Out Of Control
AIDS and the corruption of medical
science
CELIA FARBER / Harper's Magazine
1mar2006
A substantial
amount of this article has been removed (EDITED).
For complete article contact Harper's Magazine
http://www.mindfully.org/Health/2006/AIDS-Medical-Corruption1mar06.htm
Joyce
Ann Hafford was a single mother living alone with her
thirteen-year-old son, Jermal, in Memphis, Tennessee, when she
learned that she was pregnant with her second child. She worked as a
customer service representative at a company called CMC Call Center;
her son was a top student, an athlete and musician. In April 2003,
Hafford, four months pregnant, was urged by her obstetrician to take
an HIV test. She agreed, even though she was healthy and had no
reason to think she might be HIV positive. The test result came up
positive, though Hafford was tested only once, and she did not know
that pregnancy itself can cause a false positive HIV test. Her first
thought was of her unborn baby. Hafford was immediately referred to
an HIV/AIDS specialist, Dr. Edwin Thorpe, who happened to be one of
the principal investigators recruiting patients for a clinical trial
at the University of Tennessee Medical Group that was sponsored by
the Division of AIDS (DAIDS)—the chief branch of HIV/AIDS research
within the National Institutes of Health.
The objective of the trial,
PACTG 1022, was to compare the "treatment-limiting toxicities" of
two anti-HIV drug regimens. The core drugs being compared were
nelfinavir (trade name Viracept) and nevirapine (trade name Viramune).
To that regimen, in each arm, two more drugs were added—zidovudine
(AZT) and lamivudine (Epivir) in a branded combination called
Combivir. PACTG 1022 was a "safety" trial as well as an efficacy
trial, which means that pregnant women were being used as research
subjects to investigate "safety" and yet the trial was probing the
outer limits of bearable toxicity. Given the reigning beliefs about
HIV's pathogenicity, such trials are fairly commonplace, especially
in the post-1994 era, when AZT was hailed for cutting transmission
rates from mother to child.
The goal of PACTG 1022 was to
recruit at least 440 pregnant women across the nation, of which 15
were to he enrolled in the University of Tennessee Medical Group.
The plan was to assign the study's participants to one of
two groups, with each receiving three HIV drugs, starting as early
as ten weeks of gestation. Of the four drugs in this study, three
belong to the FDA's category "C," which means that safety to either
mother or fetus has not been adequately established.
Joyce Ann Hafford was
thirty-three years old and had always been healthy. She showed no
signs of any of the clinical markers associated with AIDS — her CD4
counts, which measure the lymphocytes that are used to indicate how
strong a person's immune system is, and which HIV is believed to
slowly corrode, were in the normal range, and she felt fine. In
early June 2003, she was enrolled in the trial and on June 18 took
her first doses of the drugs. "She felt very sick right away,"
recalls her older sister, Rubbie King. "Within seventy-two hours,
she had a very bad rash, welts all over her face, hands, and arms.
That was the first sign that there was a problem. I told her to call
her doctor and she did, but they just told her to put hydrocortisone
cream on it. I later learned that a rash is a very had sign, but
they didn't seem alarmed at all."
Hafford was on the drug regimen
for thirty-eight days. "Her health started to deteriorate from the
moment she went on the drugs," says King. "She was always in pain,
constantly throwing up, and finally she got to the point where all
she could do was lie down." The sisters kept the news of Hafford's
HIV test and of the trial itself from their mother, and Hafford
herself attributed her sickness and nausea to being pregnant. She
was a cheerful person, a noncomplainer, and was convinced that she
was lucky to have gotten into this trial. "She said to me, `Nell'
—that's what she called me—`I have got to get through this. I can't
let my baby get this virus.' I said, `Well, I understand that, but
you're awful sick.' But she never expressed any fear because
she thought this was going to keep her baby from being HIV positive.
She didn't even know she was in trouble."
On July 16, at her scheduled
exam, Hafford's doctor took note of the rash, which was "pruritic
and macular-papular," and also noted that she was suffering
hyperpigmentation, as well as ongoing nausea, pain, and vomiting. By
this time all she could keep down were cans of Ensure. Her blood was
drawn for lab tests, but she was not taken off the study drugs,
according to legal documents and internal NIH memos.
Eight days later, Hafford went
to the Regional Medical Center "fully symptomatic," with what legal
documents characterize as including: "yellow eyes, thirst, darkening
of her arms, tiredness, and nausea without vomiting." She also had a
rapid heartbeat and difficulty breathing. Labs were drawn, and she
was sent home, still on the drugs. The next day, July 25, Hafford
was summoned back to the hospital after her lab reports from nine
days earlier were finally reviewed. She was admitted to the
hospital's ICU with "acute and subacute necrosis of the liver,
secondary to drug toxicity, acute renal failure, anemia, septicemia,
premature separation of the placenta," and threatened "premature
labor." She was finally taken off the drugs but was already losing
consciousness. Hafford's baby, Sterling, was delivered by C-section
on July 29, and she remained conscious long enough not to hold him
but at least to see him and learn that she'd had a boy. "We joked
about it a little, when she was still coming in and out of
consciousness in ICU," Rubbie recalls. "I said to her, `You talked
about me so much when you were pregnant that that baby looks just
like me."' Hafford's last words were a request to be put on a
breathing tube. "She said she thought a breathing tube might help
her," says Rubbie. "That was the last conversation I had with my
sister." In the early morning hours of August 1, Rubbie and her
mother got a call to come to the hospital, because doctors had lost
Hafford's pulse. Jermal was sleeping, and Rubbie woke her own
daughter and instructed her not to tell Jermal anything yet. They
went to the hospital, and had been there about ten minutes when
Joyce Ann died.
Rubbie
recalls that the hospital staff said they would clean her up and
then let them sit with her. She also remembered a doctor who asked
for their home phone numbers and muttered, "You got a lawsuit."
