AS I WRITE THIS, IN THE LATE WINTER OF 2006,
WE ARE MORE THAN TWENTY YEARS into the AIDS era. Like many, a large part of my life has been
irreversibly affected by AIDS. My entire adolescence and adult life – as
well as the lives of many of my peers – have been overshadowed
by the belief in a deadly, sexually transmittable pathogen and the
attendant fear of intimacy and lack of trust that belief engenders.
To add to this impact, my chosen career has developed around the study of the
HIV model of AIDS. I received my PhD in 2002 for my work constructing mathematical
models of HIV infection, a field of study I entered in 1996. Just ten years
later, it may seem early for me to be looking back on and seriously reconsidering
my chosen field, yet here I am.
My work as a mathematical biologist has been built in large part on the paradigm
that HIV causes AIDS, and I have since come to realize that there is good evidence
that the entire basis for this theory is wrong. AIDS, it seems, is not a disease
so much as a sociopolitical construct that few people understand and even fewer
question. The issue of causation, in particular, has become beyond question – even
to bring it up is deemed irresponsible.
Why have we as a society been so quick to accept a theory for which so little
solid evidence exists? Why do we take proclamations by government institutions
like the National Institutes of Health (NIH) and the Centers for Disease Control
(CDC), via newscasters and talk show hosts, entirely on faith? The average
citizen has no idea how weak the connection really is between HIV and AIDS,
and this is the manner in which scientifically insupportable phrases like "the
AIDS virus" or "an AIDS test" have become part of the common
vernacular despite a lack of evidence for their accuracy.
When it was announced in 1984 that the cause of AIDS had been found in a retrovirus
that came to be known as HIV, there was a palpable panic. My own family was
immediately affected by this panic, since my mother had had several blood transfusions
in the early 1980s as a result of three late miscarriages she had experienced.
In the early days, we feared mosquito bites, kissing, and public toilet seats.
I can still recall the panic I felt after looking up in a public restroom and
seeing some graffiti that read "Do you have AIDS yet? If not, sit on
this toilet seat." But I was only ten years old then and, over time,
the panic subsided to more of a dull roar as it became clear that AIDS was
not as easy to "catch" as we had initially believed. Fear of going
to the bathroom or the dentist was replaced with a more realistic wariness
of having sex with anyone we didn't know really, really well. As a teenager
who was in no way promiscuous, I didn't have much to worry about.
That all changed – or so I thought – when I was twenty-one. Due
to circumstances in my personal life and a bit of paranoia that (as it turned
out, falsely and completely groundlessly) led me to believe I had somehow contracted
AIDS, I got an HIV test. I spent two weeks waiting for the results, convinced
that I would soon die, and that it would be all my fault. I believed this,
despite the fact that I was perfectly healthy, didn't use drugs, and
wasn't promiscuous – low-risk by any definition. As it happened,
the test was negative and, having felt I had been granted a reprieve, I vowed
not to take more risks and to quit worrying so much.
Over the past ten years, my attitude toward HIV and AIDS has undergone a dramatic
shift. This shift was catalyzed by the work I did as a graduate student, analyzing
mathematical models of HIV and the immune system. As a mathematician, I found
virtually every model I studied to be unrealistic. The biological assumptions
on which the models were based varied from author to author, and this made
no sense to me. It was around this time, too, that I became increasingly perplexed
by the stories I heard about long-term survivors. From my admittedly inexpert
viewpoint, the major thing these survivors all had in common – other
than HIV – was that they lived extremely healthy lifestyles. Part of
me was becoming suspicious of the claim that being HIV-positive necessarily
meant you would get AIDS.
By a rather curious twist of fate, on my way to a conference to present the
results of a model of HIV that I had proposed together with my advisor, I came
across an article by Dr. David Rasnick about AIDS and the corruption of modern
science. As I sat on the airplane reading this story, in which Dr. Rasnick
writes, "the more I examined HIV, the less it made sense that this largely
inactive, barely detectable virus could cause such devastation," everything
he wrote started making sense to me in a way that the currently accepted model
did not. I didn't have anywhere near all the information, but my instincts
told me that what he said seemed to fit.
Over the past ten years, I nevertheless continued my research into mathematical
models of HIV infection, all the while keeping open an ear for dissenting voices.
By now, I have read hundreds of articles on HIV and AIDS, many from the dissident
point of view but far, far more from that of the establishment, which unequivocally
promotes the idea that HIV causes AIDS and that the case is closed. In that
time, I even published four papers on HIV (from a modeling perspective). I
justified my contributions to a theory of which I wasn't convinced by
telling myself these were purely theoretical, mathematical constructs, never
to be applied in the real world. I suppose, in some sense also, I wanted to
keep an open mind. So why is it that only now have I decided that enough is
enough, and I can no longer in any capacity continue to support the paradigm
on which my entire career has been built?
