HIV is not the cause of AIDS

(Much of the following is taken from Henry Bauer's book, The Origin, Persistence and Failings of HIV/AIDS Theory.)

Around 1980, in Los Angeles, New York and San Francisco, there were sudden outbreaks of rare, opportunistic infections, infections that were nearly unheard of in individuals with healthy immune systems. These infections consisted mainly of Pneumocystis carinii pneumonia and Kaposi’s Sarcoma, with a little candidiasis and other fungal infections on the fringes. They happened almost exclusively in gay communities, and were called GRID, for gay related immunodeficiency. Many suspected an infectious agent was responsible.

While the myth has been established that these were healthy young men, the truth is their ages ranged between 20 and 50 years, and they were drug abusers, living what became known, in the seventies, as the fast track lifestyle. 96% of the early AIDS cases had abused poppers and most had abused other drugs as well, such as heroine. The vast majority had had STD’s, and many were habitual takers of antibiotics, creating the possibility of long term, suppressed but not eradicated venereal diseases, which are known to weaken immune systems.

Since then, Kaposi’s Sarcoma’s cause was found to be HHV-8, human herpes virus eight. There are some who think there may be co-factors, but it is now known that HIV does not cause Kaposi’s Sarcoma. To the dispassionate observer, this must seem a severe blow to the HIV/AIDS dogma. One of the two primary AIDS illnesses of those early years is not an AIDS illness. This means that all there is left to explain is an outbreak of pneumonia in a population at severe risk for weakened immune systems. It practically explains itself, does it not? There is no need to resort to a mysterious “lentivirus”, a virus that does no harm until years after infection.

Throughout the 1970’s, virologists were on the hunt for viruses that caused cancers. Robert Gallo claimed to have found one that caused leukemia, HL23V. It was later discovered not to exist (Barbacid et al., 1980; Snyder and Fleissner, 1980). By the 1980’s, that quest had been given up, and virologists were looking for ways to justify their funding. Gallo latched on to AIDS and, as he had done in 1975, claimed to find a retroviral cause. But what did he actually do?

In order to isolate a retrovirus, there are a number of things that need to be established, things agreed upon at a convention by the Pasteur Institute in 1973, and things that Gallo himself stressed as important. A retrovirus has a density of 1.16 gm/ml, so samples are placed in a centrifuge prepared with sucrose that gets progressively denser. After spinning, particles will sink until buoyancy won’t let them sink further, and retroviruses sink to, or band at, 1.16 gm/ml. EM photographs of this band must be taken to establish the presence of particles that at least look like retroviruses. Not all such particles will prove to be retroviruses, but if there are no particles with that appearance, then no retroviruses are present.

Next, after ascertaining the attributes of these virus-like particles, virgin cells must be co-cultured with the particles, and then the centrifuge process is done again. If identical particles, looking like retroviruses, are found in the virgin cells, the particles can be called retroviruses, because they look like retroviruses, have the same density as retroviruses, and also infect like them. This constitutes discovery and isolation of a retrovirus. Gallo did far less than this when he claimed to discover HIV.

He cultured T-lymphocyte cells, because the T4 lymphocytes, also called CD4 cells, were the ones that dwindled to almost nothing in AIDS patients. Fluids from this culture were co-cultured with a stock, leukemic T-cell line called HT. Under a microscope he found particles resembling viruses and detected reverse transcriptase activity (reverse transcriptase is what turns RNA into DNA and allows a virus’ RNA to merge with the DNA of an infected cell). He gave no evidence of any virus-like particles banded at 1.16 gm/ml.

At this point, what has he established? Next to nothing. Without proof of virus–like particles at 1.16 gm/ml, we don’t know whether there is the possibility of a virus. Reverse transcriptase is not unique to retroviruses, and indeed human cells have enzymes that mimic reverse transcriptase activity, so the presence of this activity in the culture does not establish the presence of a retrovirus.

Next, he mixed proteins from the culture – which may or may not have been viral proteins because viral presence was not established – with sera from AIDS patients and observed antibody reactions with the proteins. On this basis he claimed discovery of what would come to be known as HIV. But what did he actually discover?

