IS HIV GUILTY?
By Elinor Burkett
Miami Herald 23 Dec. 1990
Margaret Heckler stood behind the podium in the auditorium of the Hubert
H. Humphrey Building in Washington, D.C. Lights flooded her face, cameras
rolled, reporters clutched their notebooks expectantly.
"Today we add another miracle to the long honor roll of American medicine
and science," announced the secretary of Health and Human Services.
"Today's discovery represents the triumph of science over a dreaded
disease. Those who have disparaged this scientific search-those who have
said we weren't doing enough-have not understood how sound, solid,
significant medical research proceeds."
It was April 23, 1984. Almost 2,000 Americans were dead of AIDS. More than
100 new cases were being reported every week. For the first time since the
plague began, the government was offering shreds of hope to the dying: The
virus causing the disease had been isolated. An end to the nightmare was
finally in sight: Within six months a blood test would be available,
Heckler said; within two years a vaccine would be ready for testing.
As Heckler made her dramatic appearance on national television, Dr. Peter
Duesberg sat in his cluttered office in Berkeley, Calif., bewildered.
Duesberg is one of the world's foremost authorities on viruses. He was the
first person to map all the different gene strands that make up a
retrovirus, the very type of clever, hard-to-fight bug Heckler said was
causing AIDS. To Duesberg, Heckler's announcement just didn't make sense.
If her HIV virus was indeed the cause of AIDS, it violated the laws of
virology. He decided to withhold his applause and wait for the proof.
Six years and 90,000 deaths later, he's still waiting. And there is still
no vaccine.
In the six years since Margaret Heckler's surprise announcement, the
federal war against AIDS has become a desperate $3 billion-a-year battle
against HIV, Human Immuno-deficiency Virus. In the most intensive disease
hunt in the history of mankind, scientists have cross-sectioned and
spliced HIV. They have cultured, activated and mapped it. They have
figured out how it reproduces. They can draw you a picture of it. But they
are missing one important piece of the puzzle:
"We do not yet know how HIV causes AIDS," Dr. John Coffin of Tufts
University, a member of the international committee that named the virus,
told the delegates to the Sixth International Conference on AIDS last
June.
It is that missing link that nags at a growing number of the world's
best-known scientists. They have begun to suggest a frightening
explanation: HIV alone may not cause the disease. Or it may have nothing
to do with it.
The Doubters
By 1987, three years after the HIV discovery was announced,
retrovirologist Duesberg's doubts had hardened into a certainty that
something was wrong. For one thing, the numbers weren't adding up. Each
year since Heckler's announcement, the federal Centers for Disease Control
has projected the number of people expected to turn up with the HIV
infection. Initially, scientists were confident their projections would
prove accurate: They knew from years of experience how quickly a toxic new
virus spreads in a human population. But, the predictions were wrong. At
the end of each year, the CDC was forced to revise its estimates downward
dramatically. In 1986, for example, the CDC estimated that 1 million to
1.5 million Americans were infected with HIV. A year later, they cut that
estimate in half. HIV is not spreading at anywhere near the rate expected
of a newly introduced sexually transmitted virus. Why? No one knows.
There were other nagging problems with the HIV hypothesis:
* Two healthy people can have sex with the same HIV-infected person,
and one of them will come down with the infection after a single
encounter, while the other will still not have it after 500 encounters.
Why? No one knows.
* The vast majority of those known to be HIV-infected remain healthy
for years-and there is no proof that they will not live a normal life
span. Why? No one knows.
* Diseases presumed to signal AIDS are cropping up in individuals
without any trace of HIV. Why? No one knows.
* How could a virus found to be active in only minute quantities in
the bodies of even the sickest AIDS patients devastate the immune system
as HIV purportedly does? No one knows.
While most researchers say such apparent contradictions are to be expected
in the early stages of research into a new disease, others aren't so
certain.
"There are too many shortcomings in the theory that HIV causes all signs
of AIDS," says Luc Montagnier.
In June, when Montagnier, a French AIDS researcher announced his rejection
of the established theory, he should have provoked a sensation. After all,
Montagnier discovered HIV in the first place.
