regular traveller to Africa i always pass of safe sex info to the locals. I have one gentthere who denies HIV/Aids is real and usually bounces all kind of info at me to back up his claim. Can you please point me in the direction of a reliable source where i can produce some scientific data to prove this guy wrong. This is his latest musing... "We've been told since the mid eighties that we're all at risk from this pandemic, it's going to be the world's biggest killer. But where is it?

We're told that HIV causes AIDS but this has never been proven. In fact the HIV test isn't exclusively for HIV, but non-specific anti-bodies that could be fighting HIV and also the common cold, pregnancy etc. etc.

Don't touch anyone elses blood - if they are infected you'll get it - right? Well how come only 25% of children born to HIV positive mother get HIV? surely this should be 100%.

How come in Africa if you get the runs for 30 days and lose 10% of your body mass you're AIDS infected? yet get on a plane and fly to the UK and you're not? In fact, you can have AIDS in the US and go to Canada and not have AIDS. If you have AIDS in Canada you can come to the UK, and not have it. This pandemic is very confusing!

I've never had an AIDS test, but then again it's not a test for AIDS. It's an HIV test, but then again it's not an HIV test either. But if you fall into a catagory where you may be having one of these tests, look at all the available information. Do some research outside of the AIDS multi billion dollar industry." Unbelievable hey Dr Bob. Thanks and keep up the fight.

Response from Dr. Frascino


I've addressed this topic many times in the past. I'll reprint a few of my comments from the archives below. You can find many more with a simple search. In addition I'll post some articles from AIDS Treatment News that address these issues. It's tragic that more than a quarter of a century into the global pandemic we have to waste any time whatsoever on such indefensible rubbish and debunked myths.

Good luck convincing your buddy to pull his head out of his butt and wake up to reality. Unfortunately he may find out the hard way that he is "dead" wrong.

Dr. Bob

AMERICAN FOUNDATION FOR AIDS RESEARCH Dr. Mathilde Krim Refutes AIDS Denialists on ABC's "20/20" August 2001

On ABC's "20/20" prime-time news program on August 24, 2001, Dr. Mathilde Krim, amfAR's Founding Chairman and Chairman of the Board, offered a clear and compelling response to the small but vocal group of AIDS denialists who argue -- incorrectly -- that HIV does not cause AIDS. Interviewed by Connie Chung, Dr. Krim underscored the danger that AIDS denialists pose to preventing the spread of HIV and to amfAR's work. "To see others on spurious, disingenuous arguments fight us and undermine what we are doing is very, very difficult to accept -- and, frankly, offensive," she said.

"The [AIDS denial] theory has been so thoroughly repudiated by the science that it now resembles more fantasy than hypothesis." -- GQ Magazine

The view that HIV does not cause AIDS is rejected by all but a handful of scientists who have done little or no research with AIDS patients and has been repeatedly debunked in scientific journals ranging from Science to the Journal of the American Medical Association. Last year, over 5,000 physicians and scientists from around the world signed a statement known as the Durban Declaration, which was published in the July 6, 2000, issue of Nature and affirmed that the evidence supporting the link between HIV and AIDS is "clear-cut, exhaustive and unambiguous. . . . It is unfortunate that a few vocal people continue to deny the evidence. This position will cost countless lives."

The evidence that HIV causes AIDS is overwhelming:

HIV infection correlates with epidemic AIDS.

Numerous laboratory, clinical research, and epidemiological studies have shown significant correlation between levels of HIV production and viral load and disease prognosis.

Simian immunodeficiency virus, which is quite similar to HIV, causes AIDS in animals (and HIV-1 itself can cause immune deficiency and AIDS in chimpanzees).

Anti-HIV drugs have succeeded in reducing AIDS-related deaths by more than 80% in countries where they are available. Also in July 2000, amfAR placed a full-page statement in The New York Times that took direct aim at those who continue to dispute the fact that HIV causes AIDS. Timed to coincide with the start of the 13th International AIDS Conference in Durban, South Africa, and signed and supported by over 500 researchers and physicians, the amfAR-sponsored statement targeted those who might be persuaded by dissident claims to discontinue HIV/AIDS treatments. Please see the PDF for the full text of the statement that appeared in The New York Times.

"The evidence that HIV causes AIDS is as good as the evidence that polio is caused by a polio virus and measles by a measles virus." -- Dr. Mathilde Krim

Ultimately, AIDS denialists are promoting misinformation that encourages people to ignore treatment and prevention messages that can save lives and prevent the further spread of HIV. The number of new HIV infections in this country remains constant at between 40,000 and 50,000 annually, and the recent National HIV Prevention Conference convened in Atlanta by the Centers for Disease Control and Prevention (CDC) highlighted several disturbing trends:

After dropping sharply in the mid-1990s, the number of U.S. AIDS cases and AIDS-related deaths remained stable between mid-1998 and mid-2000, underscoring the need for early HIV testing and expanded access to prevention and treatment services. As CDC director Helene Gayle observes, "The latest data suggest that the era of dramatic declines is over [and] there are a number of signs indicating that our progress in fighting the disease is in serious jeopardy."