Since he did not even establish retroviral presence in the first two cultures, much less a single, unique retrovirus, the proteins cannot be considered as definitely viral, much less specific to one retrovirus. Indeed, it is known that one of the proteins, p24, is not specific (Agbalika et al., 1992; Mortimer et al., 1992). Therefore, the antibodies are equally unknown. However, even if the proteins were definitely specific to a unique retrovirus, there is no reason to believe that the antibodies reacting with them are monogamous. Most proteins and antibodies display cross-reactivity. So all that Gallo did was show that proteins from one AIDS patient – or possibly from the HT cell line – reacted with antibodies from some other AIDS patients (not all!).

After looking for the new putative retrovirus, he claimed to discover it in 26 of 72 AIDS patients. 26 of 72. And he claimed to find it in their sera if two of the following four conditions obtained: unbanded virus-like particles were discovered; reverse transcriptase activity was detected; antibodies reacted with proteins; virus-like particles were transmitted to bone marrow or other samples. Even his 26 “hits” are dubious.

When he went back to look for just antibodies in AIDS patients, he found that 88% of them had the antibodies he had never proven specific to HIV. It is not surprising to find antibodies in patients as sick as these men were, but even then he did not find the HIV antibodies in all of them, nor even his watered down claim of HIV in many more than a third. How did he claim to have found the cause of AIDS, then? Keep in mind, he had used the same process to “find” HL23V, except in that case he had actually published EM photos of virus-like particles banded at 1.16 gm/ml. If HL23V was found to be a chimera, why should HIV have been considered proven? The process was obviously fallible, and the process used for HIV was a watered down version of the one that had already blown up in his face in 1980.

But Gallo had the clever idea of bypassing the peer review process and running straight to the government. The Secretary of Health and Human Services announced, on April 23, 1984, that the likely cause of AIDS had been found. Over the next year, the word likely was dropped from the literature, but with no further evidence to justify this.

A word on lentiviruses is in order here. Carleton Gajdusek won a Nobel Prize for demonstrating that kuru, mad cow disease and other similar diseases were caused by a lentivirus, a virus that does its damage long after infection. This went against the germ theory of disease, where a germ entered and multiplied and was either finally overtaken by antibodies or killed the host. Germs were not supposed to lay in wait and only produce their disease years later. HIV was supposed to be one of these lentiviruses, a concept first introduced for kuru.

In 1997, Stanley Prusiner won the Nobel Prize for showing that prions, a kind of infectious protein, were actually the cause of the diseases, not a lentivirus. The very existence of lentiviruses might have been reexamined. At any rate, extraordinary claims require extraordinary evidence. A retrovirus that kills its host cell is an extraordinary claim (they need the cell to survive in order to reproduce). The idea of a lentivirus itself is an extraordinary claim. More extraordinary claims would be added later. And what for? To explain an outbreak of pneumonia among a drug abusing and sexually promiscuous segment of the population. Occam’s Razor speaks loudly and clearly on this one.

After Gallo, AIDS evolved into a different syndrome. Other researchers, using Gallo’s methods, established a few more HIV proteins. Patients in hospitals were now tested for HIV, and when enough patients with a certain disease had antibodies that reacted with these proteins, a new disease was added to the list of AIDS defining illnesses.

But we run into yet another problem here. If these new diseases were actually AIDS illnesses, why did they not break out in the early 1980’s like PCP and KS had done? Indeed, most of the illnesses were waning, not waxing. Cervical cancer, for instance, went down 50% from the period 1975-2003, declining by a few percent each year.

Deaths due to AIDS jumped in this era, but part of that was because old diseases that were already killing people were added to the list. Another reason was that AZT was given to people who might have needed nothing more than to stop abusing their bodies.

AZT was developed in the 1960’s to fight cancer. It proved so toxic that no patent was applied for; it was considered useless. With the advent of HIV/AIDS theory, AZT became a moneymaker, and a patent was petitioned in 1985 and granted in 1987. The original idea behind AZT was that it might kill the cancer cells before it killed the person, but this did not pan out. A few compromised studies – one might even say fraudulent – purported to show that AZT improved outcomes. It was not until the Concorde Study, where proper controls were used, that AZT was shown to increase, not decrease, mortality (Seligmann et al., 1994).