Montagnier now believes that HIV is "a peaceful virus" that becomes a
killer only when combined with another bug-a bug he has already isolated
and identified. This finding received none of the attention of his
original discovery. The same reaction-which is to say no reaction-had
greeted
Robert Gallo, Montagnier's American co-discoverer of HIV, when he also
suggested in print two years ago that HIV might need a co-factor to cause
AIDS. Now Gallo does not even discuss the matter.
Montagnier, however, persists-and has discovered what earlier dissenters
have found out over the years: It's no fun to challenge the common
wisdom.
Peter Duesberg, the retrovirologist, has been likened to obsessives who
believe AIDS has extraterrestrial origins. He is, CDC researcher Harold
Jaffe and his British colleague Robin Weiss wrote recently in a British
science magazine, "a flat-Earther bogged down in molecular minutiae and
miasmal theories of disease."
Two other dissenters, Robert Root-Bernstein, winner of a MacArthur "genius
grant," and Shyh-Ching Lo, director of AIDS pathology at the Armed Forces
Institute of Pathology, have been accused of quackery and endangering the
public health of the nation by key AIDS policy makers for their insistence
that HIV is not the sole cause of AIDS.
Even when they present evidence that their dissent might be justified,
nothing happens. Montagnier was not the first one who found a second
organism that may be essential to produce AIDS. A year ago this month, the
National Institute of Allergy and Infectious Disease-the agency in charge
of the war on AIDS-convened a panel of scientists to examine Shyh-Ching
Lo's discovery of an extremely toxic micro-organism in AIDS patients. When
the organism-the same mycoplasma that Montagnier would report four months
later - was injected into experimental animals, the animals quickly
sickened and died. That does not happen with HIV. Panel members quizzed Lo
for three days, and
concluded that he was onto something important.
A year later, of the $1.8 billion in federal funds NIAID spends on AIDS
research, not one dollar has been budgeted to pursue that finding.
Whodunit
The official version of AIDS: In the beginning, there is HIV (a type of
virus called a retrovirus) that hits the bloodstream with a burst of fury,
looking for one of its favorite cells-a T cell, an essential part of the
body's immune system. HIV attacks the T cells, but, initially, does not
destroy them. Most newly infected people feel nothing. Some might suffer
swollen glands or a mild fever, like a case of flu or a touch of
mononucleosis.
The symptoms quickly disappear. Most scientists believe the virus lies
almost dormant in a small number of cells, often for years, until it
somehow becomes activated. Then the infected cells suddenly mass produce
new viral particles that float through the bloodstream, attaching
themselves to previously uninfected cells.
This in itself doesn't necessarily mean disaster. Healthy bodies harbor
dozens of viruses and other bugs that never cause any noticeable harm. But
in the case of HIV, most scientists believe the virus suddenly stops
cohabiting with T cells-as it has done for years-and kills them instead.
When T cells are killed off, the body is left wide open to disease.
Bacteria, other viruses and bugs that wouldn't hurt a soul under normal
circumstances suddenly run riot. When that begins to happen, an
HIV-infected person has AIDS.
In the absence of any drug that can kill HIV without killing the body that
harbors it, scientists leading the fight against AIDS see the result as
inevitable: Once you are infected, your body cannot kill the virus. The
virus eventually destroys your immune system. You die.
If this were a murder case, the official case against HIV would be
entirely circumstantial. Nobody can see HIV destroying the immune system,
or even say how it does it.
But it isn't just the lack of proof that bothers critics of the HIV
orthodoxy. They understand that in science, there isn't always a smoking
gun. Sometimes, inferences are all you get. But in this case, they argue,
even the circumstantial evidence has gaping holes in it.
Robert Koch was a German scientist who had a peculiar obsession with
proof. Koch was born in 1843, three years after Friedrich Gustav Jacob
Henle made the stunning assertion that living organisms too small to see
with the naked eye could cause disease. Koch became one of the first
disciples of the new science of bacteriology, and he considerably advanced
it: He discovered both the organism that causes tuberculosis and the
organism that causes cholera, eventually winning the Nobel Prize for
Physiology and Medicine.
It is difficult to grasp, from the late 20th Century, what an astounding
feat that was. When scientists first began studying the world through a
microscope, they found it to be teeming with micro-organisms. There was no
way to watch them operate in living organisms. So how could the scientists
tell which were harmless, and which were killers?