There is evidence of continued increases in sexual risk behavior among both HIV-positive and HIV-negative men who have sex with men (MSM) across the U.S. A recent six-city study conducted by the CDC found that young MSM ages 23-29 are becoming HIV infected at annual rates comparable to those seen among some populations of gay men in the mid-1980s. Infection rates are especially high among African American MSM, indicating the need for targeted prevention outreach.

While representing less than one-quarter of U.S. women, African American and Latina women account for 82% of new HIV infections in this country. Injection drug use has accounted directly or indirectly for between 55% and 60% of all reported AIDS cases among black and Latina women. In addition, a recent finding that 17% of young minority MSMs also engage in sex with women highlights the role that bisexuality may be playing in placing women at risk of HIV.

New research shows that significant numbers of HIV-positive people go undiagnosed for up to a decade, forgoing life-prolonging treatment and potentially infecting others. It is estimated that half of all Americans with HIV have not been tested and do not know they are carrying the virus.

Finally, it should be noted that some denialists not only claim that anti-HIV treatment is ineffective, but that it actually causes AIDS. In reality, countless studies have affirmed that highly active antiretroviral therapy (HAART) can improve the health of people with AIDS and delay the progression of HIV disease. Likewise, there is overwhelming evidence that HAART has played a large role in the decline of AIDS-related deaths over the past several years. Certainly, there are serious toxicities associated with most of the anti-HIV drugs currently in use. But as reported in the September 8, 2000, issue of AIDS Treatment News, by forcing researchers and treatment advocates to expend unnecessary time and energy defending the link between HIV and AIDS (and the efficacy of anti-HIV treatments), the denialist movement "has diverted effort from critical questions regarding what sort of research is needed and how to speed the development of better, less toxic therapies."

Answering the AIDS Denialists: Is AIDS Real?

by Bruce Mirken December 1, 2000

Note: AIDS Treatment News has published a series of articles looking in depth at some of the bizarre ideas about AIDS, theories which are being used to persuade people to change or completely stop their medical treatment, or to ignore precautions for preventing HIV infection. One of the most bizarre is that the epidemic does not exist but is just a new name for a collection of old diseases. AIDS writer Bruce Mirken analyzes this claim and similar theories that have also been widely promoted. -- John S. James

The AIDS denialists, who dispute not only the role of HIV in AIDS but nearly all scientific knowledge about the epidemic, regularly claim that the very notion of AIDS as a distinct medical condition is a mistake. What medicine has identified as a major epidemic, they insist is nothing of the sort.

A number of variations on this theme have been put forth. Some have argued that AIDS is nothing but a "group fantasy" or "epidemic hysteria."(1) Others claim that several separate but real medical problems have been wrongly lumped together. ACT UP San Francisco has repeatedly claimed that "AIDS is over," suggesting that it did exist at one time but has somehow come to an end.

While most in the denialist camp accept some physical cause or causes for the illness we call AIDS, they claim science has fundamentally misunderstood what is going on, leading to faulty conclusions about causation.

"AIDS by definition is not new and is not a disease," the web site of HEAL Toronto declares. "AIDS is a new name for 29 old illnesses and conditions, including yeast infections, diarrhea, pneumonia, cancer and tuberculosis."(2) Christine Maggiore of the Los Angeles group Alive and Well adds that "every AIDS indicator disease occurs among people who test HIV negative," existed prior to AIDS, and has "medically proven causes that do not involve HIV."(3) AIDS, in this view, is just a new name given to these old diseases when they occur in people who test positive for HIV antibodies. Furthermore, it is claimed that inclusion of a positive HIV test in the criteria for an AIDS diagnosis has created a phony connection between these illnesses and HIV: "Pneumonia + positive HIV test = AIDS," Maggiore writes, but "Pneumonia + negative HIV test = pneumonia," thus creating "the illusion of a perfect correlation."(4)

Though factually wrong, such statements appear regularly in denialist literature.

Another complaint is that the number of AIDS cases has been artificially increased by repeated changes in the official AIDS definition. Adding more conditions to the definition, it is argued, pumps up the number of cases even though those new cases may not even be ill.(2, 4)

What Was New in 1981?

The notion that AIDS is simply "a new name for old diseases" requires ignoring years of history and reams of published medical data.

