THE AIDS HERESIES
A Case Study in Skepticism Taken Too Far
By Steven B. Harris, M.D.

"Felix qui potuit rerum cognoscere causas."--Virgil ("Fortunate is the man
who understands the causes of things.")

"It's the virus, stupid." --Dr. David D. Ho, AIDS Researcher

Contents:
ABSTRACT
INTRODUCTION: A DIALOGUE IN INDUCTIVE FRUSTRATION
Medical Induction
PART I: THE AIDS SKEPTICS AND THEIR CLAIMS
Defining AIDS
Redefining AIDS: Acquired Immune Failure Syndrome
Enter the AIDS Skeptics
HIV-Free AIDS?
Why Not AIDS Without HIV?
Did the Government Create AIDS?
The Origins of AIDS
AIDS in the 80s
Attacks on Straw Men
SIDEBAR: What Is a Retrovirus?
SIDEBAR: What Does "HIV-Positive" Mean?
References

ABSTRACT
Nobelist Kary Mullis once asked for a reference paper with the simple
statement "HIV causes AIDS." This article reviews the modern argument for
the HIV/AIDS hypothesis, covering main lines of evidence from human
epidemiology and experimental animal virus research. Special attention is
paid to the issue of how AIDS may be defined so that the possibility of AIDS
without HIV may still be theoretically discussed. Major emphasis throughout
this article is placed on the arguments of modern HIV/AIDS skeptics, Peter
Duesberg and Robert Root-Bernstein, who do not believe that HIV has a
central role in AIDS. It is concluded that HIV/AIDS skeptics have chosen
overly broad definitions of AIDS which are not clinically useful, and which
would, if employed, result in many confusing diagnoses of "AIDS" and
"HIV-free AIDS" in people with good prognoses. HIV is one of a
closely-related family of viruses which causes AIDS-like immunodeficiency
diseases in a number of animals species, and HIV/AIDS skeptics have ignored
or minimized this research in order to construct needlessly complicated
alternative hypotheses for the cause of AIDS. These alternative views are
based on correlations between AIDS and toxin exposure shown by
epidemiologists to be artificial a decade ago, but which skeptics still
refuse to abandon. Examination of the HIV/AIDS controversy thus allows us to
draw some general lessons about how skepticism in science works, and the
ways in which it can go pathologically awry.

© 1994 Steven B. Harris, M.D. Acknowledgements: My sincere thanks to Paul
Wakfer, Michael Federowicz, Larry Weber, Charles Platt, Sandra Russell, John
Richfield, and Dr. Roger Bohman of the UCLA School of Medicine, who each
provided many helpful comments on this manuscript during preparation.
Special thanks to the editor Michael Shermer and Art Director Pat Linse.

INTRODUCTION: A DIALOGUE IN INDUCTIVE FRUSTRATION

Let us suppose that you have a bright and iconoclastic friend who smokes
three packs of cigarettes a day. You remark one day that you would like to
see him quit the habit, since he is certainly increasing his chances of lung
cancer.

"Prove it," he says.

"Well," you begin, "the Surgeon General and a lot of scientists and doctors
say you should quit...."
"Come now!" says your friend, "Since when did you become a fan of The
Argument From Authority? I can find you scientists who do NOT believe I
necessarily should quit; as well as a lot of intelligent business
executives."

"Sure, but all those scientists and executives are paid by tobacco companies
or grants from the Tobacco Institute," you protest.

"Well, what do you expect?" says your friend, lighting up and taking a
satisfying drag. "Whenever scientists take an anti-establishment position,
funding is cut off. The poor scientists then don't have anyone else to
support their research but the Tobacco Institute. Do you expect them to drop
out of research just because they hold unpopular opinions?"

"Okay, let's look at the data," you say. "What about the fact that 90% of
lung cancer occurs in smokers?"
"Yes," says your friend, "and that means that 10% of it occurs in
non-smokers, doesn't it? Obviously the 'cigarettes = lung cancer' hypothesis
doesn't explain all lung cancer. Even for smokers there must be
'co-factors.' Heck, my grandfather smoked three packs a day right up to the
day he was hit by a drunk driver at the age of 92. A lot of people smoke for
a whole lifetime and never get cancer."

"Look, I didn't say the correlation was perfect!" you protest. "But it is
certainly there. Two-pack-a-day people have 13 times the lung cancer risk of
non-smokers."

"Oh, really?" your friend says, "Now, where do you get that number? I
suppose somebody did an experiment where they got together a group of
nonsmokers and randomized them to start smoking, or else stay smoke-free,
and then made sure each and every person did as told for the next 40 years,
so as not to bias the results. I must've missed that study."

"You know there is no such study. That experiment would have been
impossible, since you can't enforce a random protocol like that. People will
start or stop on their own. And besides, any experiment where you try to
keep people from quitting would be immoral, since smoking causes cancer."

"So you admit you don't have any study where the two groups of smokers and
nonsmokers are exactly equivalent, and only differing by chance or random
draw? In every study the smokers and the nonsmokers are self-selected for
their behavior and bound to be different not only in smoking behavior, but
also because of whatever made them smoke or not smoke to begin with, right?!
Not exactly great science, if you ask my layman's opinion."

"But when smokers quit, we know their risk of dying drops," you retort.

"You mean with regard to the smokers who don't quit? So what? The people who
quit smoking did so for a reason other than chance or the experimental flip
of a coin and again that means they will differ in some way other than their
not smoking. Besides, did you know that for the first year after quitting,
the risk of death for a new quitter actually goes up with regard to his
fellow smokers who keep right on smoking?"
"I knew you'd bring that up. The mortality goes up for the quitter group for
a while after they quit only because those people who quit are quite often
sick, and that's why they quit."

"If so that makes my point about self-selection, doesn't it? You're saying
that in that first year of quitting, the higher death rate of quitters is
caused by another factor in our study other than smoking--namely, sickness.
Well, so long as we're talking about such third factors, I have a hunch that
stress causes cancer, and stressed-out people take up smoking to try to
relieve the stress, and that's why there is more cancer in smokers, not
because of smoking. Moreover, maybe the act of quitting stresses people out,
and that's really why quitters die faster in that first year after quitting.
Smoking is just a marker for stress--what you scientists call a "proxy
variable."

"All this is ridiculous! You're just using your intellect to make you
believe something you want to believe for other reasons. There is
experimental evidence! Smoking causes lung cancer in lab animals! Are THEY
stressed?"

"Actually, yes--have you seen what they do to them in a modern lab? Ever
seen one of those rabbits with a leather muzzle over its nose, and a
cigarette stuck in it which it can't take out? But anyway, I don't even
believe you can find me a report of an experiment in which smoking causes
lung cancer in animals."
Back you go to the scientific literature. And you find nothing. There is no
such paper . . . .

Medical Induction

As this fact-based, fictional dialogue demonstrates, because there are many
intellectual steps which are not perfectly secure in any generalization,
even the most detailed inductive argument only goes so far toward proof. Not
only may the same evidence mean different things to different people, it is
more difficult to get people to follow a complicated inductive-reasoning
trail when they dislike, or are threatened by, the conclusion at the end.

In the medical sciences, assembling an irrefutable argument for causation is
sometimes an impossible task for the same reason it is in astronomy or
paleontology: the direct and definitive experiment cannot be done.
Scientists cannot travel back in time to watch dinosaurs, nor can they
influence the behavior of planets or stars. In medicine, a common difficulty
is that the necessary human interventive experiments to perfectly assess
"risk factors" for harm may be unethical, and so these risks cannot be
studied directly by experiment either.1 How, then, do we come to "know" what
things cause lung cancer or AIDS? For that matter, how do we come to know
with any confidence that tyrannosaurs ate meat, or what generates the sun's
energy? In other words: how do we ever infer causation from looking at
events (or records of events) which we cannot influence?

However we do it, it does seem that it can (to some extent) be done. Modern
science depends on the fact that "correct" causal relationships can often be
guessed entirely from logical and indirect observational tests of competing
theories, even where direct experimentation is not possible. This is done
using help from knowledge of simpler causal mechanisms which we have gained
from similar systems in which experimentation is possible. As Einstein
observed, one of the most amazing things about the universe is that this
kind of inference is possible at all.

Of course, the overall results of this kind of theorizing, like those of any
inductive process, are never certain. Still, whenever inferential theories
in science finally do become directly testable by some new experimental
technique, they often prove to be surprisingly sound. Why this should be
true remains the deep mystery that it was for Einstein.

It is because of an inferential process, based on many lines of evidence,
that we can be reasonably confident of the tobacco causation of much of lung
cancer, even in the absence of a definitive experimental study. In the same
way, an examination of a large body of related facts allows us reasonable
confidence about the causation of other diseases-- even a disease far more
complicated than lung cancer, and with even more money and passion involved
on both sides of the issue.

PART I
THE AIDS SKEPTICS AND THEIR CLAIMS

Should We Be Skeptical?