(That person has not resurfaced.) They hadn't been sitting with
Hafford's body long when a hospital official came in and asked the
family whether they wanted an autopsy performed. "We said yes, we
sure do," she says. The hospital official said it would have to be
at their expense—at a cost of $3,000. "We said, `We don't have
$3,000.' My sister didn't have any life insurance or anything," says
Rubbie. "She had state health care coverage, and we were already
worried about how to get the money together to bury her."
Consequently, no autopsy was done. There was a liver biopsy,
however, which revealed, according to internal communiqués of DAIDS
staff, that Hafford had died of liver failure brought on by
nevirapine toxicity.
And what was the family told
about the cause of Hafford's death?
"How did they put it?" Rubbie
answers, carefully. "They told us how safe the drug was, they never
attributed her death to the drug itself, at all. They said that her
disease, AIDS, must have progressed rapidly." But Joyce
Ann Hafford never had AIDS, or anything even on the diagnostic scale
of AIDS. "I told my mom when we were walking out of there that
morning," Rubbie recalls, "I said, `Something is wrong.' She said,
`What do you mean?' I said, `On the one hand they're telling us this
drug is so safe, on the other hand they're telling us they're
going to monitor the other patients more closely. If her disease was
progressing, they could have changed the medication.' I knew
something was wrong with their story, but I just could not put my
finger on what it was."
When they got home that morning,
they broke the news to Jermal. "I think he cried the whole day when
we told him," Rubbie recalls. "My mom had tried to prepare him. She
said, `You know, Jermal, my mom died when I was very young,' but he
was just devastated. They were like two peas in a pod those two. You
could never separate them." Later on, Jermal became consumed with
worry about how they would bury his mother, for which they had no
funds and no insurance. The community pitched in, and Hafford was
buried. "I haven't even been able to go back to her grave since she
passed," says Rubbie.
Rubbie
King is haunted by many questions, including whether her sister was
really infected with HIV,1 and also what the
long-term damage might be to Sterling, whom Rubbie is now raising,
along with Jermal and her own child. Sterling, in addition to the
drugs he was exposed to in the womb, was also on an eight-week AZT
regimen after birth. One of the reasons the family suspects Hafford
may have been a false positive is that St. Jude's Children's
Research Hospital has not released Sterling's medical records, and
although they have been told that he is now HIV negative, they never
had any evidence that he was even born positive. (All babies born to
an HIV-positive mother are born positive, but most become negative
within eighteen months.)
Hafford's family was never told
that she died of nevirapine toxicity. "They never said that. We
never knew what she had died of until we got the call from [AP
reporter] John Solomon, and he sent us the report," says Rubbie
King. "It was easier to accept that she died of a lethal disease.
That was easier to handle." The family has filed a $10 million
lawsuit against the doctors who treated Hafford, the Tennessee
Medical Group, St. Jude's Children's Research Hospital, and
Boehringer Ingelheim, the drug's manufacturer.2
Rubbie King made a final,
disturbing discovery when she was going through Hafford's medical
records: In addition to discovering that her sister had only ever
been given a single HIV test, she also came across the fifteen-page
consent form, which was unsigned.
On
August 8, 2003, Jonathan Fishbein, who had recently taken a job as
the director of the Office for Policy in Clinical Research
Operations at DAIDS, wrote an email to his boss, DAIDS director Ed
Tramont, alerting him that "there was a fulminant liver failure
resulting in death" in a DAIDS trial and that it looked like
"nevirapine was the likely culprit." He said that the FDA was being
informed. He was referring to Joyce Ann Hafford. Tramont emailed him
hack, "Ouch. Not much we can do about dumb docs!"
This email exchange came to
light in December 2004, when AP reporter John Solomon broke the
story that Fishbein was seeking whistle-blower protection, in part
because he had refused to sign off on the reprimand of an NIH
officer who had sent the FDA a safety report concerning the DAIDS
trial that launched the worldwide use of nevirapine for pregnant
women. The study was called HIVNET 012, and it began in Uganda in
1997.
The internal communiqués from
DAIDS around the time of Hafford's death made it clear that doctors
knew she had died of nevirapine toxicity. Tramont's reply to
Fishbein suggests that he thought blame could he placed squarely
with Hafford's doctors, but it was the NIH itself that had conceived
of the study as one that tested the "treatment-limiting toxicities"
of HIV drugs in pregnant women.
The conclusion of the PACTG 1022
study team was published in the journal JAIDS in July of 2004. "The
study was suspended," the authors reported, "because of greater than
expected toxicity and changes in nevirapine prescribing information."
They reported that within the nevirapine group, "one
subject developed fulminant hepatic liver failure and died, and
another developed Stevens-Johnson syndrome." Stevens-Johnson
syndrome is skin necrolysis—a severe toxic reaction that is similar
to internal third-degree burns, in which the skin detaches from the
body. Another paper, entitled "Toxicity with Continuous Nevirapine
in Pregnancy: Results from PACTG 1022," puts the results in charts,
with artful graphics. A small illustration of Hafford's liver floats
in a box, with what looks like a jagged gash running through it.
Four of the women in the nevirapine group developed hepatic
toxicity.
As
Terri Schiavo lay in her four-teenth year of a persistent vegetative
state, and the nation erupted into a classically American moral
opera over the sanctity of life, Joyce Ann Hafford's story made only
a fleeting appearance—accompanied by a photo of her holding a red
rose in an article that was also written by the AP's John Solomon.
But soon a chorus of condemnation was turned against those who were
sensationalizing Hafford's death and the growing HIVNET controversy
to condemn nevirapine, which had been branded by the AIDS industry
as a "life-saving" drug and a "very important tool" to combat HIV in
the Third World.