The official start of the AIDS epidemic dates from mid-1981, when the U.S. Centers for Disease Control and Prevention's Morbidity and Mortality Weekly Report described cases of Kaposi's sarcoma (KS) and Pneumocystis carinii pneumonia (PCP) in young, previously healthy gay men.(5, 6) Detailed reports of these and other cases, a few involving heterosexual drug injectors, were published in several medical journals later that year.

Prior to 1980 KS and PCP were extraordinarily rare in the U.S. Annual incidence of KS ranged from 2.1 to 6.1 cases for every 10 million people,(7) usually occurring in older men of European descent. The disease generally progressed slowly, with an average survival time of 8-13 years.(7, 8)

PCP was nearly as rare, and the drug used to treat it, pentamidine isothionate, could only be obtained through the CDC's Parasitic Disease Drug Service, which kept detailed statistics. Strictly a disease of people with weakened immunity due to disease, cancer chemotherapy or immune-suppressive treatment for organ transplantation, PCP had "never been convincingly demonstrated to occur in an immunologically normal adult."(9) In one study, 98 percent of patients had known immune defects, and the others were all seriously ill infants. Even though most were quite sick even before their PCP, the disease often responded well to treatment and relapses were rare.(10)

These new PCP and KS cases shattered the pattern. Most patients were young men, often in their 20s and 30s, with no identifiable reason for weakened immunity. Their KS was "fulminant, malignant"(8) and rapidly progressing. Some had both PCP and KS, and most had a cluster of other problems including persistent fever, weight loss, swollen lymph nodes, and other infections usually associated with weakened immunity, including cytomegalovirus and toxoplasmosis. This unremitting barrage set victims on a downward spiral that commonly ended in death within a year.(5, 6, 8, 9, 11, 12, 13, 14) This onslaught of infections in people with no known reason for being sick was so unusual that the usually reserved British journal The Lancet called it "bizarre" twice in one brief commentary.(15) Patients also showed unexplained weakness in their immune responses, with a consistent pattern of defects in their cellular immunity.(5, 6, 8, 9, 11, 12)

The physicians treating these patients had no doubt they were seeing a new clinical syndrome ("syndrome" is the medical term for a group of signs or symptoms that appear together and indicate a particular condition). And these doctors weren't babes in the woods. Several treated large numbers of gay men living a "fast lane" existence including multiple sex partners and recreational drugs, while others worked at urban hospitals treating many drug addicts, yet none of them had seen anything like this.(16)

The Evolving Definition of AIDS

As with any new syndrome, scientists' understanding of AIDS evolved gradually, with the most obvious and severe manifestations noticed first and rarer or subtler ones recognized later. A careful review of how the CDC has defined a case of AIDS contradicts the cartoon version presented by the denialists and shows that the definition has evolved cautiously -- perhaps too cautiously at times. (For simplicity this analysis will focus on the CDC's AIDS case definition. While not followed universally, health authorities in other industrialized countries often use the CDC's work as a starting point. The enormous subject of AIDS in Africa and other third world areas requires a separate article.) The CDC first published an AIDS case definition in September, 1982. AIDS was simply defined as "a disease, at least moderately predictive of a defect in cell-mediated immunity, occurring in a person with no known cause for diminished resistance to that disease." Thirteen specific diseases were listed.(17) HIV (then known as HTLV-III or LAV) was discovered in 1984, but the CDC waited a full year, until after a discussion at the Conference of State and Territorial Epidemiologists, before revising the AIDS definition. This new definition added a small number of conditions which would be considered AIDS-defining if they occurred in a person with a positive HIV test. But the original list of infections still triggered an AIDS diagnosis without an HIV test if they occurred in a person with depleted CD4 (T-helper) cells and no known reason for immune dysfunction.(18)

It was soon clear that patients commonly experienced a much broader array of illnesses than the indicator diseases listed by the CDC. In 1987, the agency noted, "It became apparent that some progressive, seriously disabling, even fatal conditions (e.g. encephalopathy, wasting syndrome) affecting a substantial number of HIV-infected patients were not subject to epidemiological surveillance, as they were not included in the AIDS case definition." So the agency made another cautious revision, with encephalopathy (dementia) and wasting syndrome being the most notable additions to the list of indicator conditions.(19)

But the CDC's AIDS definition was still capturing only a narrow piece of the picture, and not always the most severe piece. "There are very many people who are very ill who don't have AIDS by the CDC definition," said Los Angeles AIDS specialist Scott Hitt, M.D. (who went on to head President Clinton's AIDS Council) in 1990. "There are also people with one KS lesion (qualifying them for an AIDS diagnosis) who are doing very well."(20)