Koch, who had served as a field surgeon in the Franco-Prussian War, became
an ace detective. He developed all kinds of new investigative techniques,
including what was to become the basic rules for what constitutes
definitive proof that a specific germ causes a specific disease:
# 1. You have to find the germ in every case of the disease.
# 2. You must be able to isolate it from the body and from other germs.
# 3. It must cause sickness when injected into a healthy host.
# 4. After it does, the same germ must be retrieved from the newly
diseased person.
Koch was flexible. He understood some cases wouldn't fit neatly into his
set of rules. In those cases, however, he insisted that a simple
association should not be confused with causation. In other words, just
because everyone in your neighborhood with measles also has blond hair
does not mean that blond hair causes measles.
Koch-whose principles are still taught to every student of
epidemiology-isn't very popular among AIDS researchers these days: HIV
fails his test on three of four counts.
HIV can be isolated, both from the body and from other germs, but only
with difficulty, because even the sickest AIDS patients simply don't have
much virus to be found. With run-of-the-mill viruses, scientists can find,
at the very least, a million units of virus particles in a milliliter of
bodily fluid of a sick person. With HIV, finding even one-tenth that many
is extremely rare.
HIV fails the other tests outright. The virus cannot be found in every
case of AIDS. In 3 percent of diagnosed AIDS cases, no HIV antibodies have
been found.
No one has tried injecting HIV into a healthy human being, but scientists
have stuck all kinds of mice and rats and monkeys and chimpanzees, and
none of them got anything resembling human AIDS.
All this doesn't necessarily disprove the HIV hypothesis, as dozens of
scientists have pointed out in attacking Peter Duesberg, the HIV-doubter,
who insists on reminding everyone of Koch's postulates as frequently as
possible. HIV's failure of Koch's tests can be easily explained:
* The virus or its antibodies are not being found in all cases of AIDS
because tests for it are not yet sensitive enough, the CDC argues.
* Some germs are specific to a single species, says Dr. Peter Drotman,
a CDC medical epidemiologist. HIV may not give other animals AIDS simply
because it cannot live in the bodies of most other animals.
But the most powerful argument against the doubters is also the foundation
of HIV orthodoxy: In almost every case of the condition called AIDS-a
cluster of diseases frequently accompanied by weight loss, blindness,
incontinence and dementia-they find antibodies to HIV. That is just too
much of a coincidence to pass up.
A Matter of Time
To Robert Root-Bernstein, the number of people with AIDS who are
HIV-positive is not as interesting as the number of people who are
HIV-positive who don't have AIDS.
Root-Bernstein, the MacArthur Grant winner, was working on immune
disorders in Jonas Salk's laboratory when the discovery of HIV was
announced. Given the incredible variety of evils that were included in the
definition of AIDS-from diarrhea to dementia-Root-Bernstein was skeptical
that a single virus could be blamed for them all. Now he has another cause
for skepticism: Fewer than 5 percent of HIV-infected Americans have AIDS.
Most AIDS researchers say the rest will eventually get sick. It just takes
time. "How much time?" Root-Bernstein and others ask. The answer keeps
changing.
When HIV was first discovered, scientists at the Centers for Disease
Control suggested that most of those infected would begin to fall ill
within 12 to 18 months of infection. They didn't. So the CDC did what it
would do again and again: It raised the projected incubation time: first
to five years, then seven, then 10, and now, 15.
In the late '70s, blood samples were drawn from 6,875 sexually active gay
men in San Francisco. Scientists had never heard of AIDS or HIV when they
froze the blood for research on hepatitis B. But in 1985, when the HIV
antibody test was licensed, all that six-year-old blood from the highest
AIDS risk group in the nation suddenly became critically important. Sure
enough, 67.3 percent of the samples turned out to be HIV-positive. It's
now been 11 years since the first blood samples were taken. Only half of
the infected men have been diagnosed with AIDS.
That figure, Root-Bernstein argues, suggests that HIV alone is a poor
explanation for AIDS. But it gets even more complicated: Almost all the
frozen blood samples were from men who also had hepatitis B, syphilis,
gonorrhea and herpes. Their immune systems were already in chaos from the
massive assault-which makes them terrible predictors of how HIV would
operate in healthier blood.
Even the CDC's Peter Drotman admits it is "a nonrepresentative sample."
Nonetheless, it is the basis for the current 15-year CDC estimate of the
median HIV incubation period.