Recently, several popular lay publications (Reason, Spin, New York Native)
have run articles calling into question the theory that the viral agent with
the conclusion-asserting name, the "human immunodeficiency virus (HIV)," is
the cause of the epidemic of human acquired immune deficiency syndrome,
known as AIDS.

What do we mean by talking of the "cause" of AIDS? We know that the common
cold or the flu--indeed all infectious diseases--are in some sense "caused"
not only by the organism. Also important in the causal chain are host
factors (such as immune response), and even simple host-overwhelming
factors, such as the infectious dose of organism which enters the body
(called the "inoculum"). These additional causal factors, which have nothing
to do with the microbe itself, can be extremely important. They may in some
cases outweigh everything else. Nevertheless, because the smallpox virus
(for example) is necessary for smallpox, medical science still regards it as
"causal" in the sense that if there is no microbe, there is no illness.
Eliminate the smallpox virus from the population and one eliminates the
disease (as was in fact done in the 1970s).

Even this kind of "causal" connection between a disease syndrome and
infectious agent is what is under attack in recent articles about HIV and
AIDS. Some skeptics have claimed not only that HIV is not the only external
factor necessary for AIDS, but that if HIV were eliminated from the Earth,
at least some AIDS would still be with us. Still others have gone further
and claimed that HIV infection is totally harmless and does not even
contribute to the development of AIDS. These people believe that if HIV were
to disappear, AIDS would continue exactly as before.

In what follows, we will examine the best evidence behind what most
researchers believe is the role of HIV and other factors in AIDS. We will
also examine leading skeptical views on the causation of AIDS. Because a
great deal of published research is available on this issue, our examination
of AIDS will also let us illustrate how science closes in on cause and
effect, even when direct experimental "proof" is not available.

We will thus be interested in not only AIDS, but also larger questions about
science, and scientific debate. What makes a good scientific theory, and
what makes a poor one? Are there reasons for hope in looking at the disease
of AIDS in particular, and the workings of the biomedical scientific
"establishment" in general? Are we making any progress with AIDS, or just
wasting billions each year chasing fantasies?
This essay will argue that we are not wasting all that money, and that when
it comes to critics of the HIV/AIDS hypothesis, we have a practical case in
which skepticism has been taken too far. Science, we are happy to report,
still works, and it is making progress with AIDS. That some critics have
failed to recognize this only highlights the fact that science is only
partly an empirical enterprise, and that it also has an intuitive and
aesthetic side which is subject to arguments over taste. This is not a thing
which is taught to students in schools, but it is a concept key to
understanding most scientific controversies.

Defining AIDS

Scientific problem-solving begins with definitions, and in choosing a
definition for AIDS we run immediately into the HIV/AIDS controversy. Some
of the difficulty is that definitions, even in science, are chosen partly on
aesthetic grounds, partly on utilitarian ones.

In medical science we rarely know in detail at the molecular or even
cellular level what causes most human illness, and so in our ignorance we
are often forced to work with "disease syndromes," which are collections of
symptoms and sometimes lab tests which seem to "go together." In order to
usefully define a "disease syndrome" we need to pick our defining
characteristics so as to include all of the sick people who we are
interested in for good clinical reasons, and exclude everyone else.

What are good clinical reasons? In medicine there is not much point in
defining a new "disease" which, when present, makes no difference in either
prognosis or treatment. Nor is there any point in defining a disease so
poorly that it fails to capture all the sick people who seem to have pretty
much the same thing wrong with them from the prognosis or treatment
viewpoint. If (as always happens) we lack information about what impact
certain definitional characteristics have upon treatment or prognosis, then
we are forced to guess, as best we can, what definition will be most useful.
It is at this point, in deciding whether two people have "pretty much" the
same thing wrong with them, that aesthetic and intuitive considerations
unavoidably enter into medical science.

Utility imposes other constraints, too. A disease definition which is to be
used during a hunt for the disease's causation, should not assume any cause
which is in question. In other words, if we choose a definition for AIDS
which requires infection with the HIV virus (the current way it is done in
many countries, including the U.S.), then we will have chosen our terms so
as to be of little help in the question of whether HIV causes AIDS.
Obviously, it would be nothing remarkable if we "discovered" that 100% of
people with AIDS were infected with HIV, if we defined AIDS in such a way as
to require HIV infection.
In re-opening the question of the cause of AIDS, what we need is a modified
AIDS definition which does not involve HIV, so that the question of whether
or not all AIDS cases are infected with HIV is an empiric one, not simply a
semantic one. When we have a suitable HIV-free candidate definition for
AIDS, we can then ask two critical questions about it: 1) Have we captured
with our definition all of the people with the new medical problem that we
historically came up with the AIDS label, in order to describe and encompass
in the first place? 2) If we test our defined group, are 100% of the people
encompassed by our AIDS definition found to be infected with HIV, an
otherwise rare virus in the population? If the answer to both these
questions is yes, then HIV is promoted to a good candidate for a cause of
AIDS. If either answer is no, then the HIV/AIDS hypothesis obviously has
severe problems right from the start.

Fortunately, however, we can easily construct a workable definition of AIDS
which does not include any reference to HIV, but which still describes the
new epidemic in which we are interested. Such a definition will not be the
standard one, of course, but since the standard modern HIV-containing AIDS
definition is unusable for this purpose, both we and the AIDS skeptics are
required to construct special AIDS definitions even to continue to talk
about the problem of causation.

Redefining AIDS:

Acquired Immune Failure Syndrome

What is the best way to define AIDS without reference to HIV? Acquired
Immune Deficiency Syndrome is the name historically chosen for a new medical
syndrome which is essentially 100% fatal, and thus in defining it we are
looking for people with an immune deficiency in the range which is
life-threatening and will continue to grow relentlessly worse until life is
impossible.

One possible way to define immune deficiency would be to define it by what
problems it causes--for instance, one could pick people who have gotten
so-called "opportunistic infections" or strange infections which are seldom
if ever seen in people whose immune systems are fully functional. In the
early days of AIDS, before HIV was discovered, the syndrome was indeed
defined using such opportunistic diseases (Fig. la), and people with these
infections are still included in the federal Centers for Disease Control
(C.D.C.) clinical surveillance definition of AIDS (but now only if they are
also HIV infected). We will not be able to use this C.D.C. definition (Fig.
lc). Not only does it assume HIV infection, but for historical, political,
and technical reasons, it also is constructed in a way which does not assess
current immune status in the best way.

Why is this? The basic problem is that only a limited amount of information
about a person's immune system function flows from the bare fact that they
have an "opportunistic" infection. Certainly there is a good correlation
between immune function and what kind of opportunistic infections occur, but
the correlation is far from perfect, since opportunistic infection risk is
influenced by not only immune status, but also by the quality of what we may
term the infectious "assault" to the system. The assault in turn is
influenced by a person's physical location, infection contacts, personal
habits, and other exposure factors both known and unknown. In the end,
assault differences insure that some unlucky, highly infection-exposed
people manage to contract opportunistic infections when only mildly immune
compromised (though these are rarely fatal). By contrast, the same assault
differences insure that other people who are badly immunologically impaired
may escape opportunistic infections for an amazingly long time, simply by
missing the microbes which will kill them (Fig. 1a).

When it comes to immune function, then, it is better to have a direct test
which is not subject to uncontrolled variables such as which microbes happen
to be in the air or drinking water, and how many. Such a test exists. Quite
early in the history of AIDS, it was found that the immune defect in this
disease is peculiar, and that it most visibly involves a particular kind of
cell in blood and lymphatic tissues (lymph "nodes"), called "T-lymphocytes."
In the syndrome of AIDS, certain T-lymphocytes gradually disappear from both
blood and lymph tissues, and a simple T-lymphocyte count in the blood can
tell how serious the reduction has been in both places (since blood
lymphocytes come from the lymphatics). The arm of the immune system which is
controlled most directly by T-lymphocytes (the body's defense against
viruses and fungi) is what is most defective in AIDS, and viral and fungal
infections are the main opportunistic infections which appear and cause
death in AIDS.

AIDS is so specific in its attack that scientists eventually found that only
one subset of T-lymphocytes was initially hardest-hit. This was the
so-called CD4+ or "helper" T-lymphocyte, which has the job of stimulating
the immune system. The other major type of blood T-lymphocyte, the CD8+ or
"suppressor" lymphocyte, is involved in shutting the immune system down; in
AIDS, CD8+ lymphocyte blood numbers increase early in the disease, and are
not decreased until near the very end of the disease process, when they may
also disappear.