Part of the problem was that the only opportunistic infections that made it into the CDC's database were whatever conditions triggered a patient's initial diagnosis. CDC spokespeople acknowledged they simply didn't have the means to track the rest.(20) Pressure mounted on the agency to adopt a definition that was more reflective of the real-world clinical experience of the most seriously ill patients, and after a lengthy period of discussion and debate, the current definition went into effect in January, 1993. For the first time it allowed an AIDS diagnosis based purely on an immune system measure: a CD4 cell count below 200 or a CD4 percentage below 14. Based on strong epidemiological evidence, three conditions were also added as AIDS indicator diseases in people with HIV: invasive cervical cancer, pulmonary tuberculosis and recurrent pneumonia (defined as two or more episodes within one year).(21) One thing did not change: The core list of 12 opportunistic infections -- PCP, toxoplasmosis, etc. -- that dated from the mid-1980s would still trigger an AIDS diagnosis even without a positive HIV test.(21, 22) In other words -- and contrary to the denialists' claims -- a positive HIV test has never been required to diagnose AIDS in people with these otherwise rare illnesses. At this point it is useful to refer again to Maggiore's version of the AIDS definition, variations of which appear throughout denialist literature: "Pneumonia + positive HIV test = AIDS," but "pneumonia + negative HIV test = pneumonia." In fact, pneumocystis pneumonia triggers an AIDS diagnosis regardless of HIV status, and in HIV-positive persons, more conventional bacterial and viral pneumonias do not automatically trigger an AIDS diagnosis. To qualify as AIDS they must happen at least twice within a year, because only such multiple episodes are strongly associated with immune suppression.(21) Simply put, the "illusory correlation" so harped on by the denialists is an illusion of their own invention. Another favorite denialist complaint is that some of the toxicities of certain AIDS drugs match items in the list of AIDS-defining conditions. As with the assertions discussed above, this claim is based on a skewed and often blatantly inaccurate reading of the case definition. In any case, the list of toxicities often cited as "AIDS by prescription"(23) consists entirely of conditions whose association with HIV was well established before AZT and other antiretrovirals came into widespread use.

Duesberg's Epidemiology and Other Mysteries

A related but distinct thesis has been advanced by University of California Berkeley Prof. Peter Duesberg: AIDS is in fact several separate epidemics lumped together. Proof, he and colleague David Rasnick suggest, lies in the fact that members of different risk groups get different diseases. KS, he notes, is seen mostly in gay men, while "weight loss and tuberculosis predominate in intravenous drug users, and pneumonia and candidiasis are almost the only two of the 30 AIDS-defining diseases that are diagnosed in hemophiliacs."(24)

These "distinct, subepidemic-specific diseases," Duesberg and Rasnick argue, rule out a common cause, infectious or otherwise. They further insist that AIDS indicator conditions can be divided into those that are immune deficiency-related, like PCP, and those that aren't, such as KS. A significant proportion of AIDS cases, they note, are diagnosed based on these "non immune deficiency diseases."(24)

Duesberg's reading of the literature is, to put it gently, selective. For one thing, despite his repeated assertions to the contrary, an association between KS and weakened immunity had been well established in the medical literature prior to AIDS.(7) As for his claims about differing opportunistic infections in different risk groups, it is hardly a surprise that populations with widely varying behaviors, lifestyles and health risks would experience severe immune deficiency somewhat differently, and such differences have indeed been noted. But even a cursory glance at the medical literature quickly dynamites Duesberg's claim that these differences are so dramatic as to constitute separate epidemics. For example, five years before Duesberg and Rasnick's assertion that pneumonia and candidiasis are "almost the only two" AIDS-defining conditions seen in hemophiliacs, a European hemophiliac cohort found that of 37 diagnosed with AIDS, 6 had toxoplasmosis, 3 had wasting syndrome, 3 had dementia, 2 had MAC, 1 had CMV and 1 had lymphoma as their AIDS-diagnosing illness.(25)

The same Duesberg/Rasnick article touts both the "drug-AIDS hypothesis" and the "new name for old diseases" theory with an impressive list of references purportedly showing that AIDS-defining illnesses had been widely identified in drug users prior to and without AIDS. Duesberg's chart has at times been borrowed by other denialists.(24, 26)

But again his "evidence" wilts under close examination. For example, one reference he cites repeatedly -- as evidence that immune deficiency, candidiasis, lymphadenopathy and weight loss had been documented in heroin addicts pre-AIDS -- is a 1973 article by Pillari and Narus from the American Journal of Nursing. But the article, it turns out, isn't a study but simply an anecdotal description of patients seen in one treatment program. It gives neither numbers of cases nor occurrence rates for any of the conditions described.(27)