So-called community AIDS
activists were sprung like cuckoo birds from grandfather clocks at
the appointed hour to affirm the unwavering AIDS cathechism: AIDS
drugs save lives. To suggest otherwise is to endanger millions of
African babies. Front and center were organizations like the
Elizabeth Glaser Pediatric AIDS Foundation, which extolled the
importance of nevirapine. Elizabeth Glaser's nevirapine defenders
apparently didn't encounter a single media professional who knew, or
cared, that the organization had received $1 million from
nevirapine's maker, Boehringer Ingelheim, in 2000.3
This was no scandal but simply part of a landscape. Pharmaceutical
companies fund AIDS organizations, which in turn are quoted
uncritically in the media about how many lives their drugs save.
This time the AIDS organizations were joined by none other than the
White House, which was in the midst of promoting a major program to
make nevirapine available across Africa.4
America
is a place where people rarely say: Stop. Extreme and unnatural
things happen all the time, and nobody seems to know how to hit the
brakes. In this muscular, can-do era, we are particularly prone to
the seductions of the pharmaceutical industry, which has
successfully marketed its ever growing arsenal of drugs as the
latest American right. The buzzword is "access," which has the
advantage of short-circuiting the question of whether the drugs
actually work, and of utterly obviating the question of whether they
are even remotely safe. This situation has had particularly tragic
ramifications on the border between the class of Americans with good
health insurance, who are essentially consumers of pharmaceutical
goods, and those without insurance, some of whom get drugs "free"
but with a significant caveat attached: They agree to be
experimented on. These people, known in the industry as "recruits,"
are pulled in via doctors straight from clinics and even recruited
on the Internet into the pharmaceutical industry and the
government's web of clinical trials, thousands of which have popped
up in recent years across the nation and around the world. Such
studies help maintain the industry's carefully cultivated image of
benign concern, of charity and progress, while at the same time
feeding the experimental factories from which new blockbuster drugs
emerge. "I call them what they are: human experiments,"
says Vera Hassner Sharav, of the Alliance for Human Research
Protection in New York City. "What's happened over the last ten to
fifteen years is that profits in medicine shifted from patient care
to clinical trials, which is a huge industry now. Everybody
involved, except the subject, makes money on it, like a food chain.
At the center of it is the NIH, which quietly, while people weren't
looking, wound up becoming the partner of industry."
By June 2004, the National
Institutes of Health had registered 10,906 clinical trials in ninety
countries. The size of these trials, which range from the hundreds
to more than 10,000 people for a single study, creates a huge market
for trial participants, who are motivated by different factors in
different societies but generally by some combination of the promise
of better health care, prenatal care, free "access" to drugs, and
often—especially in the United States—cash payments. Participating
doctors, whose patient-care profits have been dwindling in recent
years because of insurance-company restrictions, beef up their
incomes by recruiting patients.
Dr.
Jonathan Fishbein is hardly a rabble-rouser. But he is a passionate
advocate of "good clinical practice," or GCP, a set of international
standards that were adopted in 1996, as clinical-trial research
boomed. The GCP handbook states: "Compliance with this standard
provides public assurance that the rights, safety, and well-being of
trial subjects are protected, consistent with the principles that
have their origin in the Declaration of Helsinki, and that the
clinical trial data are credible." During the decade prior to his
arrival at DAIDS, Fishbein had overseen and consulted on hundreds of
clinical trials for just about every pharmaceutical company.
Fishbein knew, before he took his job as director of the Office for
Policy in Clinical Research Operations at DAIDS, that there was a
troubled study haunting the whole division. Nobody was supposed to
talk about it, but it hung heavily in the air. "Something about
Uganda, that's all I knew," he says. There was a trial staged there,
a big one, that had been plagued with "problems," and there was also
a lot of talk about one particular employee connected to this trial
who would need to he disciplined. Soon he discovered just how bad
the situation was. "The HIVNET thing," he recalls, "it hit me like a
fire hose when I walked in there."
Fishbein's position was new. "It
sounded like a very important position," he says. "I was to oversee
the policies governing all the clinical-research operations, both
here and abroad." He was told he would have "go–no go" authority
over individual trials. It wasn't long before Fishbein realized that
he was, in effect, taking a job that was the equivalent of piloting
an already airborne plane. "They had all these trials going on, and
hundreds of millions of dollars flowing in every year, but there was
apparently no one in a senior position there who really had clinical
expertise—who knew all the nuances, rules, and regulations in the
day-to-day running of clinical trials." DAIDS, when Fishbein came to
work there in 2003, was running about 400 experimental trials both
in the United States and abroad.
A DAIDS project officer close to
the HIVNET study closed the door when she had her first meeting with
Fishbein. She had also crossed over from the private sector, and so
she and Fishbein shared a disillusionment over how much shoddier and
more chaotic the research culture was within the government,
compared with industry. "I'm really frightened about the stuff that
goes on here," she told him. "We really need somebody." This project
officer, who for her own protection cannot be named, told Fishbein
that the division's flagship study in Africa—HIVNET 012—had been
wracked with problems and completely lacking in regulatory
standards. She told Fishbein that the trial investigators were "out
of control," and that there was no oversight of them, and nobody
with either the inclination or the authority to make them adhere to
safety standards. What Fishbein subsequently learned entangled him
in a story with eerie echoes of John Le Carre's Constant
Gardener.
For
our purposes, the story of nevirapine begins in 1996, when the
German pharmaceutical giant Boehringer Ingelheim applied for
approval of the drug in Canada. The drug had been in development
since the early 1990s, which was a boom time for new HIV drugs.