CD4+ lymphocyte blood counts tell much of the story in AIDS and other
immunodeficiencies involving the T-lymphocyte immune system. A healthy adult
might have a CD4+ lymphocyte count of 800 to 1000, with a CD8+ count half of
this. These are normal values. Under physical stress, injury, or chronic
infection, CD4+ lymphocyte count might drop to 500 (to even less than the
CD8+ count), and mild, non-fatal opportunistic infections might be the
result. A CD4+ count less than the CD8+ count was once used as a crude
marker for AIDS, but today with progress we know that this immune state is
non- specific. In AIDS, things eventually become much worse than this, and
the worse things get, the fewer possible alternative causes are possible.

In full-blown AIDS, as defined by opportunistic infections and other
problems, the CD4+ count is usually below 200. It is at such count levels
that Kaposi's sarcoma (a tumor perhaps caused by a virus) and
life-threatening infections begin to appear, although approximately 95% of
AIDS patients survive beyond this level of decline.2 Another feature of
AIDS, however, is that inevitably the count grows worse over time. Today, in
the modern era of antibiotics and more knowledgeable care, 85% of AIDS
patients live to see their CD4+ lymphocyte count drop below 50.3 Famous AIDS
sufferer Kimberly Bergalis, for instance, had her CD4+ count drop to 41
before her disease was even diagnosed.4 Many AIDS patients today go all the
way to CD4+ counts of zero before the inevitable final infection or other
complication. It is because of the implacable and more or less irreversible
loss of vital T-cells that AIDS remains a fatal condition, with an average
time span of less than two years between the first opportunistic infection
and death.

If we wish to define AIDS in terms of immune failure, the essential question
is where do we draw the line, so as to include almost all people with the
new immunodeficiency epidemic, who are going to die from it, but exclude
everyone else? If we simply define "immune deficiency" as a sustained CD4+
lymphocyte count of less than 200 (where death begins to become more
likely), we will capture about 95% of people who die of what the C.D.C. now
defines as "AIDS" (Fig. lb).

Previous to the epidemic of AIDS, of course, people did die of immune
failure with low T-lymphocyte counts (including low CD4+ counts) for other
reasons, and they continue to do so now. Thus, we must also exclude from our
AIDS definition all those people who have one of the classic reasons for a
very low T-lymphocyte count--reasons which were well-known before the AIDS
era (cancer, malnutrition, tuberculosis, radiation, chemotherapy, etc).
These people do not have AIDS, because the historical epidemic of AIDS
consisted of people with no T-lymphocytes, and yet no known reason for it.
These people had appeared newly on the scene in the 1980's with evidence of
a fatal kind of immune failure which was acquired, meaning that it was an
epidemic problem of something "picked up" by previously healthy people.

So let us simply collect all the people we can find with CD4+ counts
remaining below 200 (for a few months) without known reason, and test them
for HIV. When we do, we find that essentially all are HIV infected, and any
who are not do not look at all like typical AIDS patients (as we will see).
This, despite the fact that only 0.3% of the general population carries this
virus. Thus, at this point we have no evidence yet to directly contradict
the simple theory that HIV causes 100% of our conservatively defined "AIDS."
AIDS skeptics will need different definitions in order to find HIV-free
AIDS. (Fig. 1d and 1e).

Enter the AIDS Skeptics

The view that HIV plays no role in AIDS has been most notably put forth by
Peter H. Duesberg, professor of molecular and cell biology at the University
of California at Berkeley. A German emigree, he was originally trained in
chemistry. On arriving in the U.S. in 1964 he began work in the field of
viral molecular biology at Berkeley, where in 1970 he co- discovered the
genetic basis for the carcinogenic action of the Rous sarcoma retrovirus. In
1987 he began publicly questioning the role of HIV in AIDS, a stand which
has made him the center of the present HIV/AIDS controversy. Duesberg's most
recent book is called Why We Will Never Win the War on AIDS (1994),
co-authored by a Berkeley graduate student and one-time protege Bryan J.
Ellison. The book has been plagued by trouble. According to a message issued
October 13, 1994 by the Group for the Scientific Reappraisal of the HIV/AIDS
Hypothesis, this manuscript was published unilaterally by Ellison without
Duesberg's consent, following failed editorial negotiations with the
original contracting publisher (St. Martin's Press). According to Duesberg,
the editor had asked for additional documentation, clarification, and
elimination of material which might be considered unfair to individuals.
Duesberg was willing to cooperate but Ellison was not. Following Ellison's
publication of the manuscript at Inside Story Communications (a newsletter
edited by Ellison), Duesberg severed relations with Ellison and is seeking
an injunction against further publication of the book. The cooperation of
James Tabulse, publisher of the Group's newsletter Rethinking AIDS, with
Ellison, has meant that the Duesberg's Group has decided to severe relations
with this publication as well. They now publish a new newsletter called
Reappraising AIDS. Since Duesberg has questioned only publication and
editorial rights for the new book and has not repudiated any of its
contents, the book is used in this essay (see page references) as a source
of Duesberg's views. A major Duesberg essay is also used.5

At the other end of the skeptic spectrum are hybrid arguments raised by
Robert Root-Bernstein, an associate professor of physiology, winner of a
MacArthur "genius" award, and author of Rethinking AIDS6, the most
carefully- documented work to yet assail the prevailing medical views on HIV
and AIDS (see page references). Root-Bernstein is less radical than
Duesberg, arguing for a somewhat less central role for HIV in AIDS than is
generally given it, but still allowing for the virus to have some part in
the etiology of the disease.

Since Duesberg's original challenge, which has been the cause of much formal
debate in the literature7, a number of scientists, physicians, and lay
persons have taken up the cause for a "re-appraisal" of the idea that HIV is
the major causal factor, or even one of the major causal factors, in AIDS.
Most respectable is the Group for the Scientific Reappraisal of the HIV/AIDS
Hypothesis, which has collected over 200 signatures of physicians and
scientists, including those of Nobelists Walter Gilbert and Kary Mullis.
This group has campaigned to remove the requirement for HIV infection from
any medical definition of AIDS, feeling that using this criterion is at best
premature, and prejudices any hunt for alternative explanations for the
disease.

Almost all critics of the AIDS/HIV hypothesis have one thing in common: they
insist on using a much broader definition of AIDS than we have proposed, a
definition which virtually guarantees that some people who fit the critics'
AIDS definition will not be HIV infected.

To be fair, there is some historical precedent for using a definition of
AIDS which relies solely on the patient developing one of a certain list of
the most serious and specific opportunistic infections, since this was the
way the disease was diagnosed before HIV testing became available in 1985
(compare Fig. 1a and ld). Today we know that almost all such people with
pre-1985 defined "AIDS" are infected with HIV--indeed this was known in late
1983, before the official announcement of viral cause was made the following
year. But today we know this figure would not quite be 100%.13 As we will
see below, there is evidence that the few HIV-negatives in this group will
be people with lesser degrees of immune suppression (higher CD4+ counts),
who will not progress to worse immune function, or quickly die. (Fig. 1c).
It seems reasonable, then, with what we know today, to simply exclude
them--since we know that this is not the characteristic picture of AIDS.
Again, it is most reasonable for our purposes to diagnose AIDS on the basis
of immune function (CD4+ levels) only, since it is immune function, not
infection status, which correlates with short-term prognosis in CD4+
immunosuppressed people.

The skeptics, however, will have none of this, and in their definitions are
seemingly less interested in clinical utility than they are in collecting
ammunition for an argument. The more broadly AIDS is defined, the more "HIV-
free AIDS" cases skeptics can assemble, and these, in turn, can be used as
evidence to the lay public that HIV cannot be the cause of AIDS.

Duesberg, for instance,5 has insisted upon retaining the early 1980's
observation that a CD4+/CD8+ lymphocyte count ratio of less than 1.0 is
often seen in AIDS, and he has decided that such a ratio, even in the
absence of opportunistic infection, is synonymous with AIDS (p. 260).
Duesberg now calls this ratio an "AIDS-defining immunodeficiency," and
counts people with this lab result as part of "HIV-negative AIDS," in his
shocking and too-often repeated statistic that there are "3,000 documented
HIV-free AIDS cases."8 Here again, Duesberg's chosen definition of AIDS is
less than useful because people with such mild immunosuppression as he uses
to define "AIDS" are not the people who are dying, or are shortly destined
to die. AIDS is nothing if not a fatal epidemic, and insisting that mildly
compromised persons who may or may not eventually get any worse be labeled
as having "AIDS," as Duesberg routinely does, only serves to confuse the
issue (Fig le).

There is a general trend for AIDS skeptics to overdramatize levels of immune
deficiency which are not clinically very significant. For example,
Root-Bernstein (p. 262), in characterizing a study of HIV-negative men newly
infected with CMV virus, notes that for a time, some of the men had
CD4+/CD8+ cell ratios of less than 0.4, a figure which he claims "represents
extreme immune suppression." During viral infections such CD4+ depressions
are transient. In AIDS, however, this ratio would typically be far less than
0.3, and thus these men would not be mistaken for the current C.D.C.
immunological definition of AIDS, even if they were HIV-positive.9 The level
of immunosuppression associated with a ratio of only 0.4 is not associated
with significant risk of death by opportunistic infection. You might wonder
how we are justified in calling a ratio of 0.4 "extreme immune suppression,"
if people rarely die from it, as they are known to do in AIDS.
Root-Bernstein does not say--indeed, does not even raise the issue. The AIDS
skeptics' overdrawn interpretation of the clinical significance of lab
results is one of the places in which absence of medical training shows most
clearly.

