All this virus nonsense is too silly to even comment on.

What people will do to make a (good) living.

HIV=AIDS Controversy: Understanding Scientific Homogeneity

bemoans the culture of conformity imposed by government-funded,
industry-driven, and media-hyped Big Science.
Blinded by Science

by David Rasnick

People think of "AIDS research" as the crucible of modern science and
technology. There are more than 100,000 scientists and doctors working
on AIDS--more than the annual number of AIDS patients in the U.S. There
are 80,000 AIDS organizations in the U.S., one for each new AIDS
patient. As a scientist who has studied AIDS for 16 years, I have
determined that AIDS has little to do with science and is not even
primarily a medical issue. AIDS is a sociological phenomenon held
together by fear, creating a kind of medical McCarthyism that has
transgressed and collapsed all the rules of science, and imposed a brew
of belief and pseudoscience on a vulnerable public.

Like most scientists, I was taught in school that science is a
self-correcting activity. All hypotheses, no matter how precious, were
put to the grindstone of the scientific process, which was designed to
preserve what was true and destroy what was false.

But this delicate state of affairs was possible only when science was
free--or, in fact, when science was broke, before the tragic union of
government and science ushered in by the Manhattan Project and the Cold
War. Nuclear physicist Ralph E. Lapp, a researcher and adviser on the
Manhattan Project, remembers what science was like before the shift:

   In those days no scientist ventured to ask the federal government
for funds. He gathered together what money he needed from private
sources or earned extra pay as a consultant to pay for his own
research. But mostly he acted as a jack-of-all-trades and built his own
equipment. Graduate students were required to take machine-shop
practice and learn glass blowing. If he needed Geiger counters he made
them himself, and he wired his own electronic circuits.

Before World War II, research and development funding for the sciences,
public and private, amounted to about $250 million per year. By 1993,
the federal share alone was $76 billion. And what has it bought us? For
the $45 billion of taxpayer money spent on AIDS so far, HIV researchers
still use statistical methodologies shown by their inventors to be
invalid and still conduct experiments without any controls. They take
causes for effects, correlations for causations, and constants for
variables. Most important, they haven't stopped AIDS. What they have
done is successfully instilled fear into human sexual relations--an
amorphous fear, which most AIDS professionals as well as journalists
argue has been valuable. I doubt even George Orwell could have imagined
that an autocratic regime would be able to successfully equate sex with
death at the end of the millennium. What the government has bought with
this money is a culture of conformity, whereby only HIV research is
funded, creating the appearance that all researchers believe HIV is the
cause of AIDS.

Let's review what readers of this column have been told many times: In
1984, National Cancer Institute virologist Robert Gallo held a press
conference, with Margaret Heckler, then the Secretary of Health and
Human Services, at his side. Gallo announced that he had found the
"probable cause of AIDS" in a retrovirus he was then calling HTLV-III
(and which had already been isolated a year earlier at the Pasteur
Institute in France).

With that announcement, Gallo had publicly leapfrogged straight across
the scientific process--across peer-review and analysis, across the
very checks and balances of science. He made no attempt to demonstrate
his claim--in fact, only 50 percent of his sample patients had any
trace of HIV--but fed it straight to the global media, which broadcast
it without hesitation. What made the move toward the viral cause of
AIDS irreversible was the fact that the federal government supported
it, if it didn't engineer it. Now a new standard of brash, unscientific
science was set, and all others took their lead from it.

Since then, the media have painted a false picture to suggest that
virtually every scientist and doctor in the world supports the HIV
hypothesis of AIDS, with the lone dissenting voice of Peter Duesberg,
who is now defunded and all but exiled from American science. In truth,
there are thousands of dissenting voices throughout the world, who have
been trying for years to get our opinions heard, counted, factored in.
The Group for the Scientific Reappraisal of the HIV Hypothesis was
founded by former Harvard professor Charles Thomas in 1991. Today more
than 500 scientists, health-care workers, and other professionals have
signed on.

What distinguishes this group? By and large, its members are not
dependent on grants from the National Institutes of Health for their
livelihood. The signatories who are Nobel laureates are immune from
bureaucratic intimidation. Many of the academic members of the group
who publicly support Duesberg are emeritus professors, whose careers
can't be terminated. Younger academics, on the other hand, who have
seen the establishment mercilessly punish and excommunicate someone of
Duesberg's stature have clearly gotten the message: They keep their
mouths shut and bow down before the golden calf of HIV.