Canada rejected nevirapine twice, once in 1996 and again in 1998,
after the drug showed no effect on so-called surrogate markers (HIV
viral load and CD4 counts) and was alarmingly toxic. In 1996, in the
United States, the FDA nonetheless gave the drug conditional
approval so that it could be used in combination with other HIV
drugs.5
By this time, Johns Hopkins AIDS
researcher Brooks Jackson had already generated major funding from
the NIH to stage a large trial for nevirapine in Kampala, Uganda,
where the benevolent dictator Yoweri Museveni had opened his country
to the lucrative promise of AIDS drug research, as well as other
kinds of pharmaceutically funded medical research. HIVNET 012,
according to its original 1997 protocol, was intended to be a
four-arm, Phase III, randomized, placebo-controlled trial.6
Its sole sponsor was listed as the National Institute of Allergy and
Infectious Diseases (NIAID), though one of the investigators was a
Boehringer employee. The "sample size" was to be 1,500 HIV-1
infected Ugandan women more than thirty-two weeks pregnant. The four
arms they would be divided into were 1) A single dose of 200mg
nevirapine at onset of labor and a single 2mg dose to the infant
forty-eight to seventy-two hours post-delivery, and 2) a
corresponding placebo group; 3) 600mg of AZT at onset of labor and
300mg until delivery, with a 4mg AZT dose for the infant lasting
seven days after birth, and 4) a corresponding placebo group. There
were to he 500 women in each "active agent" arm and 250 in each
placebo arm. The study was to last eighteen months, and its "primary
endpoints" were to see how these two regimens would
affect rates of HIV transmission from mother to child, and to
examine the "proportion of infants who are alive and free of HIV at
18 months of age." Another primary objective was to test
the "safety/tolerance" of nevirapine and AZT. HIVNET's
architects estimated that more than 4,200 HIV-positive pregnant
women would deliver at Mulago hospital each year, allowing them to
enroll eighty to eighty-five women per month. Consent forms were to
be signed by either the mother or a guardian, by signature or
"mark." One of the exclusion criteria was "participation
during current pregnancy in any other therapeutic or vaccine
perinatal trial."
Although
HIVNET was designed to be a randomized, placebo-controlled,
double-blind, Phase III trial of 1,500 mother/infant pairs, it wound
up being a no-placebo, neither double- nor even single-blind Phase
II trial of 626 mother/infant pairs. Virtually all of the parameters
outlined for HIVNET 012 were eventually shifted, amended, or done
away with altogether, beginning with perhaps the most important—the
placebo controls. By a "Letter of Amendment" dated March
9, 1998, the placebo-control arms of HIVNET were eliminated.
The study as reconstituted thus
amounted to a simple comparison of AZT and nevirapine.
On September 4, 1999, The
Lancet published HIVNET's preliminary results, reporting that
"Nevirapine lowered the risk of HIV-I transmission during the first
14–16 weeks of life by nearly 50 percent." The report concluded that
"the two regimens were well-tolerated and adverse events were
similar in the two groups." The article also reported that
thirty-eight babies had died, sixteen in the nevirapine group and
twenty-two in the AZT group. The rate of HIV transmission in the AZT
arm was 25 percent, while in the nevirapine group it was only 13
percent. As Hopkins Medical News later reported, the study
was received rapturously. "The data proved stunning. It showed that
nevirapine was 47 percent more effective than AZT and had reduced
the number of infected infants from 25 to 13 percent. Best of all,
nevirapine was inexpensive—just $4 for both doses. If implemented
widely, the drug could prevent HIV transmission in more than 300,000
new-borns a year."
With the results of the study
now published in The Lancet, Boehringer, which previously had
shown little interest in HIVNET, now pressed for FDA approval to
have nevirapine licensed for use in preventing the transmission of
HIV in pregnancy.
----EDITED SECTION----
The
HIVNET cover-up can only be understood within the larger political
context of AIDS. The emergence of this syndrome in the 1980s sparked
a medical state of emergency in which scientific controls, the rules
that are supposed to bracket the emotions and desires of individual
researchers, were frequently compromised or removed entirely. AIDS
helped turn disease into politics, and politics, at least in the
United States, is all about turning power into money.
No one has been more persistent
in calling attention to the failings of AIDS research than Peter
Duesberg, a virologist and cancer specialist at the University of
California at Berkeley. If Duesberg's name sounds familiar, it's
because he has been quite effectively branded in the international
media as the virologist who is wrong about HIV. His name entered the
popular culture in the late 1980s prestamped with wrongness. You
knew he was wrong before you knew what he had said in the first
place.
In 1987, Duesberg published a
paper in the journal Cancer Research entitled "Retroviruses
as Carcinogens and Pathogens: Expectations and Reality." He was, at
the time, at the top of the field of retrovirology, having mapped
the genetic structure of retroviruses and defined the first cancer
gene in the 1970s. He was the youngest member, at age fifty, ever
elected into the National Academy of Sciences. In this paper, which
in the words of his scientific biographer, Harvey Bialy, "sealed his
scientific fate for a dozen years," Duesberg argued that
retroviruses don't cause cancer and concluded by detailing how and
why the retrovirus HIV cannot cause AIDS.
As AIDS grew in the 1980s into a
global, multibillion-dollar juggernaut of diagnostics, drugs, and
activist organizations, whose sole target in the fight against AIDS
was HIV, condemning Duesberg became part of the moral crusade. Prior
to that 1987 paper, Duesberg was one of a handful of the most highly
funded and prized scientists in the country. Subsequently, his NIH
funding was terminated and he has received not one single federal
research dollar since his pre-1987 Outstanding Investigator Grant
ran out. Duesberg lost his lab facilities and had to move twice
within a few years to smaller labs on the Berkeley campus, where he
spent much of his time writing futile research grant proposals
asking to test his hypothesis that AIDS is a chemical syndrome,
caused by accumulated toxins from heavy drug use. He lost his
graduate students, who were warned that to emerge from his lab would
blight their careers. He was denied and had to fight for routine pay
increases by his employers at UC Berkeley, where he has tenure and
still teaches. He was "disinvited" from scientific conferences, and
colleagues even declared that they would refuse to attend any
conference that included him. Duesberg also was banished from
publishing in scientific journals that previously had welcomed his
contributions, most theatrically by the editor of Nature, Sir
John Maddox, who wrote a bizarre editorial declaring that Duesberg
would he denied the standard scientific "right of reply"
in response to personal attacks that were frequently published in
that journal. Prior to 1987, Peter Duesberg never had a single grant
proposal rejected by the NIH. Since 1991 he has written a total of
twenty-five research proposals, every single one of which has been
rejected. "They took him out, just took him right out," says Richard
Strohman, an emeritus professor of biology at UC Berkeley.