"Look," says Root-Bernstein, "if they keep going at this rate, we're going
to have people who live to 90 who were infected with the virus at 15 and
they will still be arguing that HIV causes AIDS."
But there is another glitch in AIDS epidemiology that Root-Bernstein finds
even more disturbing: An increasing number of people coming down with
infections typical of AIDS patients are turning out not to have HIV.
Four leading scientists at the Centers for Disease Control recently
suggested in Lancet, a British medical journal, that Kaposi's Sarcoma - a
form of cancer that before AIDS had only been found in elderly men - is
turning up in young gay men who indisputably do not have HIV. They
concluded that KS-one of the diseases that have always been part of the
definition of AIDS - "may be caused by an as yet unidentified infectious
agent, transmitted mainly by sexual contact."
The HIV-negative KS group differs from the 3 percent of "AIDS patients"
who do not test positive for HIV antibodies in that they have been given
the sophisticated, extremely expensive tests for the virus itself, and
come up negative.
This is a stunning development, because the very existence of AIDS was
originally hypothesized to explain why young men had diseases like KS. If
HIV was not responsible for the outbreak of Kaposi's Sarcoma, then
something else is. What? No one knows.
"Maybe these are anomalies," Root-Bernstein says, "but everyone in science
knows that the anomalies are keys. They are nature's way of telling you
that something is wrong with your dogma. Look at Copernicus, Galileo,
Einstein. That is what they keyed in on.
"If we insist that HIV is the sole cause of AIDS, then if we have people
who aren't infected developing the same symptoms as AIDS patients, we are
forced to conclude that we have a second epidemic, or a third or a
fourth."
A Murderous Microbe?
Every American adult should have a small scar on his upper arm or thigh: a
smallpox vaccination. Smallpox once was a deadly scourge-killing millions.
Vaccinations have virtually wiped it out. It's an ingenious concept: You
introduce a minuscule amount of weakened or dead disease-causing bugs into
the human system. The body responds by producing antibodies-a natural
antidote that neutralizes the invading bug. Once you have the antibodies,
you're immune. So why is it such devastating news when a person tests
positive for HIV antibodies?
Shyh-Ching Lo, the researcher in charge of AIDS programs for the Armed
Forces Institute of Pathology, doesn't believe it should be: The presence
of the antibodies to HIV-far from being a sign of doom-is proof the body
is capable of coping with the virus, Lo contends. Nobody is able to
explain how the dormant HIV particles manage to suddenly whip the
antibodies.
"There is no good explanation for why and how the virus breaks out of the
antibody protection," says Lo. "I'm not saying that HIV plays no role in
AIDS-the data shows a clear correlation with disease. But AIDS is much
more complicated than HIV."
Lo, an obscure microbiologist, with no grants or establishment support,
went looking for a new explanation. In 1986 he announced that he had found
it: a previously unknown organism that-together with HIV-caused AIDS.
For nearly three years, his theory was ignored. Shyh-Ching Lo's research
was turned down for publication almost a dozen times before the Journal of
Tropical Medicine, available in few hospital libraries and on no major
electronic databases, agreed to print his findings. His attempts to find
funding have failed. Even the presentations he has given at professional
meetings have gotten him nowhere; his colleagues don't even show up.
The problem was that Lo was using a complex new research technique he had
devised himself to come up with a revolutionary finding. Given the stakes,
no one was willing to give him the benefit of the doubt.
Until last December, when an official at the National Institute of Allergy
and Infectious Diseases decided Lo's work merited at least a closer look.
The agency brought a dozen specialists together to look at his data.
Experts in AIDS and other infectious diseases flew into San Antonio,
Texas, expecting, they admitted, to demolish Lo.
Lo laid all his cards on the table. He had detected an organism similar to
a bacteria, called a mycoplasma, in cells taken from AIDS patients. He
could not find the organism in cells of healthy individuals. When he
injected the organism into four silvered leaf monkeys, three quickly
developed low-grade fevers. All four lost weight. All four died within
seven to nine months of infection. When they were autopsied, there was
Lo's mycoplasma in their brains, livers and spleens.
Lo also reported finding the mycoplasma in the damaged tissue of six
HIV-negative human beings who had died from unspecified causes after
suffering from suspiciously AIDS-like symptoms.