Serge Lang, the legendary Yale mathematician and member of the National
Academy of Sciences, has had so many letters to editors concerning the
HIV scandal refused publication that he started sending checks along
with his letters--the equivalent of buying space in which to speak.
(Some editors were sufficiently embarrassed by this tactic that they
published Lang's letters and returned his checks.)

There are countless more stories of censorship, intimidation, and
financial and professional manipulation. But the discordant data still
sits there, indestructible and unresolved.
A few specifics: We have been told for 13 years that AIDS is
infectious, and is spreading rapidly into the heterosexual population.
If so, why have the Centers for Disease Control's estimates of the
prevalence of HIV infection in the U.S. never gone up since HIV testing
began? In fact, the estimates have gone down.

Since 1985, the U.S. government and various civilian institutions have
performed some 20 million HIV tests per year. This is where the CDC
gets its estimates of how many Americans are infected with HIV. But
because of the reduction in false positive results, the CDC's current
estimate is that there are about 750,000 HIV-infected Americans--down
from the original mid-'80s estimate of one million or more.

Another of the many anomalies: The prevalence of HIV in the general
population is equally divided between men and women. But men account
for 90 percent of all AIDS cases in the U.S., as they have throughout
the history of AIDS.

We are told that hemophiliacs are especially hard-hit by AIDS.
Seventy-five percent of the 20,000 hemophiliacs in the U.S. test
positive for HIV. The paradox is that the average lifespan of
hemophiliacs, including those who were HIV-positive, doubled during the
first decade of AIDS. In fact, the positives seemed to do better than
the negatives. But in 1987, the mortality of HIV-positive hemophiliacs
began to rise sharply. That was also the year that AZT--the drug now
openly admitted to be detrimental to AIDS patients--was first widely
prescribed to HIV-positive hemophiliacs.

When AIDS first appeared around 1980, I had just moved to the San
Francisco Bay Area to help set up a small biotech company. Soon stories
were going around about a strange new disease that was affecting the
immune systems of gay men. I viewed the new scourge as one of the most
stimulating scientific puzzles of the century. But as an organic
chemist, not an immunologist or physician, I felt there was little I
could contribute scientifically toward unraveling the mysteries of the
disease.

In 1984, when Gallo announced at that historic press conference that
the cause of AIDS had been found in HIV, all speculations about
causation came to a screeching halt. At first, I was exuberant. This
retrovirus provided the clarity we all needed. I now had an object upon
which to apply my art as an organic chemist. I began to explore the
possibilities of making inhibitors for the protease (a class of
enzymes) produced by HIV. But when I recalled that a friend at Abbott
Laboratories had been working for years on just such protease
inhibitors, I pulled out of the race.

I'm glad I did, because before long I was having serious doubts about
the viral hypothesis of AIDS. I spent countless hours, as did many
scientists, devising ingenious explanations for how HIV could destroy
the immune systems of its victims. But by the end of 1985, I was
convinced that something was fundamentally wrong with the basic
assumptions that had become entrenched in the mega-institutions of
science and medicine. The more I examined HIV, the less it made sense
that this largely inactive, barely detectable virus could cause such
devastation. How could $45 billion of taxpayer money be spent on such
an ordinary, humdrum virus? And why has the media functioned as the
public relations arm of the HIV/AIDS establishment? Uncovering
Watergate now seems trivial compared to what it will take to expose the
decade of fraud, incompetence, and flagrant lying that has been going
on behind a veil of scientific and medical jargon, credentials, and
expertise.

In The Rise and Fall of T.D. Lysenko, Russian historian Zhores Medvedev
describes the rise to power of an autocratic Soviet pseudoscientist,
who over a period of decades corrupted and nearly destroyed Soviet
biology and agriculture. Medvedev concludes that "monopoly in science
by one or another false doctrine, or even by one scientific trend, is
an external symptom of some deep-seated sickness of a society." The
general acceptance of Lysenko's perverted scientific theories--designed
to undermine Western science, primarily Darwinism--was heavily promoted
by the government-supported media. "The peculiarities of [the Soviet]
press," Medvedev writes, "made possible popular support for one or
another scientific trend selected by the political leadership, and
complete suppression of the opposition."

