From _Skeptic_ vol. 3, no. 2, 1995, pp. 42-58. (The full article goes
to page 79.)
The following article is copyright (c) 1995 by the Skeptics Society,
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Note from the editor: This article is unusual for several
reasons: 1.) It is a monograph--longer than an article but
shorter than a book; 2.) Skeptic usually features several
voices on one subject, but because of the length we decided
to allow the AIDS skeptics to respond in the next issue; 3.)
Those who do not wish to read the entire article can glean
the terms of the debate from certain subtitles and sidebars,
especially in Part 1; 4.) Dr. Harris has made an original
contribution to the discussion of the AIDS controversy in his
analysis of the definition of AIDS, in particular in his use
of Venn Diagrams to specify what is unique to AIDS and what
is not. Skeptic is honored to publish this important
contribution to the field and rather than apologize for the
length of the article,
we remind our readers that the magazine includes its usual
array of columns, essays, articles, news items, and forum
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
"It's the virus, stupid."
--Dr. David D. Ho, AIDS Researcher
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.
Copyright 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
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
"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
"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
"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
"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. Moveover,
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 . . . .
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 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
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.
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
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
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
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
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
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
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.
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-
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
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.
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 devestating 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
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
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
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
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
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 epidemiologic 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
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 epidemiologic 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
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
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 epidemiologic
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
epidemiologic 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 epidemiologic 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 moveover
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
"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.
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.
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
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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88. Los Angeles Times, Letter from P. H. Duesberg, Aug 7, 1992.
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101. No slow-toxin hypothesis like Duesberg's explains the initial
C.D.C. data from 1981-1984, which show incidence of total new AIDS cases
rising in the typical exponential fashion of a new infectious disease
spreading in a susceptible population (Farr's law). Duesberg (p. 252)
states that this exponential rise is probably due to an exponential rise
in AIDS testing, overlooking the fact that the mathematical relationship
held for these four years before the HIV test was available. The _early_
departure from exponential growth for HIV infection, apparent in the
last few years, is also in accordance with Farr's law if the simple
assumption is made that the effectively _susceptible_ population is
smaller than was first assumed, and does not include most heterosexuals.
102. AIDS 7:231 -239, 1993; also see AIDS 8:803-810, 1994. From these
papers and others it is apparent that yearly risk of progressing to AIDS
is far from constant for either persons or populations. Instead, risk in
a population rises almost linearly from the date of infection for at
least seven years, toward peaks of as much as 7% per year. This does not
prevent Duesberg from routinely treating AIDS risk rates in populations
103. The necessary technology to grow the HIV virus in culture and thus
identify it, preceded the main onset of the AIDS epidemic by only 5
years, so in this sense things might have been much, much worse. HIV,
dispite many attempts, could not be grown in the lab until 1983. Genetic
engineering of viruses also dates only from the 1970s.
104. According to the Bayesian analysis of scientific induction, it is
necessary to first have some a priori idea of the likelihood of the
truth of a proposition, before one can properly evaluate the helpfulness
of new evidence which supports it.
105. Lancet 341:863-864, 1993.
106. As Ewald (note 18) argues, promiscuous behavior, or rapid
experimental passages of a virus from one lab animal to another, may
select for more virulent strains, since in such conditions viruses do
not need to keep their hosts alive for as long.
107. Lancet 340:863, 1992.
108. Hospital Practice 29(10):41-52, 1994.
109. AIDS 8:564-5, 1994.
110. I am indebted to Dr. Louis Goodman, late professor of pharmacology
at my medical school, for this alliterative description of the three
sequential social phases in the introduction of the average medicinal
111. N Engl J Med 317:192-7, 1987; Am J Med 85(2A):208-13, 1988.
112. JAMA 262(17):2405-10, 1989; AIDS 8:313-321, 1994.
113. J Acquir Immune Defic Syndr 5:120-126, 1992.
114. N Engl J Med 322(14):941-949, 1990; N Engl J Med 326(7):437-43,
115. JAMA 272:437-442, 1994.
116. N Engl J Med 328:1686-1695, 1993.
117. N Engl J Med 330:738-743, 1994.
118. Lancet 341:889-890, 1993.
119. Am J Med 85(2A):208-213, 1988.
120. CalReport, U.C. Berkeley newspaper, Fall 1991. Interview with P.H.
Duesberg; See also Lauritsen, J. Poison by Prescription--The AZT Story.
Asklepios Press, NY, 1990.
121. Preston, R.M. The Hot Zone. Random House, NY, 1994.
122. Int Conf AIDS. 1994 Aug 7-12;10(2):80 (abstract PA0200).
Dr. Steven B. Harris is an internist, clinician, and experimental
gerontologist who receives no grant money from the government AIDS
research establishment, and does not feel himself constrained in his
opinion on this subject in any way by his academic status or
occupation. He is currently a Post Doctoral Scholar at the UCLA
Department of Pathology. A graduate of the University of Utah Medical
School, Dr. Harris has published medical research papers as well as
numerous articles on both the medical and humanistic aspects of
cryonic suspension. Dr. Harris has also done considerable research
on why dietary restriction retards the aging process, and is currently
involved in a long term research project on the nutrition of the
inhabitants of Biosphere II, the self-contained ecosystem in the