Indeed, Duesberg's paper5 and Root-Bernstein's book6 each contain
descriptions of groups of HIV-free people who are somewhat immunosuppressed
due to low CD4+ counts, or low CD4+/CD8+ ratios, but not severely so, as
defined by our straightforward criteria of having a significant risk of
infectious death due to T-lymphocyte loss. These immune deficient patients
in the AIDS skeptics' literature are presented along with the inference that
perhaps somewhere there exist people with these immune suppressive factors,
or combinations of them, who are severely T-lymphocyte immunosuppressed for
long periods of time (as AIDS patients are), and yet still without having
HIV. Duesberg and Root- Bernstein only have one difficulty in this
argument--neither has been able to actually find any such people.

HIV-Free AIDS?

Hypotheses may be disproved by the right data with relative ease, and cases
of HIV-free AIDS would disprove the idea that HIV causes AIDS, in proportion
to how often these are found (i.e., if 10% of AIDS cases were HIV-free, this
would prove that HIV is not the cause of at least 10% of AIDS). Thus,
Duesberg and Root-Bernstein are not the only ones who have been looking for
HIV-free people who are badly CD4+ lymphocyte immunosuppressed without
reason (i.e., good candidates for HIV-free AIDS). Very recently the C.D.C.
reported that after a massive search it had only been able to find less than
100 people without HIV infection across the country whose CD4+ counts were
at one time less than 300 (not quite in the AIDS-class immunosuppression
range of 200, but drawing close). This syndrome was named "ICL" (idiopathic
CD4+ lymphocytopenia), meaning "people with low CD4+ lymphocyte counts
without a medically-defined disease."

Why was ICL not simply called "HIV-free AIDS?" Critics have darkly suggested
that the reason is politics, but in fact there were problems with
considering these people as AIDS cases which had nothing to do with AIDS
politics or the HIV theory. One difficulty was that people labeled as having
"ICL" were found not to come from the AIDS risk groups. They did not use
illicit drugs, had not been exposed to blood products, and had no evidence
of sexual behavior which would have exposed them to a special infection
risk. Thus, as we will see, the most popular alternative AIDS hypotheses did
not explain these people either--a fact which did not keep them from being
mentioned in nearly every skeptical treatment of the HIV/AIDS issue. What
the skeptics had forgotten (or hoped their readers would not notice) was
that the immune deficiency of people with ICL did not seem to be acquired.10
What justification was there, then, for calling it AIDS?
Moreover, people with ICL were not only epidemiologically, but often
immunologically distinguishable from AIDS cases: their CD4+ lymphocyte
counts swung widely, and transiently, in response to infections, and were
often much higher than 300 (in contrast to people with AIDS, whose CD4+
lymphocyte counts tend to stay low and heading on an ever-downward trend).
ICL people also often had low total lymphocytes or low CD8+ lymphocyte
counts, again indicating that their immune failure did not make much
distinction between CD4+ and CD8+ lymphocytes, as classic AIDS does.
Clearly, these people did not belong to the classic AIDS groups which began
suffering with epidemic immune problems about 1980. They are not part of the
new phenomenon of AIDS, and although sometimes suffering from opportunistic
infections, did not even seem to share the implacable death rate of AIDS.10

Searches for HIV-negative people who have AIDS-type severe immune
suppression have also been taken specifically within AIDS risk groups.
Vermund reported in the United States Multicenter Cohort Study that of the
2,713 persistently HIV- negative homosexual men in the study, who had had a
total of 22,643 blood tests, only one significantly immunosuppressed man
(CD4+ lymphocyte counts persistently less than 300) was found. This man was
taking chemotherapy and radiation for cancer, and thus had a very good
reason other than his lifestyle to explain his lab results.11 If this study
is indicative, then most, if not all, male homosexuals with sustained
AIDS-range immune failure are HIV-positive, since it has proved very
difficult to find any who are HIV- negative.

Much the same seems to be true in IV drug users: in a study of 1,246
HIV-negative injecting drug users in New York City from 1984 to 1992, for
example, only four were found with CD4+ lymphocyte counts less than 300 (if
IV drug use per se was a major cause of AIDS, the number should have been
far higher). In this small group of four people, even though infected with
multiple non-HIV viruses, and with a history of heavy drug use, immune
function was stable and without the steady decline in CD4+ lymphocyte counts
over a time span of years which is characteristic of all unselected
HIV-positive cohorts.12 Thus, in this study also, the few HIV-negative
people who could be found with even near-AIDS range immunodepression, were
still not behaving medically like people with AIDS.

So far as we know, then, in the United States all people who are a part of
this new phenomenon of sustained very low (and declining) CD4+ cell counts
in high risk groups, have been infected with HIV. This does not prove that
HIV causes AIDS, but it is surely an important clue.
Why Not AIDS Without HIV?

A persistent suggestion by skeptics is that it would be proper to use as an
AIDS definition the current C.D.C. definition (which includes all
HIV-infected people who have a much expanded list of infections and other
problems), but with the HIV criteria removed. (Fig. 1d.) The problem with
this suggestion is that definitions of diseases are chosen by the C.D.C. for
maximum clinical utility, and HIV criteria in the C.D.C. AIDS definition was
not put there only to insure that there would be no HIV-free AIDS. Rather,
HIV infection in a person with opportunistic infection is known to be (alone
among all other viral infections) a very good predictor of whether immune
status will continue to decay until the person eventually succumbs to
opportunistic infections. In people with mildly compromised immune systems,
the prognostic importance of an HIV infection (which even critics admit,
without admitting causation) is large. Thus, we cannot simply remove HIV
status from the C.D.C. definition and still have the definition do what it
was designed to do, which is predict impending death by immune failure.

AIDS skeptics know that if "AIDS" is defined only in terms of today's much
broader list of "AIDS-defining" diseases and infections (which are meant to
be used only in conjunction with HIV status), it is sure to be quite true
that the definition will be far too broad to be prognostic. Such
opportunistic infections, as critics well know, sometimes happen in the
population occasionally even without the most severe CD4+ immunosuppression
which is characteristic of people who die with AIDS.

A study by Salvato illustrates this point.13 In the study, medical records
over six years for 1500 HIV-positive patients were compared with records for
1,000 HIV-negative patients who had Chronic Fatigue Immunodeficiency
Syndrome (CFIDS) and evidence of immune suppression. It was found that the
CFIDS patients had fatigue, lymphadenopathy (swollen lymph "nodes") and low
grade fevers--but that over the course of six years their problems were not
severe. Only one of them developed CD4+ lymphocyte counts less than 300
("ICL"). Still, two had yeast esophagus infections, a severe opportunistic
infection rarely seen other than in AIDS and other people severely
immunosuppressed. Three had active CMV virus disease of various
tissues--another disease very often seen in AIDS. A total of 486 patients
had evidence of yeast infection of the mouth on exam, a condition suggestive
of mild immune problems but one not limited to AIDS. The average CD4+
lymphocyte count in these patients (not including the single ICL patient)
ranged from 500-1400, with an average of 650. This was significantly lower
than normal, but much higher than typical for AIDS.

In this study, 95% of the HIV-negative patients had previously been infected
with the EBV, CMV or HHV-6 viruses, and 48% had evidence for continued viral
infection (skeptics such as Root-Bernstein have suggested that these viruses
have roles in AIDS at least as important as that of HIV, but this study
provides evidence against this idea). Most interestingly, these
immunocompromised HIV-negative patients were followed from two to six years,
and none experienced progressive CD4+ lymphocyte decline (except for the one
patient with ICL, who, with treatment of CMV infection, showed increased
CD4+ lymphocyte counts again). Such CD4+ count stability is never seen in
any random group of HIV- positive people, where average CD4+ count decline
with time would be inevitable. The authors conclude: Even after a methodical
search in a practice that sees a large number of patients with immune
problems, only 1 patient was found to have ICL. However, this study
demonstrates that patients with normal CD4 counts can develop AIDS defining
opportunistic infections . . . Upon long-term follow-up these patients do
not appear to experience progressive CD4 depletion.

Most importantly, no HIV-negative person died in the study, which
illustrates the extent to which chronically virally infected,
immune-suppressed people can approach the clinical picture of AIDS (see dark
area Fig. 1d), without crossing into the permanent and deadly immune failure
which is characteristic only of people with HIV infection.