In fact, Pillari and Narus specifically mention just one of the four conditions Duesberg attributes to them, lymphadenopathy. Candidiasis is perhaps implied by nonspecific references to "fungal infections," while immune deficiency and weight loss are implied even more vaguely and indirectly. And although Duesberg's chart lists all four conditions as "AIDS defining," nothing in the article comes remotely close to describing an illness that would meet the criteria for an AIDS diagnosis.(27)

Finally, a different spin has been put out by ACT UP San Francisco. Some of their materials echo the general denialist notion that the whole epidemic is a scam, but their most-repeated phrase in recent years has been, "AIDS is over." Such statements often refer to declining numbers of AIDS cases and deaths.(28)

But extensive evidence links those declines to improved anti-HIV treatment (for more on this see AIDS Treatment News' special issue, "Treatment and Survival," Sept. 8, 2000). And for the families of the 10,198 people who died of AIDS during 1999 according to the most recent CDC figures,(29) AIDS is certainly not over.


1. Schmidt, Casper G., "The group-fantasy origins of AIDS," in The AIDS Cult, edited by John Lauritsen and Ian Young, Asklepios USA, 1997. 2. MacDonald, Robert, "Healthy skepticism about HIV," HEAL Toronto web site, 3. Maggiore, Christine, What if Everything You Knew About AIDS Was Wrong? American Foundation For AIDS Alternatives, p. 51. 4. Maggiore, p. 1. 5. Gottlieb, MS, and others, "Pneumocystis pneumonia -- Los Angeles," Morbidity and Mortality Weekly Report, 1981: 30: 250-52. 6. Friedman-Kien, A. and others, "Kaposi's sarcoma and pneumocystis pneumonia among homosexual Men -- New York City and California," Morbidity and Mortality Weekly Report, 1981: 30: 305-08. 7. Safai, B. and Good, R., "Kaposi's sarcoma, a review and recent developments," Clinical Bulletin, 1980: 10: 62-69. 8. Friedman-Kien, A., "Disseminated Kaposi's sarcoma syndrome in young homosexual men," Journal of the American Academy of Dermatology. 1981: 5(4) 468-71. 9. Masur, H. and others, "An outbreak of community-acquired pneumocystis carinii pneumonia," New England Journal of Medicine, 1981: 305: 1431-8. 10. Walzer, Peter D. and others, "Pneumocystis carinii pneumonia in the United States," Annals of Internal Medicine, 1974: 80: 83-93. 11. Gottlieb, Michael and others, "Pneumocystis carinii pneumonia and mucosal candidiasis in previously healthy homosexual men," New England Journal of Medicine, 1981: 305: 1425-31. 12. Siegal, Frederick and others, "Severe acquired immunodeficiencies in male homosexuals, manifested by chronic perianal ulcerative herpes simplex lesions," New England Journal of Medicine, 1981: 305: 1439-44 13. Durack, David, "Opportunistic infections and Kaposi's sarcoma in homosexual men," New England Journal of Medicine, 1981: 305: 1465-7. 14. Hymes, Kenneth and others, "Kaposi's sarcoma in homosexual men -- a report of eight cases," The Lancet, 1981; ii: 598-600. 15. "Immunocompromised homosexuals," The Lancet, 1981, ii: 1325-6. 16. Shilts, Randy, And the Band Played On, updated edition, Penguin Books, 1988, chapters 2-8. 17. "Current trends update on acquired immune deficiency syndrome (AIDS) -- United States," Morbidity and Mortality Weekly Report, 1982: 31: 508-08. 18. "Current trends revision of the case definition of Acquired Immunodeficiency Syndrome for National Reporting -- United States," Morbidity and Mortality Weekly Report, 1985: 34: 373-5. 19. "Revision of the CDC Surveillance Case Definition for Acquired Immunodeficiency Syndrome," Morbidity and Mortality Weekly Report, 1987: 36(supplement no. 1S). 20. Mirken, Bruce, "AIDS Name Game: Help or Misery Turns on Obsolete Definition," Los Angeles Reader, May 25, 1990, p. 3-4. 21. "1993 revised classification system for HIV infection and expanded surveillance case definition for AIDS among adolescents and adults," Morbidity and Mortality Weekly Report, 1992: 41: RR-17. 22. Kitty Bina and Dr. Richard Selick, CDC, personal communication. 23. Maggiore, p. 30. 24. Duesberg, P. and Rasnick, D., "The AIDS dilemma: Drug diseases blamed on a passenger virus," Genetica, 104:85-132, 1998. 25. Aronstan, A. and others, "HIV infection in haemophilia -- a European cohort," Archives of Disease in Childhood, 1993: 68: 521-24. 26. Maggiore, p. 56. 27. Pillari, George, and Narus, June, "Physical effects of heroin addiction," American Journal of Nursing, 1973, 73: 2105-8. 28. ACT UP San Francisco press release, "ACT UP San Francisco launches survive AIDS campaign," March 27, 2000. 29. U.S. HIV and AIDS Cases Reported through December 1999, year-end edition, Vol. 11, no. 2.