And what was it, exactly, that
Peter Duesberg had done? He simply pointed out that no one had yet
proven that HIV is capable of causing a single disease, much less
the twenty-five diseases that are now part of the clinical
definition of AIDS.12 He pointed to a number of
paradoxes regarding HIV and argued that far from being evidence that
HIV is "mysterious" or "enigmatic," these paradoxes were evidence
that HIV is a passenger virus.
The classical tests of whether
or not a microorganism is the cause of infectious disease are known
as Koch's postulates. They state: 1) the microorganism must be found
in all cases of the disease; 2) it must be isolated from the host
and grown in pure culture; 3) it must reproduce the original disease
when introduced into a susceptible host; and 4) it must be found
present in the experimental host so infected. Although claims to the
contrary have been made, Duesberg maintains that it has never been
demonstrated that HIV satisfies all of Koch's postulates. His
exhaustive analysis of the peer-reviewed scientific literature has
revealed more than 4,000 documented AIDS cases in which there is no
trace of HIV or HIV antibodies. This number is significant, because
there are strong institutional forces deterring such descriptions
and because the vast majority of AIDS cases are never described in
formal scientific papers. In fact, most AIDS patients have no active
HIV in their systems, because the virus has been neutralized by
antibodies. (With all other viral diseases, by the way, the presence
of antibodies signals immunity from the disease. Why this is not the
case with HIV has never been demonstrated.) Generally speaking, HIV
can be isolated only by "reactivating" latent copies of the virus,
and then only with extraordinary difficulty. Viral load, one of the
clinical markers for HIV, is not a measurement of actual, live virus
in the body but the amplified fragments of DNA left over from an
infection that has been suppressed by antibodies. Another
embarrassment for the HIV hypothesis is the extraordinary latency
period between infection and the onset of disease, despite the fact
that HIV is biochemically most active within weeks of initial
infection. This latency period, which apparently grows with every
passing year, enables proponents of the theory to evade Koch's third
and fourth postulates.
The foregoing is merely a sketch
of the central mystery presented by the HIV theory of AIDS. There
are many more, which Duesberg has laid out very carefully in his
scientific papers and in a trade book published ten years ago, but
they all boil down to the central point that when it comes to AIDS,
basic scientific standards seem no longer to apply.13
AIDS is a "syndrome" defined by twenty-five diseases, all of which
exist independently of HIV. No one has ever demonstrated the
cell-killing mechanism by which HIV is supposed to cause all these
different diseases, and no one has ever demonstrated how a sexually
transmitted virus can manage to restrict itself overwhelmingly to
gay men and other AIDS risk groups instead of spreading randomly
through the population, as do all other infectious diseases. The
"overwhelming" character of the evidence for HIV's causation has
always been epidemiological; which is to say, a correlation, a
coincidence. Whenever we have AIDS, researchers say, we also have
HIV. But this correlation is a result of the official definition of
AIDS, which state, that a disease counts as AIDS only if it
corresponds with HIV antibodies. ("AIDS without HIV" has been given
a singularly unmemorable name: idiopathic CD4 lymphocytopenia.)
Given that the evidence for HIV
is coincidental, a number of research avenues suggest themselves,
yet orthodox AIDS researchers have failed to demonstrate, using
large-scale controlled studies, that the incidence of AIDS-defining
diseases is higher among individuals infected with HIV than among
the general uninfected population. Consequently, it could very well
be the case that HIV is a harmless passenger virus that infects a
small percentage of the population and is spread primarily from
mother to child, though at a relatively low rate. (This hypothesis
would tend to explain the fact that the estimated number of
HIV-positive Americans has remained constant at about 1 million
since 1985.) Nor have large-scale controlled studies been carried
out to directly test the AIDS-drug hypothesis, which holds that many
cases of AIDS are the consequence of heavy drug use, both
recreational (poppers, cocaine, methamphetamines, etc.) and medical
(AZT, etc.).14 Nor have controlled studies been
carried out to prove that hemophiliacs infected with HIV die sooner
than those who are not infected. Such studies might be expensive and
tedious, but expense has never been a serious objection to AIDS
researchers, who have spent many billions of dollars in the last
twenty years on HIV research and practically nothing on alternative
causes or even cofactors. (Even Luc Montagnier, the discoverer of
HIV, has stated repeatedly that the virus cannot cause AIDS without
contributing causes.)
Attempts to rigorously test the
ruling medical hypothesis of the age are met not with reasoned
debate but with the rhetoric of moral blackmail: Peter Duesberg
has the blood of African AIDS babies on his hands. Duesberg is evil,
a scientific psychopath. He should be imprisoned. Those who wish
to engage the AIDS research establishment in the sort of causality
debate that is carried on in most other branches of scientific
endeavor are tarred as AIDS "denialists," as if skepticism about the
pathogenicity of a retrovirus were the moral equivalent of denying
that the Nazis slaughtered 6 million Jews. Moral zeal rather than
scientific skepticism defines the field. It has been decided in
advance that HIV causes AIDS; consequently all research and all
funding must proceed from that assumption. Similarly, it was known
in advance that AZT was a "magic bullet" against HIV; the word was
out that it was a "life-saving drug" before anyone could possibly
verify this, and so scientific controls were compromised.