Lo did not argue that his mycoplasma-dubbed mycoplasma incognitus-caused
AIDS. "This might be a key co-factor that promotes disease in HIV-infected
individuals," he says. "It might be an opportunistic infection that takes
advantage of immune compromise. Or it might be the primary cause of the
disease, with HIV perhaps helping it along. All I know is that it is there
and that it changes the properties of HIV. But it is too early to know how
or what that means."
The scientists quizzed Lo for two days. They knew that tiny, bacteria-like
mycoplasmas can cause immune suppression and debilitating, chronic
diseases in animals. But in human beings, mycoplasmas are only known to
cause nonlethal diseases: light pneumonias and some genital infections.
"When I showed the mycoplasmas from my pathology studies, they didn't
believe they existed," Lo recalls. "When I showed them that the organism
existed and proved it was a mycoplasma, they said my cultures were
contaminated."
Two days later, Lo had turned skepticism into interest. "The documentation
was absolutely solid," said Joseph Tully, head of mycoplasma programs for
NIAID. Participants formally recommended further study of the link between
the mycoplasma and AIDS, and experiments with drugs that could kill the
new microbe.
One year later, NIAID has funded no such research. "We have not been
pulled into the AIDS programs in any real way," Tully says.
When asked for an interview concerning Lo's work, NIAID director Anthony
Fauci said through spokesperson Mary Jane Walker that he "will not talk
about mycoplasma or any other AIDS co-factor."
Sacrilege
Fifteen minutes just wouldn't be enough. Luc Montagnier knew it. The
announcement was too controversial, too important. If the organizers of
the Sixth International Conference on AIDS wouldn't give him more time, he
would find another way.
It was June 1990 and the conference was due to open in San Francisco in a
week. Montagnier, the French discoverer of HIV, planned to announce he had
been wrong for almost seven years. He was about to explode a bomb in the
midst of a multibillion-dollar international research and development
establishment built on the bedrock truth he had helped create.
HIV, he announced, is a benign virus that only becomes dangerous in the
presence of a second organism. His candidate: a tiny, bacteria-like bug
called a mycoplasma. In culture, HIV is harmless and passive, he told the
conferees. But when you add mycoplasma, it becomes a vicious killer.
Three months earlier, Montagnier had suggested in a French journal,
Research In Virology, that HIV and his mysterious micro-organism react
together to cause the body's cells to burst. Now he was saying that in his
test tubes, tetracycline-type antibiotics stopped the bursting. The sort
of common antibiotics that people get every day to help them battle common
diseases like pneumonia or acne. If true, Montagnier's claim might have
startling implications for the treatment of AIDS. In best of possible
worlds, it might even mean that AIDS could be treated with common
antibiotics. Still, it is such a complex disease that, in any case, the
practical uses of such a discovery would be years away.
As Montagnier spoke, Shyh-Ching Lo basked in vindication. Montagnier, the
great man of AIDS, had just hit upon exactly the same microbe as Lo. The
two had not shared their data. Separately, they had made the same
discovery.
But Lo was almost the only person in the room who was excited. Of the
12,000 people who attended the conference, only 200 came to hear
Montagnier talk, and by the time he had finished, almost half of those had
walked out.
Montagnier was used to skeptical responses and outright dismissals by
scientists, especially on this side of the Atlantic. Few American
scientists took his discovery of HIV seriously until a year later, when an
American named Robert Gallo discovered what turned out to be the same
virus. But this time Montagnier came with his HIV credentials behind him.
He had hoped for a better reception.
In a confrontation after his presentation, Jay Levy, a University of
California virologist and one of the most respected AIDS experts in the
world, insisted that while Montagnier was claiming he had made a major new
discovery, in fact he had simply allowed his experiments to be
contaminated-a mistake a graduate student might make. Here, the exchange
grew heated. Levy: "I've looked in 20 patients, and I can't find your
mycoplasma."
Montagnier: "They're just very hard to find."
At this point, Levy cut off the discussion. "We know how to look," he
said. Then he turned his back and walked away. Most of the people who
control the course of AIDS research agree with Levy. The official reaction
from CDC spokesperson Peter Drotman is typical: "It's just a hypothesis.
We don't believe it. HIV is not a benign infection."
But the small number of dissenters who had hoped Montagnier's support
would be a turning point in their struggle to be heard were horrified.