The reader who is a bit confused at this point should keep in mind simply
that the most important thing about the syndrome of AIDS is that it
inevitably and rapidly destroys the immune system and kills people. Thus,
mild CD4+ depression and opportunistic infections are not always AIDS, for
only some of these people (as it turns out, the HIV+ ones) will progress to
immune failure. It is immune failure (almost complete sustained CD4+
lymphocyte loss) and death by opportunistic infection which is
characteristic of AIDS; and it is only these people who are always HIV
infected.

Did the Government Create AIDS?

At the African-American Summit speech in New Orleans in 1989, Louis
Farrakhan told his audience: "The spread of international AIDS was an
attempt by the U.S. government to decimate the population of central
Africa." Last year he told Barbara Walters on ABC's 20/20: "Do you know
where the AIDS virus was developed? Right outside of Washington. It is my
feeling that the U.S. government is deliberately spreading AIDS." Such
paranoid and conspiratorial thinking is not uncommon in history whenever a
new and devastating plague destroys a community, as when the Jews were
blamed for the Black Death in the 14th century. But this is not the form of
AIDS skepticism which I am addressing in this essay, and needless to say
there is not a shred of evidence for such an outrageous claim.17

But what if AIDS and immune failure are not really new-- perhaps we just
look harder for them now that we recognize them? Could our new theories be
warping our views so completely that by now that we have made a new "plague"
out of something that was here all the time? Epidemiologically, what can we
fairly say about the period before 1980, keeping this possible bias in mind?

With the new ability to test old preserved tissue specimens for HIV, the
first thing that becomes apparent is that AIDS is indeed older than
1981--perhaps far older. Deaths from what has since been recognized as HIV
infection with immune failure have been seen clinically, without being
understood, for at least 35 years, and probably much longer. An HIV-infected
British sailor, who had traveled widely, is known to have died with severe
immune deficiency and HIV infection in 1959, the earliest proven case of
modern AIDS. The diagnosis was made by means of preserved autopsy tissue
specimen HIV testing, 30 years after the fact.17

This man's death alone provides good evidence that HIV is not a product of
deliberate (government or otherwise) genetic engineering, for in 1959
biologic science was simply too unsophisticated to work with lymphotropic
(lymphocyte- infecting) retroviruses like HIV, let alone engineer them.103
If it is anything at all, HIV is an accidental infection of humans with an
African primate virus. The genetic material of the most common HIV-1 strain
is most similar to that of a virus known to naturally infect chimpanzees,
and it may be that HIV's ancestors have been present in Africa, perhaps even
in humans, for a very long time--perhaps thousands of years.18,121 In West
Africa, a close cousin of the U.S. HIV-1 strain, called HIV-2, is almost
identical to several indigenous African monkey viruses, and almost certainly
has been derived from them quite recently in virus evolutionary time (less
than several centuries).

The Origins of AIDS

The story of the detective hunt for the cause of AIDS is told with wit and
clarity by Randy Shilts in the best-selling book And the Band Played On. (In
1994, Shilts, at the age of 42, became a casualty of the disease himself.)
Other good histories of the early AIDS epidemic are also available.14

In the U.S., the first AIDS or AIDS-like death that we know for sure was
also associated with HIV infection was that of a 17 year-old possibly
homosexual male, who died of strange opportunistic infections in 1968, and
whose preserved tissues also proved to be harboring HIV genetic material on
testing decades later.19 This early AIDS-sufferer had never been out of the
country, showing that the virus was already active in the Western Hemisphere
in 1968. In corroboration, a 4% fraction of preserved serum samples from IV
drug users in this era (1971-2) in the U.S. have been found to be HIV-
positive. Apparently HIV viral infection has been present in small
contingents of both drug users and homosexual men for some time in the
United States.20

Why, then, was the U.S. first hit with an AIDS epidemic only in the 1980s,
with HIV infection quickly rising to 50% in some risk-groups? The answer may
be that it was not the simple presence of HIV virus in the United States
that changed; rather it was the social milieu.

In the late 1960s drug use became far more widespread in the U.S., and the
invention of the disposable plastic injection syringe about 1970 made IV
drug abuse possible for the first time on a large scale. Also beginning
around 1969 (the date of the New York City "Stonewall" riots), homosexuals
in the U.S. began to take open political power, and concomitantly one
faction of male homosexuals began to engage in the high-infection risk
"bathhouse lifestyle" chronicled by Shilts. In addition, the American
homosexual- male community was apparently many times re-infected by many
world-traveling disease "vectors" from other countries in the 1970s,
including an airline steward named Dugas (described in Shilts as the C.D.C.
"patient zero") who traveled widely in Europe, Canada, and the U.S., died of
AIDS, and is known to have had sex with no less than 40 of the first 248
Americans to be diagnosed with AIDS by April, 1982.14
What happened in the late 1970s in the U.S. is that when a large enough
fraction of the American homosexual-male population became infected with
HIV, the U.S. blood supply, maintained with volunteer donations only,
finally became contaminated with the virus. (This started in 1978, as we
know from later testing of archived serum samples taken from homosexual men
originally for hepatitis B studies). Similar archived samples tell us that
in 1978 the U.S. plasma supply used to make clotting factor for hemophilia
treatment became HIV contaminated, no doubt primarily by IV drug users
selling plasma to support a drug habit. The dates are not
coincidental--crossover between initial HIV infected groups occurred as some
homosexual men experimented with IV drugs in the late 1970s, and male IV
drug users in large cities turned to homosexual prostitution in order to
obtain drugs. The resulting new epidemic of transfusion and hemophilia-
associated AIDS, beginning in 1982 and rising sharply in 1984, helped to
bring the acquired nature of AIDS into focus.

The small incidence of AIDS in the American homosexual- male and IV
drug-user communities before the late 1970s in no way subtracts from the
reality of the dramatic increase in AIDS which took place in the early 1980s
on the heels of exploding HIV infection rates in these groups. Although
relatively mild immune suppression has apparently always been widespread in
many AIDS risk groups, the more complete and devastating immune failure
characteristic of AIDS itself has been sporadic and rare in young
cancer-free people in any of these groups, until the 1980s.

It is, to be sure, difficult to retrospectively evaluate the health of male
homosexuals before the first prospective studies of gay men's health were
done in the 1980's AIDS era, but we can be reasonably sure that an epidemic
of deadly immune failure among young American men before 1980 would have
been duly noted by epidemiologists. AIDS skeptic Root- Bernstein documents a
few cases of unexplained opportunistic infection deaths from the medical
literature before 1980, but clearly an epidemic of immunosuppressive deaths
cannot be seen in the historical record before 1980 by any act of
imagination.
By contrast, at present AIDS shows a high and rapidly rising incidence among
young men and women in the U.S., and these deaths cannot be simply a new
label for an old problem. The reason is that total mortality and cumulated
years of life lost to premature death in young persons are observed to be
rising rapidly, with all of the change due to AIDS deaths, at the same time
other leading categories of mortality remain stable. If mere re-labeling of
deaths into different categories was a problem, these "newly recognized"
AIDS deaths would come out of other previously defined mortality categories,
and this clearly is not happening.21 AIDS, the disease, may be old; but
AIDS, the epidemic, is indeed something new.
People with hemophilia, unlike homosexual men, represent a well-defined
group with long-term documentable changes in morbidity and mortality, since
they had been well-studied as a group before the era of AIDS. This research
shows that people with hemophilia began to die of dramatically different
things, starting about 1982 (Fig 2).22 A recent check shows little evidence
of a special incidence of opportunistic diseases in people with hemophilia
in the U.S. from the turn of the century up to 1979, although a low
incidence of AIDS could not be ruled out in this study, mostly because some
cases of fatal pneumonia had no identified infecting organism,23 and because
people with hemophilia as a group are immunosuppressed enough to be somewhat
more susceptible than normal to bacterial infections. Significantly,
however, in the years before AIDS, people with hemophilia had never been
noted to be particularly susceptible to the more obvious fungal infections,
such as candida esophagitis, common to AIDS patients and others with
low-lymphocyte type immune deficiency. After 1984, however, this type of
AIDS-associated opportunistic infection and immune failure rapidly became
the single most common cause of death in people with hemophilia in the
U.S.24

The rise in total mortality risk in people with hemophilia was sudden: total
mortality in this population, which had been stable in 1982 and 1983,
suddenly increased by a factor of approximately 900% in the first quarter of
1984.25 Such an increase in raw numbers of deaths was consistent with an
epidemic, or some new very toxic contamination of the clotting factor
supply. It is not consistent with slower social changes, slower toxin or
immune suppression models, multifactorial causation models, or the idea that
people with hemophilia were actually at no greater risk than before (i.e.,
that again perhaps there had been some kind of "cause of death" re-labeling
in response to AIDS hysteria). (Fig. 2.) Mortality figures in hemophilia
patients also showed something else important, which was that the new deaths
of the late 1980s, by virtue of all being judged "AIDS," demonstrated that
most or all of them occurred in people with hemophilia who were
HIV-positive. Since these deaths accounted more or less for the entire new
increase in mortality, it could be inferred that the mortality rate for
HIV-negative people with hemophilia did not increase much in the 1980s, if
at all.