So drug abusers and sufferers of multiple STD’s in the early 1980’s experience immune system collapse. Then, anyone with non-specific proteins and/or antibodies is put in the category of AIDS, which increases the death toll. AZT further increases it. All the while, there is no isolation of the virus (Bess et al., 1997; Gluschankof at al., 1997; Papadopulos, 1997; Pease, 2005, 127-9) , no proof that it exists, not enough correlation between HIV and AIDS even if one were to accept that Gallo isolated a virus, and no good reason to believe that a retrovirus, whose believers do not even claim to find it in more than one out of every one hundred T-cells, would wipe out the cells it needs to propagate. By 1997, we could add that the very idea of a lentivirus was questionable.

In 2004, David Rasnick gave a good summary of what is meant by “isolation” of HIV in modern virology. The ultimate test that the establishment offers is what’s called a co-culture technique where you take a sample of the individual’s blood cells, white blood cells. You cannot find HIV now in this sample. All you have are these blood cells. But then you culture these cells with some special cells that Robert Gallo generated some years ago. You have to throw in some powerful chemicals, phytohemaglutinin or IL-2, for example, to force these cells to do anything. The idea is to wake up the patient’s cells to start producing RNA; and then this RNA will be coated in a protein, and possibly then there will be viral particles produced in the medium. These viral particles now will go infect the other cells that you added, and then you will amplify by a period of time the replication of these viral particles in the laboratory, what we call in vitro. Now, these particles did not exist in the patient, in the human being, the person that you got this sample from. You created them in the laboratory. And by creating these virus particles in the laboratory, people say they have isolated HIV from a human being. They have not done any such thing.

In 1993, the definition of AIDS was changed again, in the United States, to be anyone who got a positive on an HIV test and a one-time CD4 count below 200. It has never been shown that a low CD4 count is necessary and sufficient to wreck the immune system (Seligmann et al., 1994; Cohen, 2001, 150). Indeed, sitting out in the sun might lower your count enough, but now, the correlation between HIV and AIDS was tautological. If you had HIV and a low CD4 count, even if you weren’t sick, you had AIDS. If you had AIDS symptoms but did not set off an HIV test, you had idiopathic CD4 T-cell lymphopenia. It should be noted that a large part of the decreased mortality in AIDS patients came from the fact that they were now not necessarily unhealthy. The cessation of AZT was also a blessing, and though the newer drugs were dangerous too, they were given in lower doses (low enough that hormesis now can go some way to explaining improved health outcomes).

So now we have people with HIV who have AIDS. We have people with HIV who do not get AIDS, or who remain healthy even after that one-time low CD4 count. We have people without HIV who remain healthy. And we have people without HIV who get what would have been called AIDS before 1993, but is now called the aforementioned infelicitous idiopathic CD4 T-cell lymphopenia. How exactly is HIV responsible for AIDS any more than, say, freckles are? I imagine there is a similar distribution, with the exception that AIDS diseases do indicate an increased risk of being HIV positive, for reasons that will be explained later.

Because the definition of AIDS has changed so much over time (and indeed varies today from country to country – find me another disease which you can contract in, say, Africa and cure yourself merely by flying to Uruguay), it can be difficult to get a good grasp on the issue. Nevertheless, a picture has emerged that looks nothing like a sexually transmitted disease.

The prevalence of HIV does not correlate well with the presence of other STD’s in a population. For instance, numerous studies in French Polynesia, Hong Kong, Singapore, Thailand, Papua New Guinea and Malaysia found that while STD’s were declining, HIV rates were increasing. A large study in Uganda of efforts to reduce transmission of STD’s noted that gonorrhea, herpes and syphilis had indeed decreased, but the infection rate of HIV remained unchanged (Kamali et al., 2003; Stephenson and Cowan, 2003).

300 Pakistani truckers, a group constantly fingered as spreaders of contagion, found a 12% syphilis rate. 50% had had sex with prostitutes and 20% had had sex with other men. 65% never once used a condom, and only 5% had used a condom during their last sexual encounter. Not a single one had HIV (Shah et al., 2002).