ISSN # 1052-4207 Copyright 2000 by John S. James. Permission granted for noncommercial reproduction, provided that our address and phone number are included if more than short quotations are used.


Has Anti-HIV Treatment Cut AIDS Deaths? November 3, 2000

How Do We Know That the Drugs Used to Treat AIDS Work?

The Bottom Line

Since 1995 the number of deaths from AIDS in the United States has dropped from nearly 50,000 per year to less than 17,000. Deaths have dropped in Europe and Canada too. Doctors and scientists believe that fewer people are dying because many have been helped by new treatments which work against HIV, the virus that causes AIDS. But some people claim that HIV doesn't really cause AIDS. These people, called "AIDS deniers," "denialists" or "AIDS dissidents," say the new drugs haven't reduced AIDS deaths. Some even claim that the medicines actually make people get sick and die.

How Do We Know That the Drugs Used to Treat AIDS Work?

How were the "drug cocktails" developed?

When the AIDS epidemic began in 1981, there were no drugs to fight HIV. When the first drugs became available in the late 1980s, patients generally used only one of them at a time. But in December, 1995, the first of a new kind of anti-HIV drug, called protease inhibitors, was approved. Scientists discovered that they worked best when used together with at least two of the older drugs. These combinations are known as "cocktails" or "HAART," which stands for "Highly Active Anti-Retroviral Therapy." Doctors saw many of their sickest patients get better when they started HAART.

When did AIDS deaths start to drop?

Some AIDS deniers say that AIDS deaths were dropping before HAART became available, so the drugs couldn't be the cause. That is not true. The most AIDS deaths ever in the United States happened in 1995, when almost 50,000 people died of AIDS. The first protease inhibitor was approved for sale that December, and soon HAART began to be used widely. In 1996 the number of deaths dropped below 37,000.

After rising every year since 1981, 1996 was the first year that AIDS deaths ever dropped. The number of deaths dropped again in 1997 and 1998.

Did other things affect AIDS death rates?

Yes, the rise in AIDS deaths began to slow down in the early 1990s for two reasons: First, as we learned more about AIDS in the early 1980s, many people began using condoms or having fewer sexual partners. The spread of HIV slowed, but because HIV takes about 10 years to cause AIDS, it took until the 1990s for safer sex to slow the rise in AIDS cases and deaths.

Second, doctors learned more about how to treat AIDS. Even before HAART, doctors were learning to combine anti-HIV drugs and got better at preventing or treating many of the infections that kill people with AIDS.

These better treatments were already starting to slow down the increase in AIDS deaths. But HAART dramatically added to that improvement.

How do scientists decide if medicines work?

Scientists study new medicines in what are called clinical trials: One group of patients takes only their regular medicines, while the other group takes the new drug being tested. Then the groups are compared to see who does better. These trials showed that patients on HAART stay healthier and live longer than those taking just one or two anti-HIV drugs.

What other ways do scientists learn about new drugs?

To better understand what helps people stay healthy, scientists do cohort studies. A cohort is simply a group of people who are alike in some way -- such as having HIV infection. Some cohort studies involve all types of people with HIV -- young, old, male, female, etc. Others look at certain groups, like women or gay men. In a cohort study, scientists try to learn as much as they can about people's daily experiences in order to see what helps them. The volunteers come in regularly to have blood tests, and at the same time the scientists ask about things that may affect their health -- like what they eat, whether they smoke, drink alcohol or take any medicines.

These studies can be very large, with many thousands of people, and often go on for many years. All the information from these thousands of people helps doctors learn what things help or hurt people over a long period of time.

What do cohort studies say about anti-HIV drugs?

These studies have told us that people on anti-HIV treatment almost always do better than those on no treatment, and people taking HAART live longer and stay healthier than people who take only 1 or 2 drugs.

One of the largest HIV/AIDS cohorts began in 1990. This "Adult/Adolescent Spectrum of Disease Project" has studied over 49,000 people with HIV. By January, 1998, 9,280 had died. Patients on any anti-HIV treatment were less likely to die than those with similar illness who weren't taking anti-HIV medicine. People not taking anti-HIV drugs were 6 times as likely to die as comparable patients on 3-drug HAART combinations.

Another cohort, the HIV Outpatient Study, has followed over 3,500 HIV patients in eight U.S. cities since 1992. In this group, people not taking any anti-HIV treatment were four and a half times as likely to die as comparable patients taking combinations that included a protease inhibitor. Several large studies in Europe have shown the same kind of result.