How significant was the increase in death rate for HIV- positives in this
group? In one Journal of the American Medical Association study it was found
that in a cohort of 111 people with hemophilia infected with HIV in the
early 1980s, one third had died by 1992.26 Imagine any group of this age (a
high school class, perhaps) and imagine an overall 33% mortality rate in
less than 10 years. Of the estimated 10,000 people with hemophilia to have
been infected with HIV in the early 1980s in the United States, a quarter
had been reported to the C.D.C. to have died of AIDS by July of 1993.

Such death rates were especially shocking in view of strides in hemophilia
treatment which had been made in the years before. Total life expectancy in
people with hemophilia had risen as clotting factor treatment became
available through the 1970s, until by 1980 it was nearly normal.23 After
1984, however, life expectancy in this group began a steep decline, and by
the early 1990s was at a lower level than at any time since before World War
II.24 In the 1980s, total mortality for hemophilia increased in all age
groups above nine years of age, and age at death shifted markedly to lower
ages, decreasing from 57 years of age in 1979-1981 to 40 years of age in
1987-1989.27 (Fig. 2.)

About 50% of people with hemophilia in the U.S. had been HIV infected by
early 1986, when screening and treatment of the clotting factor concentrate
stopped HIV spread.28 Still, the long latency of the virus (as long as 15
years for 50% progression to AIDS in this group) caused death rates to rise
for long after the window of new HIV infection closed.

The fact that there was a massive and silent HIV infection of half of the
people with hemophilia in the early 1980s is beyond question, even for
skeptics. The AIDS skeptics' quest to divorce this event from the epidemic
of deaths by AIDS in this same group over the next decade has resulted in
some remarkable and curious statements about hemophilia mortality. Duesberg,
for instance (p. 216) quotes only older statistics for hemophilia patients
from the pre-1986 period, before AIDS deaths became very large. His practice
of using randomly reported AIDS and mortality data for people with this
disease (which is often notoriously unreliable in the best of
circumstances29), instead of the much more reliable cohort study data, also
results in figures which minimize the impact of AIDS. Cohort data shows
mortality in hemophilia patients to be far higher than Duesberg
acknowledges.30

Duesberg has not been alone in ignoring major trends in hemophilia mortality
in the last decade. The very misleading statement that people with
hemophilia are living "longer than ever" today is one of the standards among
the HIV/AIDS skeptic community. Root-Bernstein does no better than Duesberg
at providing updated information in this area, offering one paper's 1979
pre-AIDS statistics,23 without update and without qualification, to
represent contemporary life expectancy in people with hemophilia in 1993 (p.
247). This represents very sloppy scholarship (something which stands out
particularly in Root-Bernstein), but the oversight does allow the author to
skip discussion of the pronounced and otherwise awkward peak in life
expectancy for hemophilia in the middle 1980s.

Duesberg, though he seems to believe that people with hemophilia have
suffered no mortality increases in the age of AIDS, does suggest that people
with hemophilia live longer than ever due to recent factor concentrate
development, and thus live long enough to die of immunosuppression caused by
longer treatments with clotting factor concentrate, instead of from
hemophilia (p. 220). Although clotting factor does indeed appear to be
mildly immunosuppressive (albeit in a different way than AIDS--CD4+
lymphocyte counts are not affected), the main problem with the hypothesis
that clotting factor itself causes AIDS is that two studies of HIV-positive
people with hemophilia have found that HIV infection, and not clotting
factor use, is the critical risk for AIDS. These studies found that once a
person is HIV-positive, risk of AIDS is not related to amount of clotting
factor used or severity or type of hemophilia--effects that would have been
expected if clotting factor carried a significant immune risk independent of
its HIV content.31 Available statistics thus strongly suggest that the known
association of clotting factor use and AIDS risk is merely due to the
increased risk of being infected with HIV the more clotting factor has been
consumed; once HIV infection has occurred, it does not matter how much
clotting factor is used.109

AIDS in the 80s

Historically, what happened in the U.S. in 1981 was that in increasing
numbers homosexual men began coming to physicians with very, very low CD4+
lymphocyte blood counts (but not lowered counts for other subtypes of
lymphocytes), a destroyed immune system with lymphatic tissue destruction,
opportunistic infections, and Kaposi's sarcoma. No one who had treated
diseases in the male homosexual community could remember having seen
anything remotely like what had began happening on an increasingly large
scale in the early 1980s.

The year 1981 was not (in retrospect) exactly when the problem started, but
rather when the problem first grew large enough in the U.S. to be brought to
the attention of the federally-run Centers for Disease Control in Atlanta.
It was in the Summer of 1981 that alert physicians brought to the attention
of the C.D.C. a mini-epidemic of immunodeficiency and pneumonia caused by
unusual organisms (a fungus called Pneumocystis carinii, and a virus called
CMV) in homosexual men in Los Angeles.

Because many of the first people to contract AIDS had had sexual contact
with each other, C.D.C. researchers thought they might be looking at an
unknown sexually-transmitted infectious disease. They also toyed for a time
with the idea that sex-stimulant-chemical use or illicit narcotic use, both
very common among the first cases of AIDS, might be somehow causing
immunosuppression. Perhaps sexual contact was a red herring--or merely a
marker for a small and fairly tight-knit sub-community of people who shared
common interests in non- sexual activities which might be damaging their
immune systems.
Those physicians treating infectious diseases in homosexual men thought not,
however. Dr. Joel Weisman, one of the first doctors to put the AIDS puzzle
together, noted that initially, within the male homosexual community, the
disease seemed to follow lines of sexual contact more than it did drug or
sex habits. Not all homosexual men were so promiscuous as to make
contact-tracing impossible; Weisman observed that promiscuous men did not
always contract the disease, but on the other hand, that even men with few
sexual contacts were coming down with the disease if they had had sexual
contact with the wrong person. In fact, men with severe immunodeficiency
were eventually found to form sexual contact networks, of the kind that have
always been seen by researchers using the classic epidemiological tools for
tracing sexually transmitted disease chains. The difference, however, was
that for AIDS the contact networks stretched over years, indicating an
infectious agent (if there was one) with a very long latency. Still,
investigators found that of the first 19 cases of AIDS reported in Los
Angeles, nine had direct or indirect (one intermediate partner) sexual
contact with a single French-Canadian airline steward (previously
mentioned), a man who was also sick with immunodeficiency.

Then, starting in 1982, reports began to come into the C.D.C. of the same
CD4+ lymphocyte and lymphatic-tissue- destroying immune failure syndrome
occurring this time in U.S. citizens who had received transfusions. Soon
also came reports that an identical immune deficiency of a new severe
variety was now being seen in men with hemophilia, a genetic disease in
which sufferers must be injected with concentrates of protein clotting
factors made from donated blood plasma. Reports of the first people with
hemophilia and AIDS emphasized that, in these people, none of the same drug
or male-homosexual behavioral factors were present that had been seen in the
first group of AIDS sufferers.15

Further, the same was true of those with "transfusion- related AIDS," who
also did not fit into drug-using or male- homosexual lifestyles, and did not
resemble them in sex or age either. Former tennis star Arthur Ashe is a
well-known modern example. Ashe, like many of those with transfusion-
related AIDS, had never had an intimate connection with anyone else with an
immune problem, except for a history of blood transfusions years in the
past, during the time in which transfusions were associated with AIDS.
In late 1982 all this worried epidemiologists as the reports continued to
come in. They knew that another viral disease called hepatitis B ("serum
hepatitis") was also transmitted epidemically as a sexually transmitted
disease in homosexual men, but much more rarely in homosexual women or
heterosexuals in the U.S. Hepatitis B had historically also shown up early
in people with hemophilia, who because of their large pooled blood-product
exposure have historically seemed to be first to suffer from any new
organism infecting the blood supply. Hepatitis B had also been known to be
one of the worst disease-causing contaminants in donated blood for general
transfusion. Thus, the same three groups of people who had historically been
infected with a new epidemic of hepatitis B in the 1970s, had now started
coming down with AIDS. Hepatitis B was also a disease of IV drug users who
shared needles, and it was not long before the first reports of IV drug
users with AIDS came in.

By 1983, the C.D.C. was sure it had a new infectious disease on its hands,
similar in epidemiology to hepatitis B but with a longer latency period.
Analysis of the habits of donors of the blood components that went into
those people who had later developed AIDS, indicated one thing different
about the donors: it was found that blood products AIDS patients had
received had more often come from people who themselves were at "high-risk"
for AIDS due to promiscuous male homosexual behavior. On the other hand,
matched case- controls who had been transfused identically from the same
blood bank but had not developed AIDS after transfusion, were found to be
not nearly as likely to have gotten blood components from anyone in a
"high-risk group."