Medvedev easily could have been describing the way our government's
public-health institutions have commandeered the AIDS debate. Because
the NIH and Dr. Anthony S. Fauci, director of the National Institute of
Allergy and Infectious Diseases, control funding of virtually all
academic research, they can with impunity cut off funds to dissenting
voices. Editors of peer-reviewed journals are pressured not to publish
papers critical of the HIV hypothesis. Journalists who interview
dissenting scientists are denied access to government sources, and
accused of acting "immorally." The result is a world in which the
once-cherished process of scientific discourse is treated as social
deviance--and punished as such.

In AIDS, perhaps the most devastating effect of this new antiscience is
in the realm of clinical trials. Most drugs that are approved by the
FDA must complete three phases of human clinical trials--phase I for
toxicity, phase II for short-term effectiveness, and phase III, the
most vital, for the ultimate measure of morbidity and mortality (that
is, whether the drugs actually benefit patients).

None of the recently lauded HIV protease inhibitors approved by the FDA
has yet completed a phase III clinical trial.

In order to satisfy the requirements for licensing, however, two phase
III protease inhibitor clinical trials recently got under way: a
1,200-patient Boston-centered study and a 3,300-patient trial in
Europe. (With AZT, only the Europeans kept their study going long
enough to see the true results, despite the fierce protestations of
activists and health care workers. In the end, the so-called Concorde
study gave us the answer about AZT--it did not work.) But on February
25, a Boston Globe headline trumpeted: AIDS Trial Terminated; 3-Drug
Therapy Hailed. The article reported that 63 of the 579 Boston trial
subjects receiving two drugs had died or developed new AIDS-associated
illnesses, while only 33 of the 577 individuals receiving the new
three-drug "cocktail" had died or gotten sicker. It also mentioned
that, as late as mid-January, a "peek" at the results of the two drug
regimens had concluded that they had not "yet diverged enough to
warrant stopping the study."

When the triumphant results were reported, Fauci dramatically announced
that the trial had provided evidence that combination treatments
including protease inhibitors "can reduce the risk of death" from AIDS.

You don't have to be a scientist to follow the logical difficulties
here. It seems highly unlikely that between mid-January and
mid-February, the data had changed enough to stop the phase III trial.
Even the leader of the Boston trial admitted that there was no
statistical difference between the deaths in the two treatment groups.
When the study was concluded, there were eight deaths among those
taking three drugs, compared with 18 deaths among those taking two.
Using these mortality figures at face value is a little like using the
halftime score in a basketball game to determine the winner. As
everyone knows, the lead can oscillate back and forth throughout the
game. The same is true of clinical trials.

In short, we don't know if the combination therapies work to "reduce
the risk of death," because it hasn't been proven. So why did Fauci and
his allies halt the phase III trial before it yielded statistically
significant results?

Protease inhibitors were internationally hailed as miracle drugs in
1996, without the benefit of proof. As long as phase III trials were
under way, they posed a dangerous uncertainty. A completed trial that
resulted in an unsatisfactory result would be difficult to explain
away. From the HIV/AIDS establishment's perspective, the safest course
of action was to stop the game, declare victory, and hope nobody would
call them on it.

AIDS research has become a virtual puppet for the titanic, symbiotic
forces of industry and government. I recently attended a small, elite
conference focusing on the "chemotherapy of AIDS," where 43 of the 100
people present were pharmaceutical company representatives who ran to
the phones after each session to call in the results. (Is this Wall
Street or science?) During one session, I asked a leading proponent of
cocktail therapies how the patients receiving the cocktails were doing.
He said that some were healthy enough to work. Then I asked whether,
during the course of therapy, the 20 individuals did better, stayed the
same, or got worse. He did not answer. It was an embarrassing moment
for the audience. Then I asked: "Your patients should have done better,
right?" Again, he was speechless.

Even more disturbingly, one presenter suggested that "clinical
endpoints are dead" in phase III trials. In other words, he believes
that clinical trials will no longer use morbidity and mortality as
endpoints--they will no longer be designed to determine whether drugs
actually work. The excuse given for dropping phase III clinical trials
is that they are unethical and too costly; we are henceforth supposed
to assume that the drugs under evaluation reduce morbidity and
mortality before this has actually been demonstrated.