In San Francisco, the Department of Public Health has kept track of about 95 percent of the city's AIDS patients. Patients taking combinations that included a protease inhibitor were 57 percent less likely to die than people who didn't take any anti-HIV treatment.

The Bottom Line

Anti-HIV drugs are strong medicines that can have serious side effects. And there is still more we need to learn about how to use them to get the best results. But large studies done around the world have all found the same thing: Anti-HIV treatment has helped thousands of people infected with HIV to live longer and stay healthier. The evidence shows that anti-HIV drugs have played a big part in reducing AIDS deaths.

See our Web site ( for a PDF version of AIDS Treatment News #354.

ISSN # 1052-4207 Copyright 2000 by John S. James. Permission granted for noncommercial reproduction, provided that our address and phone number are included if more than short quotations are used.

AIDS TREATMENT NEWS AIDS Treatment Improves Survival: Answering the "AIDS Denialists" by Bruce Mirken September 8, 2000


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 denialists 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.

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ISSN # 1052-4207 Copyright 2000 by John S. James. Permission granted for noncommercial reproduction, provided that our address and phone number are included if more than short quotations are used.

AIDS TREATMENT NEWS AIDS Denialists: How to Respond by John S. James

May 5, 2000

For over ten years self-styled "AIDS dissidents" have said that HIV does not cause AIDS, that AIDS is not a contagious disease, that HIV is a harmless retrovirus (some say, instead, that HIV does not exist), that AIDS treatments are poisons which themselves cause the disease, and that the AIDS epidemic is a huge medical fraud promoted by corrupt pharmaceutical companies, scientists, and doctors. This movement has learned to appeal to very different agendas; and along with heavy doses of misinformation it weaves some accurate facts and emotional, social, and political truths. It has hidden funding, celebrity endorsements, and corporate journalists who can get its views publicized in mass media as news. It does not conduct medical research nor take care of patients, but has more than a decade of experience in learning how to debate and look credible. Our concern is not the ideas -- we agree that all sorts of ideas should be explored and debated -- but rather the direct translation of casual speculation and debating points into the medical care of patients with life-threatening illness, which is strongly encouraged by many of the "dissidents."

In the U.S., where AIDS treatments usually have been accessible to patients who need them, this movement has made noise for many years, but has found only a tiny constituency of believers who will put their lives at risk by rejecting all medical advice in favor of the rhetoric and debate. But recently it has been revitalized by tapping into other agendas in developing countries, where people have been told that they are going to die and have no chance of treatment, because the drugs have been priced far beyond their reach (by U.S. and international government policies to protect the interests of major corporations, as well as by corporate greed). The "dissidents" (we believe a better term is "AIDS denialists") have found a new audience among leaders and publics who are understandingly suspicious of a Western- dominated, heavily corporate mainstream which pursues its own profit above all else, and offers millions of people around the world nothing but death.

These issues will be prominent in the next few weeks, through the XIII International AIDS Conference in Durban, South Africa, July 9-14, 2000. This conference, by far the largest in the world, happens only once every two years; this is the first meeting in a developing country. And South Africa is the only country in the world where the AIDS denialists have ever been recognized by a head of state (see "South Africa 'AIDS Dissident' Dispute: Time to Stop and Think," AIDS Treatment News #340, April 7, 2000).

How to Answer

For years most AIDS doctors and scientists have seen the denialists as a lunatic fringe best ignored in hopes that it would go away. They did not want to bring it more attention, or spend their time rehashing issues that were settled years ago in the scientific community. And few of them were prepared for this debate -- for while they have spent their time treating patients or conducting medical research, the other side has spent years doing nothing but debating, learning what goes over and what does not in various forums, and learning how to use the Internet, where anything can be made to look credible.

Many now agree that refusing to answer is a mistake. AIDS professionals and activists often forget that the world looks different to people who do not have the same access they do. We have had long conversations with sincere, intelligent people, including patients and journalists, who had clearly been influenced by the denialists and who told us that we were the first person they had ever found who would talk to them to defend the "mainstream" view. Their doctors would not discuss it, nor would any researchers they asked. Most people do not have the background or training to judge a technical scientific argument themselves; instead, they look at how they are being treated. When one side will not give them the time of day on the issue while the other is always available, they may believe those they can talk to, without hearing any other view. While some researchers and activists have answered the denialists (for Web links, see, it has long been difficult for patients to find understandable and effective written answers to some of their claims. So if one does answer the denialists' arguments, what form should the answers take? We have discussed this with a number of activists, and there is clearly an emerging consensus: (1) The denialist position consists of about 5 to 10 major points (depending on how you count them -- we list 7 below), which are repeated again and again. Each must be addressed separately, with separate flyers or brochures which healthcare and service professionals can give to clients to address their individual concerns.