Condom use does not affect transmission rates of HIV (Wawer et al., 2005, 1406; Padian et al., 1987).

Given that the probability of transmission of HIV is one in one thousand sexual contacts, it is hard to understand the magnitude of HIV (Chakrabarty et al., 2001).

Rabkin et al., 1987, found that there was no correlation between the prevalence of HIV and exposure to prostitutes.

Horsburgh et al., 1990; Brown, 2006; and Kelley et al., 1986 found low to no seroconversions in looking at prison systems in Nevada, Georgia and the military.

Finally, no STD displays a regular infection rate across gender, geographical and racial lines, but HIV does. Babies test HIV+ more often than teenagers, but the older one gets, the more likely one is to be HIV+ until around age fifty or so, and then it drops off. No matter the rate of infection, the ratio remains roughly constant. Urban areas test HIV+ more often than rural areas. Blacks test HIV+ more often than whites. Men more than women. There is an explanation for this, but it has nothing to do with an infectious agent.

Real STD’s, on the other hand, vary through time. They change geographic foci, as well as sexual and racial proportions. Syphilis, around the time we became aware of AIDS, was primarily a disease of white, homosexual men. In 1990, however, there was an outbreak in black communities, affecting both men and women. Over a two decade period, relative rates of infection of males and females changed by a factor of over two. More recently, gonorrhea, in the span of just five years, went up 22% in whites, but down 19% in blacks.

Things can change very quickly with a real STD. The states in 2003 with the highest rates of gonorrhea infection included only six of the 11 states with the highest rates in 2001. For adult inmates, only half of the top eight states in 2001 were in the top eight in 2003. Between 1997 and 2003, syphilis increased in the West and Northwest, remained stable in the Midwest, and decreased in the South (www.cdc.gov/std/2004STD-Conf/Slides/A-sessions/A7/Heffelfinger.pps, accessed March 25, 2006).

There is no such occurrence with HIV. The infection ratios have remained stable since testing began.

Nor does HIV behave like a virus passed along through contact with dirty needles. Kruger et al., 1990 found, at a drug clinic, that intravenous drug users (IDU) who used clean needles had a 34% infection rate of HIV, whereas the ones who shared needles had a 19% infection rate. People who use clean needles have less hepatitis B, according to one study, but ten times greater frequency of HIV infection (Bruneau et al., 1997). Correlations between dirty IDU and HIV infection rates were searched for, but not discovered. Instead, HIV infection rates were found to correlate only with race and geography (Lange et al., 1988). Vlahor et al., 1989 found zero spread of HIV from IDU in Maryland prisons.

Even more convincing is the fact that health care workers almost never contract HIV. Despite the fact that about a 1,000 health care workers a year contract some disease through workplace accidents, only a few dozen, representing a handful a year, are thought to have contracted their HIV through a needle stick, or some other accident. This is by no means proven, as the testing done for HIV is done with kits that come with disclaimers saying they should not be used to determine HIV infection.

Viral load test: The Amplicor HIV-1 Monitor test is not intended to be used as a screening test for HIV or as a diagnostic test to confirm the presence of HIV infection.

Western Blot test: Do not use this kit as the sole basis of diagnosing HIV-1 infection.

ELISA test: EIA testing alone cannot be used to diagnose AIDS, even if the recommended investigation of reactive specimens suggests a high probability that the antibody to HIV-1 is present […]there is no recognized standard for establishing the presence and absence of HIV-1 antibody in human blood (emphasis mine).

The regularity of HIV infection ratios bears some comment here, especially with respect to race. As mentioned, blacks always test higher for HIV than whites and Asians. The problem with this is that, according to HIV/AIDS theory, one gets AIDS from choosing to engage in risky behavior. Notwithstanding the evidence presented above, it is thought that AIDS is primarily a sexually transmitted disease, with a significant portion getting it from dirty needles. Though it is true that babies are said to acquire it from the mother, the mother herself must have engaged in sex without a condom, or injected herself with a dirty needles according to the orthodox theory.