To date, there is still no clinical trial that has proven that the
protease inhibitors--either taken alone or in combination with other
antiviral drugs--reduce the mortality of AIDS patients.

The HIV cult has transported AIDS beyond the domain of science and
medicine, and into the realm of mythology. The discourse is controlled
by powerful individuals and institutions with a professional or
financial stake in HIV, who take it upon themselves to be the sole
purveyors of "truth." Government institutions have compounded the
difficulty of arriving at a true understanding of AIDS by doing
everything in their power to suppress the views of scientists who
disagree with established opinions.

Yet there is always hope for the future; those willing to challenge
orthodoxy still believe that science will ultimately return to its
moorings and that their message will be heard. I am reminded of former
Supreme Court Justice William O. Douglas's warnings against the tyranny
of conformity and the injury it does to freedom of expression and
thought. As he wrote in Freedom of the Mind: "The curious man--the
dissenter--the innovator--the one who taunts and teases or makes
caricature of our prejudices is often our salvation. Yet throughout
history he has been burned or booed, hanged or exiled, imprisioned or
tortured, for pricking the bubble of contemporary dogma."

HIV=AIDS Controversy: Theatre of the Absurd

The following report on the Gordon Conference on the Chemotherapy of
AIDS originally appeared in Reappraising AIDS, vol. 5, no. 3, March
1997.
Reappraising AIDS is a monthly publication of The Group for the
Scientific Reappraisal of the HIV/AIDS Hypothesis. For more
information, contact Paul Philpott, publisher/editor at:
philpott@wwnet.com.

Non-Infectious HIV is Pathogenic
Exclusive report from important AIDS conference

by David Rasnick, Ph.D.

I just returned from my first AIDS conference, the Gordon Conference on
the Chemotherapy of AIDS, held March 9-14 in Ventura, California. I
went to present a poster of a paper that refuted one of the fundamental
concepts of the prevailing HIV-AIDS model. The paper had just been
published in a scientific journal, and I was eager to defend it against
the scrutiny of my peers.

Also I knew that David Ho and his co-workers would be making
presentations advancing the HIV model. I was determined to subject
their ideas to scientific scrutiny face-to-face.

Gordon conferences are some of the world?s most prestigious
scientific gatherings. Unlike nearly all other conferences, which seek
to maximize the number of paying participants, Gordon conferences are
generally limited to 100 attendees, all of whom must apply for
acceptance. This makes them serious and productive events. All
participants get a chance to attend every presentation, and to meet and
question every presenter, either during formal Q&A periods, or
informally during the social breaks.

Over my 20-year career as a pharmaceutical drug designer, I ?ve
attended about nine Gordon Conferences, where I have presented papers.
Usually those conferences related to my specialty: proteases and the
drugs that inhibit them.

Ho Charms Critics

Of the 100 attendees, 90% were American, and 43% were pharmaceutical
company employees. I noticed something new to me at a Gordon
Conference: a non-scientist participant, specifically, a representative
of Project Inform, a political group devoted to promoting the HIV
hypothesis.

The six-day event began on a Sunday. The special opening lecture was
given by David Ho, director of NYU Medical School?s Aaron-Diamond
AIDS Center, and Time?s 1996 Man of the Year.

His talk was titled, ?Chemotheraphy and Pathogenesis.?
Surprisingly, I was not the only critic in the audience.

Somebody in the front row challenged Ho?s criteria for what
constitutes an assay of infectious virus, a challenge that has profound
implications for the basic tool of contemporary HIV science: the viral
load test. He also disputed the mathematical basis of Ho?s
?virological mayhem? model, the paradigm upon which HO wants to
base ?anti-HIV? therapy.

The specifics of these objections were never made clear because Ho
sidestepped the questions with the skill of a seasoned bureaucrat, and
in doing so chewed up all the discussion time.

Another surprise was an obvious lack of Ho supporters in the audience.
In subsequent breaks I found several others who openly rejected the
validity of the ?viral load? test and Ho?s model of HIV/T4-cell
dynamics.