Peter Duesberg: "There was Montagnier, the Jesus of HIV, and they threw
him out of the temple."
"Who were these people who are so much wiser, so much smarter than Luc
Montagnier?" asks Harry Rubin, the dean of American retrovirology. "Heb
became an outlaw as soon as he started saying that HIV might not be the
only cause of AIDS.
"The minute someone suggests that the orthodoxy might be wrong, the
establishment starts to call him crazy or a quack. One week you're a great
scientist; the next week, you're a jerk. Science has become the new church
of America and is closing off all room for creative, productive dissent."
Rubin has been mocked as a has-been, an old fool.
But no one has felt the heat more keenly than Peter Duesberg, the most
aggressive of HIV's disbelievers-the only one who insists that HIV has
nothing to do with AIDS.
Three years ago Duesberg began arguing in print that HIV was no more
harmful than any of the other myriad viruses and bacteria that live in our
bodies and are contained by our immune systems. He is not surprised at the
gaps in the evidence. After all, he says, how can a virus be so vicious
when it first enters the body, then turn around and play dead for 10, 20,
30 years? What kind of virus one day, out of nowhere, springs into action
to destroy a person's immune system with no provocation?
Levy, the UC AIDS researcher, and others insist that HIV is just that-a
time-bomb virus that lies dormant in the body until-for some unknown
reason-it modifies its own genetic structure and transforms into a
fast-growing, virulent, deadly virus.
Poppycock, insists Duesberg. "No virus has ever behaved that way."
Duesberg is accustomed to being listened to, praised and funded for his
work. After all, he is the man who discovered the viral gene that can
cause cancer, and was rewarded with membership in the prestigious National
Academy of Sciences. He was the first man to draw a genetic map of a
retrovirus. Now Duesberg is, in his own words, "the enemy within."
When National Public Radio attempted to stage a debate between Duesberg
and a supporter of the HIV hypothesis, it could find no one willing to
confront him. "Critiquing a dubious theory would take time away from more
productive efforts," Anthony Fauci, head of NIAID, told NPR producers.
For 22 years, Duesberg had no trouble finding federal funding for his
research. For the past five years, he has been the recipient of an
Outstanding Investigator Grant from the National Institutes of Health, one
of the most prestigious, and liberating, sources of research funding in
American science. But on Oct. 26, the Berkeley professor of molecular and
cell biology was turned down for continuation of the grant.
The committee reviewing his application wrote: "Despite the applicant's
eminent track record, the relatively low past productivity, the logically
and functionally flawed rationale, and the poor prospect of the proposed
study for advancing knowledge in important areas, greatly weakens the
overall merit of this application."
Duesberg argues that the review committee was "penalizing me for
developing concepts contrary to those of the committee members." Committee
members say that it is illegal for them to discuss the grant termination
further.
The Worst Possible News
What is AIDS? According to the federal government, it is a 10-page
single-spaced collection of diseases, conditions under which the diseases
must occur, test parameters and pure deduction. The only thing that holds
this mind-numbing definition together is: HIV. If you have certain kinds
of pneumonia and HIV, you have AIDS. If you have those kinds of pneumonia
and you don't test positive for HIV, you're just a poor slob who has been
around too many people spewing pneumonia germs.
If HIV is not the sole cause of AIDS, then the effort to fight the disease
is in chaos. In fact, we wouldn't even know what disease-or how many
different diseases-we are fighting. HIV is the glue that holds together an
amorphous syndrome of usually common and nonlethal ailments that are
hitting uncommon groups of people or becoming strangely lethal.
If HIV is not the sole cause of AIDS, then five years of desperate
searching for a way to kill a virus in already infected people-a feat that
has never been accomplished with any virus-might have been spent more
productively on another course of research.
For scientists, the idea at this late date that HIV is not a lone assassin
is the worst possible news. In the bars outside medical conferences and in
off-the-record conversations, dozens of AIDS researchers admit they are
disturbed by the persistent failure of the most monumental medical
research effort in the nation's history to yield clear proof that HIV is a
lone assassin.
Yet in public, and on-the-record, few will express those doubts. "I'd bet
my professional reputation that something more than HIV is involved in
this disease," said one federally funded AIDS researcher. "But I wouldn't
bet my grants, my ability to work."