(2) The back-and-forth debate format is not especially useful here, because it tends to turn on technical points, asking readers to make their own decisions on the scientific merits of the issue, which most people are not prepared to do. A better format is to explain what the denialists are saying, then show with two or three examples that their arguments are not credible -- that the assertions on which they ask others to base life-and-death decisions usually leave out far more compelling information than they include. Most importantly, we need to explain what is really going on in treatment and research -- the human story as well as the medical/scientific one, a reality more interesting than the stick-figure ideologies of the denialists. Here we should avoid the argumentative style of trying to score points against the other side. Instead, follow the truth wherever it may lead; when there is truth in the denialist case, by all means acknowledge it.

(3) Eventually we will need an in-depth, well-referenced document explaining the issues to healthcare and AIDS service professionals, and also to patients and anyone else who wants this detailed information. (For an example of what part of this document might look like, see the article by Bruce Mirken which we published in our last issue, "Answering the AIDS Denialists: CD4 (T-Cell) Counts, and Viral Load," AIDS Treatment News #341, April 21, 2000. This article addresses one of the seven or so major denialist assertions, which we list below. The other six articles still need to be written.) (4) From this in-depth document can come the flyers, brochures, videos, Web sites, and other media.

Seven Deadly Deceptions

Here is our list of the major denialist arguments. As noted above, the problem is not unorthodox ideas, but their immediate translation into personal medical advice, usually to tell patients to reject all medical care for HIV or AIDS, as well as suggesting that safer sex and other infection- control precautions can be ignored. So for each of the seven points, we include the corresponding action item. We are continually amazed at how casually sheer speculation gets translated into life-and-death decisions.

* HIV is harmless (or does not exist), and AIDS is not contagious -- so sexual and other precautions are unnecessary.

* The HIV test is unreliable -- so don't get tested.

* AIDS drugs are poisons, pushed by doctors corrupted by the pharmaceutical industry -- so don't take any of them, no matter what your doctor says -- or don't go to a doctor at all, especially if you feel well.

* Viral load and CD4 tests are useless -- so don't use them.

* AIDS deaths would have gone down anyway, even without new treatments -- so you don't need medical care.

* AIDS is over, or never existed, or only affected small risk groups -- so there is no important need for medical research on AIDS or HIV, or for AIDS services.

* The free speech of dissenters has been suppressed -- so you can't believe anything you hear.

Note: We omitted the idea that AIDS was created in a government laboratory to kill African Americans, gay people, or others. This conspiracy theory is widespread in some communities, but usually does not urge people to reject medical care, or safer sex or other precautions against infection.

Note on "Denialists" vs. "Dissidents"

Some of these medical ideologists are upset with the term "AIDS denialists"; they prefer "AIDS dissidents," which suggests parallels with such historic examples as anti-totalitarian dissidents, or Galileo.

We use "denialists" because it is more specific and descriptive. There can be many kinds of AIDS dissent. But the denialists regularly deny that precautions against infection are necessary, deny that HIV testing is appropriate, deny that any approved treatments should be used (or CD4 or viral load tests to monitor disease progression), deny that treatment saves lives, and often deny that AIDS is a real epidemic, or even a real medical condition. The problem is not ideas, but the organized efforts to practice bizarre medicine, telling people with a major illness to reject care entirely. Denialists have convinced pregnant women or mothers of HIV-positive children to reject treatment universally recommended by their doctors -- then harvested publicity from court cases which result. In the U.S. and other countries where treatment is available, they have found few who will sacrifice their own lives; but now they are going to South Africa and elsewhere in the developing world, seeking to deny medical care to people who will have little or no voice in the decision, while also impeding public-health campaigns to slow the spread of HIV infection. The issue here is not freedom to express ideas; no one is stopping that. The issue is destructiveness by a handful of professional or semi-professional denialists whose ideas and behavior have failed to win them the respect they want.

The AIDS denialist movement will be remembered if it can do serious damage to worldwide efforts to control the pandemic. Otherwise it will be largely forgotten, like similar movements during other epidemics in the past.

ISSN # 1052-4207 Copyright 2000 by John S. James. Permission granted for noncommercial reproduction, provided that our address and phone number are included if more than short quotations are used.

AIDS TREATMENT NEWS Answering the AIDS Denialists: CD4 (T-Cell) Counts, and Viral Load By Bruce Mirken

April 21, 2000

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®]), 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 199, 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 1,604-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 1,170-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 negelcted to refute theories expressed by self-styled AIDS dissidents -- 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, Also, see

References 1. ACT UP Hollywood home page, 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 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 o

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