Ho could easily become the next Anthony Fauci, who?as Director of the
NIH?s Institute of Allergies and Infectious Diseases?is the
government?s reigning king of HIV science. Ho is far more charming
than Fauci and is coated with several layers of Teflon. Regrettably, Ho
left the conference early Tuesday morning so I never got to talk with
him. But I did get to take up the validity of the viral load test with
one of his collaborators.

Cocktails Don't Help Patients

Martin Markowitz?co-author on some of Ho?s most famous papers,
including the 1995 Nature article that introduced the virological
mayhem model and popularized the viral load test?stayed through the
Wednesday presentations, and I was able to question him several times.

The first instance occurred during the question period of a lecture he
gave on treating early HIV infection. He and Ho have been treating a
cohort of 20 patients for close to a year with protease inhibitor/AZT
cocktails. The study is on-going and no results have been published, so
Markowitz was discussing preliminary data. According to him, most of
the subjects already had AIDS symptoms at the start of the experimental
therapy?including five who?d previously been
hospitalized?although a few had no history of symptoms.

Once the therapy began, HIV ?viral load? for each patient dropped
below the level of detection and has stayed that way, Markowitz said.
He considered this an indication that the therapy was a good one.

But did eliminating viral load make the patients healthier? Markowitz
had nothing to say about this during his lecture. Surely if the
patients had gotten better when their HIV viral load went down,
Markowitz would have bragged about it. But the subject didn?t come up
until I raised it in the question period.

How are we doing? I asked. ?Some are healthy enough to work,? he
said happily. The implication was that were it not for the cocktails,
these patients would not be healthy enough to work, but I suspected
this was not the case.

Markowitz?s smile vanished when I asked, During the 11 months on
therapy, when their viral loads were undetectable, did your patients do
better, stay the same, or do worse? He didn?t say a word. It was an
embarrassing moment for the audience.

I interrupted the uncomfortable silence by restating the question. Your
patients should be doing better, right? Again Markowitz was speechless.
He either didn?t know how his patients had done over the course of
therapy (which is very unlikely) or they were not doing well?despite
having HIV ?viral loads? of zero. During this revealing silence the
lecture was ended by the announcement of a coffee break.

I left with one of my curiosities satisfied: the press accounts of
miracles attributed to cocktail therapy?the fabled ?Lazarus
effect??weren?t showing up in scientific studies.

No Viable Drug-Resistant Virus

Monday and Tuesday afternoons were set aside for poster sessions. Since
my paper on the kinetics of HIV protease undermined a crucial aspect of
the current dogma, I wasn?t sure how my poster would be received.

The paper, ?Kinetics Analysis of Consecutive HIV Proteolytic
Cleavages of the gag-pol Polyprotein,? addressed the popular
assumption that when antiviral therapy fails, it is because HIV has
mutated into resistant forms (Rasnick, March 7, 1997, Journal of
Biological Chemistry). In particular, the assumption that when protease
inhibitor therapy fails, it is due to the emergence of HIV strains
characterized by mutant proteases that are resistant to the inhibitors.

This belief is central to the HIV model. Protease inhibitors,
especially when combined with AZT into a cocktail, often cause HIV
?viral load? to disappear. When ?viral load? counts start going
back up or when AIDS symptoms manifest, it is assumed that new mutant
strains of HIV have emerged, ones with proteases that resist the
inhibitors.

But my calculations show that these theoretical mutant proteases could
not be a part of a fully-functioning HIV. In order to produce a
fully-functioning HIV, the protease must cut an HIV super protein at
eight different sites. Inhibitors work by plugging-up the protease?s
cutting site, blocking it from snipping the HIV super-protein into nine
functioning parts.

A protease that would not accept an inhibitor into its active
site?one that was resistant to the effects of these drugs?would
also not be able to accept the HIV super protein into its active site.
That the protease has to make eight successful cuts under these
circumstances makes it demonstrably impossible that a resistant form
could produce functional virus.

I noted that there is not one example in the literature of a human
infected with viable, infectious HIV that possesses an
inhibitor-resistant mutant protease. All the inhibitor-resistant
mutants described so far were obtained from the proviral DNA of
non-infectious virus. There was no reason, then, to think that ?drug
resistance? could explain instances where protease inhibitors failed
to resolve AIDS or eliminate HIV ?viral load.?