As a mathematician, I was taught early on about the importance of clear definitions.
AIDS, if you consider its definition, is far from clear and is in fact not
even a consistent entity. The classification AIDS was introduced in the early
1980s not as a disease but as a surveillance tool to help doctors and public
health officials understand and control a strange, new syndrome affecting mostly
young gay men. In the two decades intervening, that classification has evolved
into something quite different. AIDS today bears little or no resemblance to
the syndrome for which it was named. For one thing, the definition has actually
been changed by the CDC several times, continually expanding to include ever
more diseases (all of which existed for decades prior to AIDS) and, sometimes,
no disease whatsoever. More than half of all AIDS diagnoses in the past several
years in the United States have been made on the basis of a T-cell count and
a "confirmed" positive antibody test – in other words, a
deadly disease has been diagnosed over and over again on the basis of no clinical
disease at all. And the leading cause of death in HIV-positives in the last
few years has been liver failure, not an AIDS-defining disease in any way,
but rather an acknowledged side effect of protease inhibitors, which asymptomatic
individuals take in massive daily doses, for years.
The epidemiology of HIV and AIDS is puzzling and unclear as well. Despite the
fact that AIDS cases increased rapidly from their initial observation in the
early 1980s and reached a peak in 1993 before declining rapidly, the number
of HIV-positive individuals in the US has remained constant at one million
since the advent of widespread HIV antibody testing. This cannot be due to
anti-HIV therapy, since the annual mortality rate of North American HIV-positives
who are treated with anti-HIV drugs is much higher – between 6.7% and
8.8% – than would be the approximately one to two percent of the global
mortality rate of HIV-positives if all AIDS cases were fatal in a given year.
Even more strangely, HIV has been present everywhere in the US, in every population
tested, including repeat blood donors and military recruits, at a virtually
constant rate since testing began in 1985. It is deeply confusing that a virus
thought to have been brought to the AIDS epicenters of New York, San Francisco,
and Los Angeles in the early 1970s could possibly have spread so rapidly at
first, yet have stopped spreading completely as soon as testing began.
Returning for a moment to the mathematical modeling, one aspect that had always
puzzled me was the lack of agreement on how to accurately represent the actual
biological mechanism of immune impairment. AIDS is said to be caused by a dramatic
loss of the immune system's T-cells, said loss being presumably caused
by HIV. Why then could no one agree on how to mathematically model the dynamics
of the fundamental disease process – that is, how T-cells are actually
killed by HIV? Early models assumed that HIV killed T-cells directly, by what
is referred to as lysis. An infected cell lyses, or bursts, when the internal
viral burden is so high that it can no longer be contained, just like your
grocery bag breaks when it's too full. This is in fact the accepted mechanism
of pathogenesis for virtually all other viruses. But it became clear that HIV
did not in fact kill T-cells in this manner, and this concept was abandoned,
to be replaced by various other ones, each of which resulted in very different
models and, therefore, different predictions. Which model was correct never
was clear.
As it turns out, the reason there was no consensus mathematically as to how
HIV killed T-cells was because there was no biological consensus. There still
isn't. HIV is possibly the most studied microbe in history – certainly
it is the best-funded – yet there is still no agreed-upon mechanism of
pathogenesis. Worse than that, there are no data to support the hypothesis
that HIV kills T-cells at all. HIV doesn't kill T-cells in the test tube.
HIV mostly just sits there, as it does in people – if it can be found
at all. In Robert Gallo's seminal 1984 paper, in which he claims "proof" that
HIV causes AIDS, actual HIV could be found in only 26 out of 72 AIDS patients.
To date, actual HIV remains an elusive target in those with AIDS or in those
who are simply HIV-positive.
This is starkly illustrated by the continued use of antibody tests to diagnose
HIV infection. Antibody tests are fairly standard to test for certain microbes,
but for anything other than HIV, the main reason antibody tests are used in
place of direct tests (that is, actually looking for the bacteria or virus
itself) is because they are generally much easier and cheaper than direct testing.
Most importantly, such antibody tests have been rigorously verified against
the gold standard of microbial isolation. This stands in vivid contrast to
HIV, for which antibody tests are used because there exists no test for the
actual virus.
As to so-called "viral load," most people are not aware that tests
for viral load are neither licensed nor recommended by the FDA to diagnose
HIV infection. This is why an "AIDS test" is still an antibody
test. Viral load, however, is used to estimate the health status of those already
diagnosed HIV-positive. However, there are very good reasons to believe viral
load does not work at all.
Viral load uses either PCR or a technique called branched-chained DNA amplification
(bDNA). PCR is the same technique used for DNA fingerprinting at crime scenes
where only trace amounts of materials can be found. PCR essentially mass-produces
DNA or RNA so that it can be seen. If something has to be mass-produced even
to be seen, and the result of that mass-production is used to estimate how
much of a pathogen exists, it might lead a person to wonder how relevant the
pathogen was in the first place.