If there is fear about questioning the established line of thought, it is
not because there is any conspiracy against skeptics: It is the intuitive
understanding that the last thing anybody wants to hear is what the
skeptics are saying. It is just too scary.
"What epidemiologist or federal official wants to admit that the entire
thrust of research and education might be misguided?" asks Robin Haueter,
an AIDS activist in New York City. "What person with AIDS wants to
consider the horrendous thought that we have wasted five years of
research, that the end might not be anywhere in sight?" *
On Tue, 11 May 2004 17:40:48 -0400, "PaulKing"
<aimulti@aimultimedia.com> wrote:
Another distortion and lie, even in the context of Elinor Burkett's
ravings.
http://www.aegis.com/news/mh/1990/MH901207.html
Written in 1990 when Luc felt HIV required something like Mycoplasma
infection to result in AIDS (a co-factor). He looked and looked and
realized his theory, though having some tantalizing observations to
support it from Dr. Lo, was unable to find it in all HIV+ people with
AIDS.
Mycoplasma may WELL serve as an enhancing co-infection. Indeed, it
seems to play a critical role in chronic fatigue. It is not, however,
a co-factor.
Some background on mycoplasma infections:
http://www2.provlab.ab.ca/bugs/biologos/9702mypl.htm
An intriguing article suggests that it is probably a good idea to be
tested for this infection. (see below)
George M. Carter
***
Coronato S. [Mycoplasmas and AIDS] [Article in Spanish] Rev Argent
Microbiol. 1997 Jul-Sep;29(3):157-66.
Catedra de Patologia II, Facultad de Medicina, Universidad Nacional de
La Plata, Argentina.
AIDS is a complex illness due to HIV type 1 and 2 infection. It is
characterized by an important immunodeficiency mainly caused by
depletion of CD4+ T lymphocytes. The reasons for this depletion have
not been sufficiently clarified yet. In 1986, Shy Ching Lo astonished
the scientific community with reported evidence concerning the direct
role played by mycoplasma in the etiopathology of AIDS. Since then,
different theories have pointed to mycoplasma as cofactors, commensals
or opportunistic agents. Although in vivo and in vitro experiments are
controversial they suggest a possible mechanism that would explain the
synergism between both agents: the mycoplasma belonging to normal
intestinal flora could move to urethra, oropharynx or blood due to
high risk sexual practice. There it would proliferate favoured by
early immunological disorders related to HIV. It has been speculated
that several microorganisms including mycoplasma, acting as
superantigens, could induce a chronic CD4+ and CD8+ T lymphocytes
activation resulting in apoptosis of the infected lymphocytes. The
release of cytokines induced by mycoplasma could influence the
progression of the disease.
***
Ainsworth JG, Hourshid S, Easterbrook PJ, Gilroy CB, Weber JN,
Taylor-obinson D. Mycoplasma species in rapid and slow HIV
progressors. Int J STD AIDS. 2000 Feb;11(2):76-9.
Division of Medicine, Imperial College School of Medicine, St Mary's
Hospital, London, UK.
We determined the relationship between the presence of Mycoplasma
fermentans and Mycoplasma penetrans and the rate of progression of
HIV-associated disease in a nested case-control study based on a
cohort of 159 HIV-infected patients with different rates of disease
progression. Study participants were divided into 3 progression
groups: non-progressors who had been HIV-1 seropositive for at least 9
years and had remained asymptomatic with a CD4 cell count of >
500/mm3; slow progressors who had been HIV-1 seropositive for at least
9 years and whose CD4 cell count had fallen below 500 cells, and who
had developed symptomatic disease or AIDS; and rapid progressors who
had developed AIDS within 5 years of HIV infection. Peripheral blood
mononuclear cells (PBMCs) were collected at enrollment and examined by
mycoplasma polymerase chain reaction (PCR) assays. Three (7%) of 46
non-progressors, 3 (3%) of 86 slow progressors, and 2 (7%) of 27 rapid
progressors were M. fermentans positive. The PBMCs from 91 subjects
were tested for M. penetrans DNA and none was positive. The small
proportion of M. fermentans-positive patients indicates that the
mycoplasma cannot be important in the development of AIDS in the large
majority of patients. Furthermore, no association was found between
its presence and more rapid HIV disease progression.
***
Ainsworth JG, Easterbrook PJ, Clarke J, Gilroy CB, Taylor-Robinson D.