While it is no secret that blacks choose to commit crimes more often than whites, this difference disappears when one disaggregates the data and proper controls are applied. A group of whites raised in the same condition, and living in the same circumstances, as a group of blacks will commit crimes at the same rate. With HIV infection, there is no disaggregation of the data that levels the infection rates between blacks and whites. Blacks ALWAYS test positive with greater frequency, whether they were raised with a father or not, whether they were raised in the suburbs or the ghetto, whether they were raised on welfare or not, in poverty or plenty, north or south, east or west. But HIV is contracted through poor decision making… this is tantamount to saying that no matter how educated, well raised, rich or well-placed a black is, he will always make riskier choices, with respect to sex without a condom and drug use, than a white. The testing for HIV is invalidated on this one point alone.

The orthodox explanation for AIDS is invalidated on many more points. For instance, ever since testing began – and testing has been widespread for well over two decades – the number of HIV infected in the United States has hovered at just over one million people. This is true all the way back to 1985, at the start of testing. But why the ups and downs in AIDS cases? Should not the HIV infection rate run parallel to, albeit slightly ahead of, the AIDS rate? And if about a million people were already infected in 1985, how did it spread so quickly, given the extremely low transmission rates? And why were HIV infection rates not necessarily highest where AIDS first showed up (Burke et al., 1990)? Why did HIV infection not radiate out from the original centers of AIDS, New York, Los Angeles and San Francisco?

And why were 90% of the early cases male, given that the male/female ratio of HIV infection was already, by 1985, nowhere near nine to one. Among military applicants, males and females had equal infection rates (Burke et al., 1990). Even in the late eighties a large disparity persisted, and it was not until the addition of cervical cancer to the list, in 1993, that the AIDS ratio was brought in line with the HIV ratio.

Why did blood transfusions in San Francisco before 1985, despite being about 6-7% from gay men, not spread HIV, except in one possible case which itself is doubtful, given the child’s health before transfusion?

Why can’t the virus be isolated? Why do people get AIDS without HIV (idiopathic CD4 T-cell lymphopenia)? Why do many people who test positive for HIV not get AIDS? Why can’t the method of CD4 destruction be determined?

AIDS theory has become like Ptolemy’s theory of the solar system, epicycles and more epicycles. Instead of a simple, clean theory, we get all manner of nonsense. To explain the number of HIV infected people living in good health, an increasingly long gestation period was attributed to the disease, going against the standard germ theory. A lentivirus was invoked, and still is, despite the fact that the very foundation for acceptance of the existence of lentiviruses was blown up by the mid-nineties. This particular retrovirus, aside from being a lentivirus, also destroyed the cells it needed to reproduce. When curious differences were found in the many different putative cultures of HIV, it was claimed that the virus must mutate at an unprecedented rate. The differences are not surprising, given that HIV is never purified and whatever it is they are seeing will be different based on the individual whose mycoplasma, cellular debris and other material inhabit the culture with the alleged HIV. What is surprising, or at least disappointing, is that scientists will not recognize the epicycles they are creating.

Perhaps the most absurd epicycle is immune restoration syndrome. Many healthy individuals who test positive for HIV are given dangerous drug cocktails and consequently develop health issues, like inflammation, opportunistic infections, liver damage and swollen lymph glands. The orthodox explanation? This is just the body’s way of reacting to its immune system being restored (Davaro and Himlan, 1999; DeSimone, Pomerantz and Babinchak, 2000). This reminds me of nothing so much as the South Park episode where Kyle and Stan’s dads are convinced that global warming has brought on a new ice age, and they venture into the streets, in the middle of summer, dressed like Roald Amundsen. When they feel like they are burning up, they attribute it to the warm feeling one gets at the onset of hypothermia.

So what does a positive on an HIV test mean? Probably nothing more than immune system distress, nothing to take lightly, but there is no one specific condition causing it. Some people, when their immune systems are under stress, react in such a way as to set off an HIV test. And the antibodies to the diseases found in 90% of AIDS patients react with the supposed HIV proteins (Muller et al., 1991; Kashala et al., 1994). A person’s genetic makeup, and how it relates to their immune system, will also affect how likely it is to set off an HIV test.

