Why I Quit HIV (Research)

[Guest guest]

Jagannath Chatterjee <jagchat01

Mon May 1, 2006 3:30 am

Why I Quit HIV (Research)

 

a great opinion piece from a mathematical biologist that has devoted

her academic career to HIV modeling:

 

http://www.lewrockwell.com/orig7/culshaw1.html

 

 

 

 

 

Why I Quit HIV

 

by Rebecca V. Culshaw

 

 

 

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 – has 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 HIV

model of AIDS. I received my Ph.D. in 2002 for my work constructing

mathematical models of HIV infection, a field of study I entered in

1996. Just ten years later, it might 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 NIH and the 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 no 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. " This was 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 they all had in common – other than HIV –

was that they lived extremely healthy lifestyles. Part of me was

becoming suspicious that being HIV-positive didn't necessarily mean

you would ever get AIDS.

 

By a rather curious twist of fate, it was on my way to a conference to

present the results of a model of HIV that I had proposed together

with my advisor, that 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 he said " 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 an ear

open 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 I wasn't convinced of 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, it 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. In

spite of 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 U.S.

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 1–2% 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 U.S., 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 are T-cells 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. It

doesn't in the test tube. It 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 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

they 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. But there are very

good reasons to believe it 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 to even be seen, and the result of

that mass-production is used to estimate how much of a pathogen there

is, 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? 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 – but 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). But few people

know that the criteria for a positive WB vary 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 of 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. And 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.

 

March 3, 2006

 

Rebecca V. Culshaw, Ph.D. [send her mail], is a mathematical biologist

who has been working on mathematical models of HIV infection for the

past ten years. She received her Ph.D. (mathematics with a

specialization in mathematical biology) from Dalhousie University in

Canada in 2002 and is currently employed as an Assistant Professor of

Mathematics at a university in Texas.

 

2006 LewRockwell.com