The second major point of my kinetics analysis was that since the viral
load test at best measures 99.8% non-infectious viral particles, it
should be replaced by an assay that measures the level of infectious
HIV particles in blood plasma. I was certain that this proposal would
be greeted by a chorus of disapproval. Surprisingly, that did not
happen.

No one disputed anything I said. A number of people, including Jack
Erickson?an HIV protease expert from the National Cancer
Institute?openly agreed with my analysis and conclusions.

Chasing Markowitz

Erickson left my poster and walked straight over to Markowitz, who was
at the other end of the room. I knew Erickson wanted to discuss with
Markowitz the points of my poster, and I went over to join them.

Sure enough, my poster was the topic. Markowitz greeted me with a
smile. Perhaps he did not yet recognize me from his earlier lecture. I
started asking about the infectivity assay used in the March 1996
article he wrote with Ho (Science 271, p. 1582), which I held in my
hand. The paper concerned the administration of cocktail therapy to
five patients. Prior to this treatment, the patients had HIV ?viral
loads? between 12,000 and 643,000 (per ml of plasma). After therapy
began, the viral loads for each patient went to zero, and stayed at
zero for the duration of the study.

I wanted to know about patient 105, the one who started with the
largest viral load, 643,000. He was the only patient for which
?tissue culture infectious doses? (TCID) were measured. Prior to
therapy?when his ?viral load? was 643,000?he had 1,000
infectious doses of HIV (per ml of plasma). Two days after initiating
therapy, his infectious doses dropped to zero, but his ?viral load?
had not dropped below 500,000.

I wanted to know the relationship between the ?viral load? figure
and the infectious dose figure. I started by asking, Did one
?infectious dose? correspond to one infectious HIV?

Yes, Markowitz said, one infectious dose equaled one infectious virus.
How did you determine that an HIV (a ?dose?) was infectious? By
looking for the p24 protein?

Yes, Markowtiz replied. Detection of p24 was accepted as evidence of a
fully functioning virus.

Well, I said, p24 is not good enough.

With this, I figured our scientific discourse would proceed along
predictable lines. He would ask me why p24 ?wasn?t good enough.?
I would explain, as documented in my paper, that p24 has been shown by
many researchers, including John Erickson, not to be a reliable
indicator of infectious virus. I was prepared with references to defend
this statement. But Markowitz didn?t bite.

As following his lecture when I had asked about the health of his
patients, Markowitz simply said nothing.

I turned my attention to the disparity between the ?viral load? and
infectious dose figures. If infectious doses equaled infectious HIV
particles, then the difference between patient 105?s infectious doses
and his ?viral load? must represent non-infectious HIV particles.

I showed Markowitz the graph he and Ho et al. had published for patient
105. In one case a viral load of 643,000 corresponded with 1,000
infectious HIV particles, and in another case a viral load of over
500,000 corresponded to zero infectious HIV particles. Markowitz agreed
with my interpretation of the data.

So I asked him, What was the significance of the hundreds of thousands
of non-infectious viral particles per ml that you detected in the blood
plasma of patient 105? He frowned, and seemed not to know what to do
next. His puzzled look and silence lasted about 30 seconds. Then he
simply turned and walked away.

It was the first time a scientist had ever run away from me. Typically
scientists are bull dogs. They fight for their position. But the HIV
guys don?t. They run.

I noticed at this time that Erickson had vanished. He?d slipped away
sometime during this strange exchange with Markowitz, and I never spoke
to him again.
Were it not for Erickson?s devotion to HIV, he and I could have been
buddies and colleagues. He is otherwise a sharp scientist who knows
enzymes and the technical particulars quite well. Regrettably, though,
he yields to the virologists and physicians when it comes to HIV
pathogenesis, and he takes his cues from the folks who run the HIV
show.

As for Markowitz, I was determined to get an answer to my question. I
cornered him two more times. On both occasions I had to literally stop
him from walking away. In each instance I repeated my question about
the significance of all that non-infectious HIV.

Both times he ran off without answering the question. In the midst of
his second retreat he turned and called back with a meaningless
response, devoid of even a hint of scientific or logistical merit:
?Trust me!?

I cried back, ?Trust has nothing to do with it!? It was an absurd
exchange, and I would have laughed were it not so pathetic.

Dashed Hopes

If I was going to get responses for my remaining questions, I would
need a stationary target.