This initial study concluded that there was only a 1% chance that the
statistical association of transfusion- associated AIDS with the lifestyle
of the blood-donor would be as close as it was found to be, if only chance
had determined the lifestyles of the donors of blood to people who later
became sick. Such a chance association would have been expected if there was
no contamination, and instead there was something about normal transfusion
blood itself, or perhaps some other factor unrelated to transfusion, that
was causing AIDS in transfusion recipients.16 The remarkable fact--from
which there was no escape--was that AIDS in a transfusion recipient
predicted the lifestyle of a blood- donor he or she had never met (a donor
which generally turned out to be a promiscuous homosexual man who had
thought himself to be perfectly healthy). Nothing but an infectious agent
could explain a statistical connection between a blood donor's sexual
habits, and risk to the person receiving the blood. As for drugs or immune
toxins, it was impossible to believe that any chemical toxin could be
present in a relatively small amount of blood component coming from a single
nominally healthy person, in sufficient quantities to cause total immune
failure in the recipient, and do it years after the transfusion.

Eventually, with many cases like Arthur Ashe's on record (but showing up in
the early 1980s, earlier than Ashe's did), AIDS looked epidemiologically
very much like hepatitis B. The hunt was on for the microbe, or microbes,
which caused the new syndrome. When the virus now known as HIV finally hit
the world news in the Spring of 1984, there was a great deal of skepticism
in the scientific and lay communities alike. With the ability to test for
antibodies to HIV in 1985, however, there came a way of powerfully sifting
through putative causal factors for AIDS, and comparing them with the factor
of past HIV infection. HIV infection has emerged from these tests as the
clear champion of competing AIDS-causation theories, convincing at present
all but the most die-hard skeptics.14

Attacks on Straw Men

It is an unfortunate fact that a great deal of the debate over AIDS and HIV
has been over what rhetoricians call "straw men." A straw man is an argument
or viewpoint set up in a debate only for the purpose of being knocked down,
and one which the opposite side never really defended or held; or one which
is not very important to the central issue of the debate, even if it has
been held. Straw man arguments often result from debaters talking "past each
other," without understanding the opposing side's position. In the HIV/AIDS
debate, straw men set up by heretics have most often been medical hypotheses
which have previously been put forth in the context of the HIV theory and
which have turned out to be wrong, but which were never important
corollaries necessarily deduced from the idea that HIV causes AIDS. Other
straw men are ideas that the orthodox scientific "establishment" never put
forth seriously at all, though they may be attacked vigorously by heretics
as though they are current medical dogma. We will presently see samples of
both.

An example of an epidemiological straw man is the timing of HIV arrival in
the Western hemisphere. Root-Bernstein discusses cases of possible AIDS as
far back as 1932, notes documented HIV infection with AIDS as far back as
1968 in the U.S., and argues that these data are anomalous (p. 2) if the
virus was transferred for the first time to the Western hemisphere around
1978, as was originally thought. And so they are. But if the HIV virus was
transferred much earlier than 1978 to the new world, and remained at low
levels in male homosexuals and injecting drug users in America until
changing social factors in the 1970s encouraged its spread (exactly as
Root-Bernstein himself indirectly suggests), no real damage would be done to
a suitably modified HIV/AIDS theory.

An example of a bad prediction made by the orthodox medical establishment
which is not necessarily derivative of the HIV theory, was (or is) the
official idea that AIDS is due to be a heterosexual pandemic in America any
time now. It is argued by Duesberg (p. 203), that the "viral hypothesis" has
failed to predict the course of the AIDS epidemic--namely that AIDS has (at
least so far) shown no clear inclination to spread rapidly by a complete
heterosexual-sexual-transmission mechanism in the U.S., even though it
apparently does so in Africa. It is also asserted in a related argument by
Root- Bernstein that the HIV/AIDS hypothesis does not explain the
generally-low measured levels of HIV virus in semen, the low (but not zero)
rate of HIV infection in mates of HIV-positive men with hemophilia, or the
nearly zero rate of infection in U.S. heterosexual prostitutes (unless they
are drug users). If AIDS is an infectious disease, ask the skeptics, then
why does HIV not infect very well?

All these arguments are against straw men. There is nothing in the HIV/AIDS
theory which demands that any particular transmission mechanism be the chief
cause of the spread of HIV infection in any given place, or which demands
that the HIV virus be as infectious in one locality as another. For example,
it now seems likely from many studies that sexual transmission of HIV often
requires mucosal tissue trauma, which is much more likely with anal
intercourse, and/or a concomitant inflammation or ulcer from a second
sexually transmitted disease. Because transmission may be inefficient even
so, promiscuity also greatly enhances the chance of HIV spread. These
requirement(s) for efficient HIV sexual transfer easily explain the
difference between spread of HIV in tropical Africa vs. the developed
countries. They also adequately explain why a disease which spreads well
sexually only in populations with an extreme level of both promiscuity and
rectal mucosal trauma (i.e., one sub-segment of American homosexual men) has
not yet become a generally spreading sexually-transmitted disease epidemic
in the U.S.

It is not that the HIV/AIDS heretics have not come across such explanations.
Root-Bernstein, in a good discussion of the epidemiology of AIDS, admits
that there is nothing especially strange about a sexually transmitted
disease which spreads easily in homosexual males but not heterosexuals in
the U.S. Both syphilis and hepatitis B in the 1970s have been examples of
such a phenomenon, and the "odd" differential epidemiology of both diseases
with regard to sexual- preference groups is easily explained by differential
behavior in the homosexual and heterosexual populations in those years.

Duesberg argues that a disease which restricts itself to classes of people
in America, but not in Africa, cannot be explained by a micro-organism. But
while he is doing so, fellow heretic Root-Bernstein (pp. 281-303) is noting
that infectious epidemiology in one group of American homosexual males, who
might be sexually infected with giardia, parasites, amoebas, hepatitis A,
and B, shigella, salmonella, etc., may resemble far more the disease
epidemiology of some African countries than that of heterosexuals living
next door (p. 290). In this, an AIDS caused by an infectious agent such as
HIV may behave just as AIDS statistics suggest it does, and yet merely
follow a pattern already amply demonstrated before AIDS, with many another
infectious disease. Root- Bernstein is sometimes too competent a scholar for
his own good. His Chapters 8 and 9--which address the epidemiological
differences and commonalities of U.S. homosexual men and African
heterosexuals due to sexual practices and social changes which appeared
newly in the 1970s and 1980s--not only believably explains and refutes most
of Duesberg's epidemiological problems with AIDS (p. 209), but also does the
same with many of Root-Bernstein's own epidemiological problems, raised in
Chapter 1.

Unfortunately, Root-Bernstein is willing to let lifestyle and habit
differences explain epidemiological differences when it suits his argument's
needs, but much less willing to consider them when they don't. An
illustrative example occurs as Root-Bernstein discusses the rectal traumas
and infections which occur during certain male homosexual practices, writing
of these (p. 283-4): "It is now accepted that such injuries and infections
greatly increase the risk of concurrent infections (HIV or otherwise) and of
semen gaining access to the immune system following anal intercourse."

Yet when Root-Bernstein discusses the statistical association of AIDS with
receptive anal intercourse (p.225) he shows an odd difficulty with the same
concept: "One possibility is that it is much easier to transmit HIV to a
receptive partner than from a receptive partner. No other sexually
transmitted disease behaves this way, however . . . . HIV would be the first
disease agent to be able to make the discrimination, unless some other
factor is involved."

Here, unfortunately, Root-Bernstein is wrong, and wrong for the very reasons
that he himself discusses in the quote preceding the last. Much like HIV,
hepatitis B infection in homosexual men also correlates with rectal trauma
and receptive anal intercourse,32 and there is little reason to believe that
the "other factor" is anything other than the fairly straightforward
mechanical injury that Root-Bernstein has already helpfully identified for
us (see reference 33 for statistical development of a "rectal trauma index"
which partly predicts risk of HIV infection). It is a characteristic of
Root-Bernstein's style of argument that it makes causal mechanisms as
mysteriously complicated as possible--very often far more complicated than
required to explain the facts.