Journalists (myself included) who reported at the time that the drug
apparently was killing patients were labeled "AZT refuseniks" and
even "murderers."
The nevirapine debate follows
the same histrionic, antiscientific pattern. Because of his concerns
about the toxicity of this and other antiretroviral drugs, President
Thabo Mbeki of South Africa was pilloried in the international press
as pharmaceutical companies and their well-funded "activist"
ambassadors repeated their mantra about "life-saving drugs." So,
too, was Jonathan Fishbein, who never questioned the premise that
HIV causes AIDS, tarred and feathered for pointing out that the NIH
flagship study on nevirapine was a complete disaster. Fishbein's
failure to fall into line, his failure to understand in advance of
experimental proof that nevirapine was too important to fail, meant
that the AIDS bureaucracy's neutralizing antibodies had to be
activated to destroy them.
In the end, the NIH failed to
silence Fishbein. In late December 2005, he won his case and was
retroactively reinstated at the agency, though he won't be returning
to DAIDS. He is unable to discuss the terms of his settlement, but
he has promised to continue his commitment to research integrity and
the protection of human research subjects. Peter Duesberg has been
less successful, though there are signs of rehabilitation.
Regardless of whether Duesberg
is right about HIV, his case, like Fishbein's, lays bare the
political machinery of American science, and reveals its reflexive
hostility to ideas that challenge the dominant paradigm. Such
hostility is not unusual in the history of science,15
but the contemporary situation is dramatically different from those
faced by maverick scientists in the past. Today's scientists are
almost wholly dependent upon the goodwill of government researchers
and powerful peer-review boards, who control a financial network
binding together the National Institutes of Health, academia, and
the biotech and pharmaceutical industries. Many scientists live in
fear of losing their funding. "Nobody is safe," one NIH-funded
researcher told me. "The scientific-medical complex is a $2 trillion
industry," says former drug developer Dr. David Rasnick, who now
works on nutrition-based AIDS programs in Pretoria, South Africa.
"You can buy a tremendous amount of consensus for that kind of
money."
"You
have to write a grant a year almost. And you have to write four to
get one, if you're any good. I got out just in time.
Everybody who's still in there says the same thing," says Berkeley's
Strohman. "Before the biotech boom, we never had this incessant
urging to produce something useful, meaning profitable. Everybody is
caught up in it. Grants, millions of dollars flowing into
laboratories, careers and stars being made. The only way to be a
successful scientist today is to follow consensus. If you're going
to produce something and put it on the market you don't want any
goddamn surprises. You've got the next quarter to report and you don't
want any bad news. It's all about the short term now. Science has
totally capitulated to corporate interests. Given their power and
money, it's going to be very hard to work our way out of
this."
Duesberg has never been afraid
to challenge consensus, but contrary to what many in the AIDS
establishment would have us believe, he is very far from being a
scientific psychopath.16 In 1997, on the brink of
scientific demise in the U.S., Duesberg was quietly invited back to
his native Germany to resume his cancer research. During this time,
commuting biannually between Mannheim and Berkeley, Duesberg
formulated and tested a theory that shifts the focus of cancer
causation from the "mutant gene" theory that has reigned for about
three decades to a simpler explanation that revives an abandoned
thread of research from early in the twentieth century, which
posited that cancer is caused by chromosomal malfunction, now known
as "aneuploidy."
Harvey Bialy, the founding
scientific editor of Nature Biotechnology, a sister journal
to Nature, recently spent four years writing a scientific
biography of Duesberg entitled Oncogenes, Aneuploidy, and AIDS.
The book is a history of the papers, review articles, and letters
that Duesberg published between 1983 and 2003, and the responses
they generated. I asked him why he wrote the book. "I am persuaded
that aneuploidy is the initiating event in carcinogenesis",
Bialy said. "Peter has found the genetic basis for cancer. The most
immediate application of it will be early diagnosis."
"When aneuploidy, or genetic
instability, or whatever linguistic term you want to use, gets
reincarnated as the dominant theoretical explanation for the genesis
of cancer, Peter Duesberg will be recognized as a major contributor
to that," Bialy said. "I wanted to make sure that his contributions
were not swept aside or ignored." I asked him about the AIDS
controversy. "AIDS is a political thing, and Peter's stuck in it.
There's nothing to discuss anymore on that." Bialy made a critical
point. Science is amoral and should be. There is no right and wrong,
only correct and incorrect. "Duesberg," Bialy said, "is a
classical molecular biologist. All he is interested in is
rigorously testing dueling hypotheses. The twin pillars, AIDS and
oncogenes, both are crumbling because of the questions Peter
Duesberg put into motion."
"The basis of speciation is
changing the content and the number of chromosomes," says Duesberg.
"Cancer is essentially a failed speciation. It's not mutation.
Cancer is a species. A really bad breast, lung, or prostate
cancer has seventy, eighty, or more chromosomes. Those are the real
had guys they're way outside our species. But it's a rare kind of
species that as a parasite is more successful in its host than the
normal host cell is."
There has been considerable
international interest in Duesberg's new research.17
In January 2004, he hosted a conference on aneuploidy and invited
fifty cancer researchers from around the world who also have been
working on the connections between aneuploidy and cancer. Seventy
showed up, including such luminaries as Thomas Ried, the National
Cancer Institute's head of cancer genomics, Gert Auer from the
Karolinska Institute in Stockholm, and Walter Giaretti, who heads
the equivalent of the NCI in Italy. And on May 31 of last year, amid
considerable tension, Duesberg was invited by the National Cancer
Institute to give a talk at the NIH. The auditorium crackled with
nervous tension as people filed in and took their seats. His talk
was succinct and laced with his characteristic irony, but the
questions afterward were civilized, with no tangible hostility. All
was not forgiven, however. After the talk, while Duesberg remained
at the podium talking to a group of people from the audience, I
noticed a very angry-looking NIH publicist standing at the back of
the room admonishing a colleague, a scientist, who'd posed a
question that somehow connected aneuploidy to HIV. "You opened it
up," she scolded. "We got through it okay, but you opened it up."