An association of disseminated Mycoplasma fermentans in HIV-1 positive
patients with non-Hodgkin's lymphoma. Int J STD AIDS. 2001
Aug;12(8):499-504.
Genitourinary Medicine Section, Division of Medicine, Imperial College
School of Medicine, St Mary's Hospital, London, UK.
We examined the relationship between the haematogenous dissemination
of Mycoplasma fermentans and non-Hodgkin's lymphoma (NHL) in 265 HIV-1
positive patients. A polymerase chain reaction (PCR) assay was used to
detect M. fermentans in peripheral blood mononuclear cells (PBMCs)
from 50 patients enrolled consecutively from an HIV outpatient clinic
in 1991 (cohort 1), 56 patients with lower respiratory tract infection
who underwent bronchoscopy in 1992 (cohort 2), and 159 patients who
were enrolled into a natural history cohort study in 1994 (cohort 3).
The incidence of NHL among the patients was determined in 1998. The
PBMCs of 29 patients (10.9%) were positive for M. fermentans (8 in
cohort 1, 13 in cohort 2 and 8 in cohort 3) and 11 patients (4.2%)
developed NHL which was confirmed histologically (3 in cohort 1, 4 in
cohort 2 and 4 in cohort 3). We found a statistically significant
association between the presence of M. fermentans and the development
of NHL in the combined cohort (risk ratio [RR]=6.78 [95% confidence
interval (CI) 2.21--20.84], P=0.003 Fisher's exact test [FET]). This
association remained significant even after adjustment in a
multivariate analysis for CD4 cell count and HIV disease status at the
time of M. fermentans testing (RR=7.97 [95% CI=2.16--29.47], P=0.002).
***
An older in vitro study:
Sasaki T, Sasaki Y, Kita M, Suzuki K, Watanabe H, Honda M. Evidence
that Lo's mycoplasma (Mycoplasma fermentans incognitus) is not a
unique strain among Mycoplasma fermentans strains. J Clin Microbiol.
1992 Sep;30(9):2435-40.
Department of General Biologics Control, National Institute of Health,
Tokyo, Japan.
Mycoplasma fermentans incognitus has attracted much interest either as
a cofactor for the progression of AIDS or as a pathogenic agent in
non-AIDS-related diseases (S.-C. Lo, M. S. Dawson, P. B. Newton III,
M. A. Sonoda, J. W.-K. Shih, W. F. Engler, R. Y.-H. Wang, and D. J.
Wear, Am. J. Trop. Med. Hyg. 41:364-376, 1989; S.-C. Lo, M. S. Dawson,
M. Wong, P. B. Newton III, M. A. Sonoda, W. F. Engler, R.Y.-H Wang, J.
W.-K. Shih, H. J. Alter, and D. J. Wear, Am. J. Trop. Med. Hyg.
41:601-616, 1989; S.-C. Lo, J.W.-K. Shih, N.-Y. Yang, C.-Y. Ou, and R.
Y.-H. Wang, Am. J. Trop. Med. Hyg. 40:213-226, 1989). In the present
study, the genetic and serologic properties of the incognitus strain
and other M. fermentans strains were compared. Furthermore, the
replication of human immunodeficiency virus type 1 (HIV-1), determined
by reverse transcriptase activity and HIV-1 p24 antigen level, in
peripheral blood mononuclear cells was evaluated after stimulation
with mycoplasma cell lysates. The psb-2.2 viruslike infectious agent
DNA probe, used to identify the incognitus strain in the tissues of
AIDS and non-AIDS patients by Lo et al. (Am. J. Trop. Med. Hyg.
41:364-376 and 40:213-226, 1989), showed reaction patterns similar to
those of two M. fermentans strains isolated from cell cultures but not
to that of the type strain PG18. Restriction enzyme patterns of the
incognitus strain with EcoRI and HindIII were also similar to those of
M. fermentans strains isolated from cell cultures. There were no
remarkable differences in the immunoblot profiles between the
incognitus strain and the other M. fermentans strains. These results
suggest that the incognitus strain is not a unique strain among M.
fermentans strains. Further, cell lysates of each M. fermentans strain
could also enhance the replication of HIV-1 to a level similar to that
of the incognitus strain as determined by the reverse transcriptase
activity and the amount of the p24 antigen.