Root-Bernstein, eager to draw attention to any factor other than HIV in the
causation of AIDS, does not take into account the most obvious physical
factors: "what is clear from existing studies," he asserts (p. 45), "is that
HIV is extremely difficult to transfer to a healthy individual." In fact,
existing studies establish no such thing. Studies quoted by Root-Bernstein
never demonstrate that only "unhealthy" people in known risk groups contract
HIV, only that certain traumatized risk groups (promiscuous gay men,
hemophiliacs, transfusion recipients) are on average somewhat unhealthy to
begin with. This, of course, is not the same thing. Indeed, there is
evidence that within risk groups, even the healthiest of individuals
(immunologically) are capable of contracting HIV. Although men with
hemophilia and homosexual men are on average mildly immunosuppressed even in
the absence of HIV, it is by no means true that all are. A study of army
recruits (surely a carefully screened group for health) shows that those who
seroconvert to HIV (demonstrating new HIV infection) may initially (by the
criterion of CD4+ count) have immunity which is in the normal range. This is
true in other groups as well.34

Perhaps the most bloated straw man assailed by Root- Bernstein (and the one
that provides the major theme of his book) is the idea that the causal agent
of an infectious disease such as AIDS must be both necessary and sufficient
to cause the disease in every sense of the terms; and moreover that since
Dept. of Health and Human Services Secretary Margaret Heckler's dramatic
announcement in 1984, most scientists have considered HIV to play this very
role for AIDS. Root-Bernstein spends much time attacking what he calls the
"HIV-only" theory of AIDS, an idea which actually has never flown, except
possibly in the popular press or the occasional scientist who expresses a
rash opinion (Dr. Robert Gallo, official co-discoverer of HIV, must by now
badly regret his hyperbole about HIV being able to cause AIDS in Clark
Kent35). The subtitle warning of Root-Bernstein's book is The Tragic Cost of
Premature Consensus, and it appears from the book that it is upon the
"HIV-only" theory of AIDS that the "premature consensus" of the
establishment is in dire danger of settling, if it has not already.

Fortunately, it can safely be said that no such thing is occurring in the
biomedical consensus, or about to. This does not prevent Root-Bernstein (p.
331) from logically blasting the somewhat cartoonish view he attributes to
medical science: "Two of the most important implications of the HIV- only
theory of AIDS are that all the risk groups should develop AIDS at
approximately the same rate following HIV infection and that the symptoms
they manifest should, on the whole, be the same."

Alas for Root-Bernstein, however, since AIDS has from the beginning involved
opportunistic infection organisms which vary in prevalence among
populations, and since there has been reason to believe from the first that
AIDS risk varies greatly with the biological age of the HIV-infected person,
scientists have never, even at the beginning, seriously considered such a
theory as Root-Bernstein here lays out: One logical implication is that the
immunological status of an infected person should be irrelevant to
susceptibility to contagion or to the progression from infection to disease.
Acquisition of the retrovirus should be the sole factor determining whether
an individual develops AIDS. Everyone should be at equal risk for AIDS, just
as everyone is at equal risk for hepatitis B virus, syphilis, or measles.

The most troubling thing about such writing is that an unwary lay reader may
leave Root-Bernstein's book with the impression that the author has
single-handedly discovered that infectious disease risks depend partly on
host immune defenses and host behaviors and environments. The reader might
well decide further that the biomedical community today does not in general
think in terms of individuals having differing resistances to various
diseases, and is accepting such advanced ideas only under duress, due to
political pressures resulting from the penetrating logic of popular writers
such as Root-Bernstein, who are "re-thinking AIDS."

The facts are more mundane. Obviously, since no microbe infects 100% of
people exposed to it, or even causes disease in 100% of the people it
infects (not even HIV has been shown to do this), there must be other
factors to explain why some exposed people become ill with ANY infectious
agent (viral, bacterial or parasitic), and some do not. Medical science
certainly recognizes such factors, but does not use them to argue that there
is in general something badly wrong with the germ theory of disease.
Instead, as discussed earlier, medical scientists regard "causality" in
infectious disease in merely the sense of "necessity" (i.e., the "causal"
microbe is necessary, but not sufficient). Medicine has not regarded the
pathogenesis of any natural infection in terms of a "germ only" theory such
as Root-Bernstein describes, since Pasteur, referring to disease, said: "The
seed is nothing, and the soil is everything." Thus, Root-Bernstein spends
many chapters assailing an idea that physicians have not held since the late
19th century, and certainly have never generally held in the case of AIDS.

No infectious agent is usually "sufficient" to cause disease in a natural
host, although in a laboratory (or perhaps very occasionally in nature) it
may be sometimes true that the dose may be so high as to make host
resistance almost irrelevant. Naturally-occurring infectious disease
organisms at reasonable doses, however, always rely on a chink of some kind
in host immunity with regard to that particular microbe (this is not to say
that we must consider any host that is successfully infected to be
"immunocompromised"--that would cheapen and overly broaden this useful
term). The idea that deficiencies in host defense in some sense "permit" all
or most infections is indeed a standard medical teaching,36 although a lay
reader of Root- Bernstein might be surprised to learn of it after Root-
Bernstein finishes misrepresenting the standard views of modern medicine.

"Why is there such a huge and medically unprecedented variation in time
between HIV infection and death from AIDS?" asks Root-Bernstein (p. 89). The
answer to this rhetorical question is that such variation is not medically
unprecedented. Other infectious diseases, from malaria to syphilis to
tuberculosis to viral hepatitis, may kill years after initial infection--or
within a much shorter time. In a cohort of newly-infected people, any study
of a chronic infectious disease cannot help but produce steady increases in
the "average" time between infection and death, as deaths accumulate slowly
while the study follows the infected cohort prospectively onward in time.

"No theory based solely on HIV can explain the phenomenon of variable times
of death," writes Root-Bernstein (p. 89). This is correct so far as it goes,
but it says much less than it seems to, for this much is true of every
infectious disease known, including other infectious diseases which may have
latency times to death fully as long as those for HIV. Too much of
Root-Bernstein's Rethinking AIDS consists of arguments that the HIV
hypothesis needs to be re-thought because HIV infection supposedly has
strange properties-- properties which on close examination turn out to be
broadly similar to those of many other infectious diseases.

SIDEBAR: What Is a Retrovirus?

A retrovirus is a virus which has its genetic structure encoded into RNA,
but which reproduces by turning it back into DNA during an infection. Once
inside a living cell, retroviruses are able to synthesize virus DNA-copy
molecules using the virus's RNA genetic molecules as a template, or "master"
(this process proceeds retrograde to the normal "DNA-->RNA" information flow
in cells, hence the name). To do this job a unique enzyme molecule called
"reverse transcriptase" is used by the virus. Since this enzyme is not found
in normal cells the virus itself must carry it. This enzyme and the process
it catalyzes are so unusual in biology that H. Temin and D. Baltimore were
awarded the 1975 Nobel Prize in Medicine for discovering it.

Once the DNA-copy of a retrovirus (called a pro-virus) is made, it is often
inserted into the DNA of the cell being infected. Now an actual part of the
genetic code of the cell, the retrovirus genetic information is hidden from
the immune system, which would otherwise destroy the virus inside the cell,
or destroy the entire cell. All humans harbor some foreign retroviral DNA
actually integrated or inserted into the DNA in most of their body cells. In
this sense, we all share some of the fate of the scientist in the remake of
the movie The Fly, a matter-transporter victim whose DNA is not pure and not
entirely human, but who cannot do anything about it because there are no
"tweezers" fine enough, or discriminating enough, for the job. Some of the
foreign DNA in each of our cells is from retroviruses which went into hiding
eons ago in our ancestors, and are now reproduced automatically along with
our normal cells, and have long since "forgotten" how to get themselves back
out of our DNA.

SIDEBAR: What Does "HIV-Positive" Mean?

Antibodies are blood proteins made by immune cells, which stick very
specifically to microbial invaders, targeting them for destruction by the
immune system. For many years after an infection by a microbe, antibodies
specific to that microbe can be detected in the blood. A person who tests
positive for antibodies to HIV by two different kinds of lab tests, is said
to be "HIV-positive."

In the case of infection with the average microbe, a person may test
antibody positive for years or even a lifetime after the microbe is
completely gone from the body. For the chronic viruses which hide in cell
nuclei, however (retroviruses like HIV; and also CMV, EBV, and other herpes-
class viruses), the presence of antibody is generally a clue to the
continued presence of the virus, active or inactive, somewhere in the body.
In some cases modern sensitive tests for viral DNA can actually detect these
hidden viruses directly.

Over the years since the discovery of HIV, critics of the HIV/AIDS
hypothesis have had to struggle to keep up with sensitivity increases in HIV
testing. Initially, critics complained that HIV virus was not present in
most HIV- positive people. When it became clear that infectious virus could
be found in almost 100% of such people (if cultures were done correctly)
critics claimed that most HIV was dormant until reactivated in culture. With
new sensitive tests for HIV RNA showing that HIV virus is active in the
body's lymph nodes, critics have fallen back to the position that it may be
active, but not active enough. This is a question which can only be answered
indirectly, by other studies. Ellison and Duesberg assert (p. 124) that HIV
is rarely to be found budding from cells in patients, and that "...in most
individuals with AIDS, no virus particles can be found anywhere in the
body," implying that this absolves the virus from any disease role.
Actually, however, even actively reproducing HIV may spend very little of
its total life-cycle budding through a cell membrane or floating free as a
particle in the blood before being picked up by another cell. Studies of
viral RNA in the body show that there may be anywhere from roughly 10
million, to as much as one billion particles or actively replicating HIV
genomes in a gram of lymph tissue--a significant amount by the standards of
most other kinds of virus.122

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