As the questioner tried to defend himself, a thick-set man who'd
been standing in the circle said loudly, as though intending to
broadcast it across the room: "Well, at least if he's wrong about
this he won't he killing millions of people."
Nobel laureate Kary Mullis, who
discovered the revolutionary DNA technique called the polymerase
chain reaction, has long been a supporter of Duesberg, but he has
grown weary of the AIDS wars and the political attacks on contrarian
scientists. "Look, there's no sociological mystery here," he told
me. "It's just people's income and position being
threatened by the things Peter Duesberg is saying. That's why
they're so nasty. In the AIDS field, there is a widespread neurosis
among scientists, but the frenzy with which people approach the HIV
debate has slacked off, because there's just so much slowly
accumulating evidence against them. It's really hard for them to
deal with it. They made a really big mistake and they're not ever
going to fix it. They're still poisoning people."
Duesberg thinks that up to 75
percent of AIDS cases in the West can he attributed to drug
toxicity. If toxic AIDS therapies were discontinued, he says,
thousands of lives could be saved virtually overnight . And when
it comes to Africa, he agrees with those who argue that AIDS in
Africa is best understood as an umbrella term for a number of old
diseases, formerly known by other names, that currently do not
command high rates of international aid. The money spent on
antiretroviral drugs would be better spent on sanitation and
improving access to safe drinking water (the absence of which kills
1.4 million children a year).
It's too late to save people
like Joyce Ann Hafford, but it is possible that an open and honest
debate about the risks of current AIDS treatments and the scientific
questions concerning HIV could save others.
REFERENCES
1
HIV tests detect footprints, never the animal itself. These
footprints, antibodies, are identified by means of molecular protein
weights, and were limited to two in 1984, when the first test was
developed and patented, but over the years expanded to include many
proteins previously not associated with HIV. Like most Americans,
Hafford thought that a single HIV-positive test meant that she "had"
HIV—a surefire death sentence. But a majority of HIV-positive tests,
when retested, come back indeterminate or negative. In many cases,
different results emerge from the same blood tested in different
labs. There are currently at least eleven different criteria for how
many and what proteins at which hand density signal "positive." The
most stringent criteria (four hands) are upheld in Australia and
France; the least stringent (two hands), in Africa, where an HIV
test is not even required as part of an AIDS diagnosis. The U.S.
standard is three reactive hands. It has been pointed out that a
person could revert to being HIV negative simply by buying a plane
ticket from Uganda to Australia.
2
Dr. Thorpe declined to comment, citing ongoing litigation, as did
the Tennessee Medical Group, the Regional Medical Center at Memphis,
and St. Jude's Children's Research Hospital.
3
"Our mission of eradicating AIDS is always informed and driven by
the best available science, not by donations," said Mark Isaac,
Elizabeth Glazer's vice president for policy, when asked to comment.
"The full body of research, as well as our extensive experience,
validates the safety and efficacy of single-dose nevirapine as one
of several options to prevent mother-to-child transmission of HIV."
4
Africa, as the news media never tires of telling us, has become
ground zero of the AIDS epidemic. The clinical definition of AIDS in
Africa, however, is stunningly broad and generic, and was seemingly
designed to be little other than a signal for funding. It is in no
way comparable to Western definitions. The "Bangui definition" of
AIDS was established in the city of Bangui in the Central African
Republic, at a conference in 1985. The definition requires neither a
positive HIV test nor a low T-cell count, as in the West, but only
the presence of chronic diarrhea, fever, significant weight loss,
and asthenia, as well as other minor symptoms. These happen to be
the symptoms of chronic malnutrition, malaria, parasitic infections,
and other common African illnesses. (In 1994 the definition was
updated to suggest the use of HIV tests, but in practice they are
prohibitively expensive.) Even when HIV tests are performed, many
diseases that are endemic to Africa, such as malaria and TB, are
known to cause false positives. The statistical picture of AIDS in
Africa, consequently, is a communal projection based on very rough
estimates of HIV positives, culled from select and small samples,
which are extrapolated across the continent using computer models
and highly questionable assumptions.
5
Asked to comment about the Hafford case, HIVNET 012, and the larger
nevirapine controversy, Boehringer Ingelheim provided the following
statement: "Viramune ® (nevirapine) was an innovation in anti-HIV
treatment as the first member of the nonnucleoside reverse
transcriptase inhibitor (NNRTI) class of drugs. Now in its tenth
year of use, Viramune has been used as a treatment in more than
800,000 patient-years worldwide."
6
The study was originally titled "HIVNET 012: A Phase III
Placebo-Controlled Trial to Determine the Efficacy of Oral AZT and
the Efficacy of Oral Nevirapine for the Prevention of Vertical
Transmission of HIV-1 Infection in Pregnant Ugandan Women and Their
Neonates." "Randomization" means that people are randomly chosen for
one arm of the study or another, a procedure that is supposed to
even out the variables that could affect the outcome. "Placebo
controls" are the bedrock of drug testing and are the only way to
know whether the treatment is effective. Phase I trials involve a
small group of people, twenty to eighty, and are focused on safety
and side effects. In Phase II trials the drug is given to an
expanded cohort, between 100 and 300, to further evaluate safety and
begin to study effectiveness. Phase III drug trials expand further
the number of people enrolled, often to more than 1,000, and are
meant to confirm a drug's effectiveness, monitor side effects, and
compare it with other treatments commonly used. A small Phase I
trial preceded HIVNET 012 that studied the safety, primarily, of
nevirapine in pregnant women but also looked at efficacy. It was
called HIVNET 006, and it enrolled twenty-one pregnant women for
initial study. Of twenty-two infants born, four died. There were
twelve "serious adverse events" reported. The study also showed that
there was no lowering of viral load in the mothers who took the
study drug (the industry's agreed-upon standard for interrupting
maternal transmission).