I found one at the week?s most frightening session: Wednesday
night?s special lecture by John Mellors of the University of
Pittsburgh Medical Center?s Graduate School of Public Health. The
topic: ?Chemotherapy of HIV-1 Infection: The Past, Present, and
Future.?

Mellors painted an accurate picture of the dismal history of HIV
chemotherapy prior to the current era of protease inhibitor/AZT
cocktails. I found myself nodding in agreement as he listed many
serious mistakes inherent in traditional therapy, which used a single
nucleoside analog, like AZT. Perhaps Mellors was a sensible and
independent thinker, the sort I?m used to dealing with at Gordon
conferences that don?t focus on AIDS.

My hopes were dashed when he got to what he labeled the greatest
mistake of the past ten years: treating AIDS patients with single
rather than multiple ?antiviral? drugs.

That?s when it hit me: there was nothing courageous about Mellors?s
critique of the old therapy. In fact, it?s the fashion now to
recognize mono nucleoside protocols as flops?so long as cocktail
therapy is promoted in their place, which is what Mellors was doing.
But the failure of mono therapy was obvious long before protease
inhibitors came along.

One Quarter Basketball Game

Mellors?s talk assumed its frightening aspect with the appearance of
a slide announcing: ?viral load? and T4-counting?rather than
clinical symptoms.

He justified this by saying that the recent termination of study
ACTG-320 last February put the final nail in the coffin of future
clinical endpoint trials.

ACTG-320 was a phase III clinical trial involving almost 1200 people,
roughly half taking two AZT-style drugs, and the rest taking a cocktail
consisting of those same two nucleoside analogs plus a protease
inhibitor. The trial was stopped early for reasons that are unclear.

When the records were unblinded, the data showed that only 8 patients
had died in the cocktail group, versus 18 in the group not taking the
protease inhibitor. Based on these figures, Mellors and the rest of the
medical establishment are saying that cocktail therapy reduces
mortality 50% compared to treatment without protease inhibitors.

Mellors regards the results of ACTG-320 as conclusive on two counts:
one, that cocktail therapy reduces mortality by half, and two, that
this benefit is predicted by ?viral load.? Studies of future
treatments should merely look for fluctuations in ?viral load? he
believes. Waiting for patients to die?or for other ?clinical
endpoints? to manifest?would be unethical and unnecessary since
?viral load? measurements supposedly predict who will and who
won?t succumb to AIDS.

But the leader of the trial, Scott Hammer of Boston?s Beth Israel
Deaconess Medical Center, admitted that ACTG-320 had not proceeded long
enough for differences in the two treatment groups to have reached
statistical significance (Boston Globe, Feb 25). In over two decades
earning my living as a scientist, I?ve never before witnessed
scientists drawing conclusions of such import based on statistically
insignificant data.

The concept of statistical significance is essential to the scientific
method. Experimental results obtain meaning only after qualifying as
statistically significant. Imagine declaring the winner of a basketball
game after the first quarter, or the champion of the World Series after
the first game.

Mellors didn?t mention statistical significance, and I didn?t get a
chance to ask about it during discussion time. So I don?t know how he
might handle this objection, which I consider to be fatal.

Instead, Mellors accepts ACTG-320 as definitive, and sufficient to
justify using surrogate markers as the sole criteria of whether or not
therapies and drugs actually benefit patients. And he?s not the only
one. I?m afraid that the mood in AIDS drug research favors
Mellors?s view. I?ve heard others call for the end of statistically
insignificant results of ACTG-320.

This is particularly frightening considering my earlier exchanges with
Markowitz, who could claim no improvement in his patients who?d had
their ?viral loads? reduced to zero for extended periods of time,
and who could attach no clinical meaning to the ?viral load? test.

If the Markowitzs and the Mellors of the world have their way, the
American public is in grave danger.

Killer Corpses

In the discussion period of Mellors?s lecture, I decided to return to
the questions that I?d wanted Markowitz to answer, about the meaning
of ?viral load.? After all, that was the heart of the matter:
Mellors?s call to discard clinical endpoints was only as valid as the
?viral load? figures with which he wished to replace them.

For starters, I wanted to compare his answers to Markowitz?s. So I
repeated my question about the relation between ?viral load? and
infectious doses. Mellors responded by proclaiming, ?Viral load has
nothing to do with infectivity!?