This explains why a positive result on such a test does correlate with decreased life expectancy, but also why the infection ratios discussed above do not significantly vary. It explains why Hispanics in the west of the US have lower infection rates than Hispanics in the east (western Hispanics tend to come from Mexico, whereas eastern Hispanics tend to come from Cuba, the Dominican Republic and Puerto Rico, whose inhabitants have much African ancestry). It explains why 30% of HIV negative blood transfusions develop antibodies to the p24 protein (Genesca et al., 1989), or why a transfusion of one’s own HIV negative, irradiated blood produces antibodies to HIV proteins (Kozhemiakin and Bondarenko, 1992).

It explains why HIV-free animals given HAART and other cocktails experience AIDS symptoms.

It explains why a few percent of Africans test HIV positive despite no sexual experience at all (Gisselquist et al., 2002).

It explains why only drug-using prostitutes have high prevalence of HIV (Rosenberg and Weiner, 1988).

And why Fiala, 2000, found that the prevalence of HIV in non-drug-using prostitutes was 1.5%, but in drug using prostitutes was 32%.

And why drug addicts in treatment have lower HIV prevalence the longer they have stayed clean (Moss et al., 1994).

It explains the numerous cases of HIV positives reverting to HIV negative status.

And why patients admitted to hospitals for conditions having nothing to do with AIDS or HIV show the same range of HIV prevalence as people at clinics for venereal disease (sources numerous).

And why HIV prevalence is higher for critically ill patients than for the least ill patients (MMWR, 1987b).

And why seroprevalence in emergency departments correlated only with “penetrative trauma” like gunshot and stab wounds (Kelen et al., 1988).

And why a survey of autopsies in Philadelphia showed significantly higher prevalence than in the general population, and it increased with the degree of trauma associated with death: 1.88% for death due to natural causes, 1.96% in accidental deaths, 2.27% for suicides and 3.74% for homicides (Resnick et al., 1991). A survey of autopsies in San Francisco found an 18% infection rate among those without any history of immunodeficiency or any laboratory or pathologic indication of AIDS (Coleman et al., 1986).

And why applicants for military service average about 3 HIV positives per 10,000, but this rate is reduced to half for those who passed the fitness test (AMSA 2004).

And why, given that the Marines require the highest levels of fitness, the incidence of HIV is less than half in the Marines what it is in sailors (Garland et al., 1989) or soldiers (AMSA 1996, 2004; Kelley et al., 1990; McNeil et al., 1989, 1991; Renzullo et al., 1995, 2001).

And why the probability of testing HIV positive increases with the number of previous hospital admissions (Renzullo et al., 1991).

And why a large percentage of African babies, born HIV positive, have HIV negative mothers (Gisselquist et al., 2002).

And why “Professor Richard Lee of the Department of Anthropology at the University of Toronto has discovered that the San people of Botswana and Namibia have mysteriously low HIV infection rates even though these countries are known for their extremely high AIDS mortality statistics” (www.news.utoronto.ca/bin6/060728-2466.asp, July 28, 2006). The San people are genetically distinct from the other West Africans of those countries.

The evidence against the orthodox theory is massive, while the evidence for it is virtually nonexistent. Despite this, people do not see, perhaps do not want to see, the truth. HIV is a fiction, and AIDS is a real but rather amorphous condition, a grab-bag of all sorts of problems. Merely suggesting this will make people angry. Mark Wainberg even suggested changing the US Constitution so that Peter Duesberg and people like him could be put in jail.

It is no surprise that vested interests in the AIDS orthodoxy would react this way, but what about everyone else? Why does no one want to consider the evidence, and why do so many get so vitriolic at mere disagreement over the theory? Perhaps Bertrand Russell can elucidate this:

If an opinion contrary to your own makes you angry, that is a sign that you are subconsciously aware of having no good reason for thinking as you do. If someone maintains that two and two are five, or that Iceland is on the Equator you feel pity rather than anger… the most savage controversies are those about matters as to which there is no good evidence either way… So whenever you find yourself getting angry about a difference of opinion, be on your guard, you will probably find, on examination, that your belief is going beyond what the evidence warrants.