7
Brooks Jackson declined to comment for this article. Laura Guay
responded with the following statement: "Several in-depth reviews of
the conduct and results of the HIVNET 012 trial as well as the data
collected from subsequent trials and PMTCT programs, have
substantiated the HIVNET 012 conclusions that Nevirapine is safe and
effective in preventing mother-to-child HIV transmission. Nevirapine
remains one of the most important tools for the prevention of
mother-to-child HIV transmission in the developing world, where
there are still hundreds of thousands of HIV-infected pregnant women
who do not have access to any HIV testing, antiretroviral therapy,
or HIV care at all. For many programs struggling to establish PMTCT
programs with limited resources, Nevirapine is often the only option
available." Family Health International, the NIH contractor
originally responsible for monitoring HIVNET 012, contested the
Westat report and said that the results of the study had been
validated by the NIH and the Institute of Medicine.
8
Smith and Luzar have been forbidden by the NIH to speak to the press
about HIVNET. Luzar was deposed by Fishbein's attorney in his
wrongful-termination lawsuit, Stephen Kohn, in December 2004, and
this account is partially based on her deposition.
9
At this point the story grows ever more complicated, as Fishbein
supported Luzar in a sexual-harassment claim against Kagan.
10
An internal NIH investigation, which was obtained by the Associated
Press last summer, vindicated many of Fishbein's charges and
concluded that "it is clear that DAIDS is a troubled organization,"
and that the Fishbein case "is clearly a sketch of a deeper issue."
Kagan and Tramont did not return repeated calls for comment.
Instead, an NIH spokesman, Dr. Cliff Lane, said that the agency
stands by HIVNET 012.
11
AZT, which was developed as a chemotherapeutic agent in 1964 but
shelved because of its extreme toxicity, is a DNA chain terminator,
which means that it brings DNA synthesis to a halt. It is therefore
an extremely efficient cell killer. HIV is a retrotirus, and as such
replicates itself by inserting its genes into a cell's genome so
that when the cell divides a new copy of the virus is produced. AZT
prevents the replication of HIV by killing infected T-cells;
unfortunately, it kills all dividing cells indiscriminately, whether
they are infected with a retrovirus or not, and will very quickly
decimate even a healthy person's immune system. AZT's manufacturer,
GlaxoSmith Kline, chose not to comment for this article.
12
HIV was declared the probable cause of AIDS in a U.S. government
press conference in 1984. It was claimed that the virus had been
discovered by NIH researcher Robert Gallo. In fact, Gallo had not
discovered HTLV-III (Human T-cell Lymphotropic Virus III, as it was
known before it was rechristened with the more memorable name HIV) .
That honor belongs primarily to Luc Montagnier, of the Pasteur
Institute, who had sent Gallo a sample of the virus.
13
It has been claimed that HIV somehow causes cell death even when it
is not present by remote programmed "suicidal" mechanisms. Some
researchers claim that HIV exploits special receptors on human
T-cells that, due to a hypothetical genetic mutation, many
"Caucasian Europeans" lack, but most Africans have. What's
interesting is that many gay men also seem to possess these
mysterious receptors, as do intravenous drug users and transfusion
recipients.
It is claimed that although HIV does not kill the laboratory T-cells
used to manufacture AIDS tests, it does kill T-cells in the human
body, even though it infects only a very small proportion of them,
typically an average of 0.1 percent. HIV does not sicken or kill
chimpanzees, though they do produce antibodies. It was recently
claimed that HIV appears to be evolving into a form less dangerous
to human beings. Such unproven hypotheses about the ingenuity of HIV
proliferate in the popular and scientific media like the seasonal
flu. Seldom do journalists insist on good hard evidence for these
assertions.
14
There is ample statistical and epidemiological evidence linking the
rise of mass drug abuse in the late Sixties and Seventies with the
sudden appearance of AIDS. The overwhelming majority of AIDS
patients with Karposi's sarcoma, for example, have been heavy users
of nitrate inhalers, or "poppers." The case of "super AIDS" that was
recently reported in New York turned out upon closer examination to
he an individual with an extraordinarily heavy methamphetamine
habit.
15
Few today remember the controversies over scurvy and pellagra,
which, until the discovery of vitamin C and niacin, were blamed by
the medical establishment on mysterious infectious agents. Those who
pointed out, even before they knew the cause, that dietary changes
cured both conditions were dismissed as flat-earthers.
16
Nor is Duesberg alone in dissenting from AIDS orthodoxy. More than
2,300 people, mostly scientists and doctors, including Nobelists in
chemistry and medicine, have signed the petition of the Group for
the Scientific Reappraisal of the HIV-AIDS Hypothesis, which calls
for a more independent and skeptical approach to the question of
AIDS causality.
17
Even so, the National Cancer Institute still refuses to fund him.
Duesberg has submitted five grant proposals to study aneuploidy, and
all have been rejected. One of the most influential cancer
researchers in the country, Bert Vogelstein, Clayton Professor of
Oncology and Pathology at Johns Hopkins University, has written a
letter urging the NCI to reconsider. "1 agree with him that
aneuploidy is an essential part of cancer," Vogelstein wrote. "Dr.
Duesberg continues to have a major impact on this burgeoning area of
research, through his careful experimental observations as well as
through his thoughtful reviews and critiques of the subject. There
is no question that he is a world leader in this field of
investigation."
|