Ah-ha! Now I had a second HIV big shot admitting that the ?viral
load? figures did not indicate infectious HIV.

Assuming that ?viral load? testing accurately counted HIV, and that
infectious dose testing accurately counted infectious HIV, I offered my
99.8% figure from the Ho/Markowitz paper as the fraction of circulating
HIV that was non-infectious.

Non-infectious HIV, then, is the source of RNA and proteins?including
protease?from which the genetics and other characteristics of HIV are
derived.

He agreed. (How could he not?)

Now I had him. Since non-infectious viruses have no conceivable
clinical relevancy, then neither could any data derived from them.

What?s the significance of all the non-infectious HIV? I asked. I had
no idea how he could work himself out of this corner, but even I was
stunned by his response: ?The non-infectious particles [HIV] are
pathogenic.?

Now here was a first. I don?t think that anybody?s ever gone on
record before proposing that non-infectious virus could cause disease.

I sat there flabbergasted, noticing the murmur that had broken out. In
my astonished state I realized there was nothing else to be said.

In the meantime, the session was declared over, the time allotted for
discussion having been exhausted by my cross examination, with no one
else having had time to pose questions.

My God, I thought. Talk about a rich source of research opportunity.
The pathogenicity of non-infectious viruses. Anybody familiar with the
antibody response and the premise of vaccinations can appreciate the
revolutionary nature (and implausibility) of this idea.

My sense is that the audience did, given the intense murmuring, which
continued even after the lecture had been dismissed. On the way out of
the room an Indian scientist grabbed my arm and asked, ?Did you hear
that??

Indeed I had. AIDS was caused by a deadly army of viral corpses.

Curing the Healthy

Though I looked far and wide, I could find not a single controlled
experiment discussed anywhere at the conference. It appears that the
only thing that exists in the entire world of AIDS is HIV. Anything bad
that happens to HIV-positive people is due to HIV; any improvement is
due to therapy.

There was even one presenter who took credit for curing people who
accidentally pricked themselves with needles tainted by HIV-positive
blood. The patients were ?aggressively? treated immediately with
antiviral drugs, and didn?t become positive. The scientist claimed
this protocol was what prevented seroconversion one time in a thousand,
a fact he did not mention. And neither did anybody else, though this
fact is well known, and the attendees were all certified ?AIDS
experts.?

Not only was he claiming credit for the effects of statistical
probability, he was also claiming to have cured healthy people...and
nobody called him on it. These HIV supporters are so desperate for good
news that they?ll say and accept anything that agrees with the HIV
model.

Cold Shoulder

Early on it was clear that certain people at the meeting already knew
of me. They avoided me.

Others, though, initially showed interest when I raised my objections.
It was obvious that these problems were not new to them, they had just
never discussed them before?or been around anyone who wanted to.
However, once these potential allies continued the discussions with
people like Markowitz?scientists with status and influence?then
they as well avoided me from then on.

I found it a lonely business acting like a scientist at an AIDS
conference.

Postscript:

Breaking the Rules

I know the rules of the Gordon conferences and have abided by them
since attending my first one in 1980: no press, no cameras, no
recording devices. Nothing revealed at a Gordon conference is to appear
in print except by the original authors. You can take all the notes you
like, and discuss the information with colleagues all you want. You
just can?t put it into public domain via print.

I openly acknowledge that my report breaks these rules. I don?t do
this lightly. Gordon conferences are my favorite meetings. However, the
HIV/AIDS scandal has compelled me to take this action. The information
on what is wrong with the prevailing HIV dogma is almost totally hidden
from the public. The travesty of the HIV protease inhibitor clinical
trial results, for example, was clearly evident at this particular
Gordon Conference, as well as one I attended in 1994 (see RA Aug.,
1996). This information is just too important to be kept from the
tax-payers and consumer who fund it all.

The rules might seem sinister, but they aren?t. They enable
scientists to present preliminary results without fear of being scooped
by colleagues, or being held accountable for mistakes. Ordinarily these
rules promote honest scientific discussion and exchange of ideas. But
the AIDS industry has adopted them to hide facts that shouldn?t be
secrets.

I hope I have done the right thing. I might be banned from future
conferences. ?D. Rasnick.