Specifically, how could something so hard
to find, even using the most sensitive and sophisticated technology, completely
decimate the immune system? The bDNA, while not magnifying anything directly,
nevertheless looks only for fragments of DNA believed, but not proven, to be
components of the genome of HIV. Yet there is no evidence to say that these
fragments don't exist in other genetic sequences unrelated to HIV or
to any virus. It is worth noting at this point that viral load, like antibody
tests, has never been verified against the gold standard of HIV isolation;
bDNA uses PCR as a gold standard, PCR uses antibody tests as a gold standard,
and antibody tests use each other. None use HIV itself.
There is good reason to believe the antibody tests are flawed as well. The
two types of tests routinely used are the ELISA and the Western Blot (WB).
The
current testing protocol is to "verify" a
positive ELISA with the "more specific" WB (which has actually
been banned from diagnostic use in the UK because it is so unreliable). Few
people know, however, that the criteria for a positive WB varies from country
to country and even from lab to lab. Put bluntly, a person's HIV status
could well change depending on the testing venue. It is also possible to test
"WB indeterminate," which translates to any one of "uninfected," "possibly
infected," or even, absurdly, "partly infected" under the
current interpretation. This conundrum is confounded by the fact that the proteins
comprising the different reactive "bands" on the WB test are all
claimed to be specific to HIV, raising the question of how a truly uninfected
individual could possess antibodies to even one HIV-specific protein.
I have come to sincerely believe that these HIV tests do immeasurably more
harm than good, due to their astounding lack of specificity and standardization.
I can buy the idea that anonymous screening of the blood supply for some nonspecific
marker of ill health (which, due to cross reactivity with many known pathogens,
a positive HIV antibody test often seems to be) is useful. I cannot buy the
idea that any individual needs to have a diagnostic HIV test. A negative test
may not be accurate (whatever that means), but a positive one can create utter
havoc and destruction in a person's life – all for a virus that
most likely does absolutely nothing. I do not feel it is going too far to say
that these tests ought to be banned for diagnostic purposes.
The real victims in this mess are those whose lives are turned upside-down
by the stigma of an HIV diagnosis. These people, most of whom are perfectly
healthy, are encouraged to avoid intimacy and are further branded with the
implication that they were somehow dreadfully foolish and careless. Worse,
they are encouraged to take massive daily doses of some of the most toxic drugs
ever manufactured. HIV, for many years, has fulfilled the role of a microscopic
terrorist. People have lost their jobs, been denied entry into the Armed Forces,
been refused residency in and even entry into some countries, even been charged
with assault or murder for having consensual sex; babies have been taken from
their mothers and had toxic medications forced down their throats. There is
no precedent for this type of behavior, as it is all in the name of a completely
unproven, fundamentally flawed hypothesis, on the basis of highly suspect,
indirect tests for supposed infection with an allegedly deadly virus, a virus
that has never been observed to do much of anything.
As to the question of what does cause AIDS, if it is not HIV, there are many
plausible explanations given by people known to be experts. Before the discovery
of HIV, AIDS was assumed to be a lifestyle syndrome caused mostly by indiscriminate
use of recreational drugs. Immunosuppression has multiple causes, from an overload
of microbes to malnutrition. Probably all these are true causes of AIDS. Immune
deficiency has many manifestations, and a syndrome with many manifestations
is likely multicausal as well. Suffice it to say that the HIV hypothesis of
AIDS has offered nothing but predictions – of its spread, of the availability
of a vaccine, of a forthcoming animal model, and so on – that have not
materialized, and it has not saved a single life.
After ten years involved in the academic side of HIV research, as well as in
the academic world at-large, I truly believe that the blame for the universal,
unconditional, faith-based acceptance of such a flawed theory falls squarely
on the shoulders of those among us who have actively endorsed a completely
unproven hypothesis in the interests of furthering our careers. Of course,
hypotheses in science deserve to be studied, but no hypothesis should be accepted
as fact before it is proven, particularly one whose blind acceptance has such
dire consequences.
For over twenty years, the general public has been greatly misled and ill-informed.
As someone who has been raised by parents who taught me from a young age never
to believe anything just because "everyone else accepts it to be true," I
can no longer just sit by and do nothing, thereby contributing to this craziness.
The craziness has gone on long enough. As humans – as honest academics
and scientists – the only thing we can do is allow the truth to come
to light.
Rebecca V. Culshaw, PhD is a mathematical biologist who has been working
on mathematical models of HIV infection for the past ten years. She
received her PhD (mathematics with a specialization in mathematical
biology) from Dalhousie University in Canada and is currently an Assistant
Professor of Mathematics at a university in Texas.
This article first appeared on www.lewrockwell.com and has been reprinted
with the author's permission.
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