THE AIDS HERESIES
A Case Study of Skepticism Taken Too Far
(c) 1994 Steven B. Harris, M.D.
_Felix qui potuit rerum cognoscere causas._
[Fortunate is the man who understands the causes of things.]
Roman maxim
"It's the virus, stupid."
Dr. David D. Ho
AIDS Researcher
A Dialogue In Inductive Frustration
Let us suppose that you have a bright and iconocl¬astic friend
who
smokes three packs of cigaret¬tes a day. You remark one day
that you
would like to see your friend quit the habit, since he
is certainly
increas¬ing his chances of lung cancer.
"Prove it," says your friend.
"Well," you begin, "the Surgeon General and a lot of
scienti¬sts 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, too, as well as a lot of
intellig¬ent business
executi¬ves."
"Sure, but all those scientists and all those executives are
paid by
tobacco companies or grants from the Tobacco Institu¬te,"
you protest.
"Well, what do you expect?" says your friend, lighting up and
taking a
satisfying drag. "Whenever any scientist takes an anti©establ¬ish¬ment,
anti©government position like that, all
grant funding is cut off. Didn't
you know that? The poor
scientists then don't have anyone else to support
their research
_but_ the Tobacco Institute. Do you expect them to starve
or
drop out of research just because they hold unpopular opinions?"
"Okay, let's look at the facts," you say. "What about the
fact that
90% of lung cancer occurs in smokers?"
"Yes," says your friend, "and that means that 10% of itÜj grandfa¬ther
smoked 3 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 association was statistically
perfect!" you
protest. "But it is certainly there. Two©pack©aªday 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
nonsmok¬ers 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 b e
immoral, since smoking causes
cancer."
"Sort of circular argument there," sighs your friend,
admiring a smoke
ring, "since that is what remains to be proved.
So you admit you don't
have any study where the two groups of
smokers and nonsmokers are exactly
equivale¬nt, and only differing
by
chance or random draw? In every study the smokers and the
nonsmokers are self©selected for their behavior, aren't they?
And bound to be different not only in smoking behavior, but also
because of whatever made them smoke or not smoke to begin with!
So
your experimental `controls' are inadequate, even if I do say
so. Not
exactly great s¬cience, if you ask my layman's opinion."
"But darnit, when smokers quit, we know their risk of dying
drops!"
"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, I'm sure, and again
that means they will
differ in some way OTHER than their not
smok ing. Again you don't have a
proper "control group" of nonªsmokers who had that very same reason, but
were _prevented_ from
quitting. Look here: did you know that for the
first year after
quitti¬ng, the risk of death for a new quitter actually
goes UP
wi th 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?
These
aren't true controlled experim¬ents. You're saying that inÜj
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 be cause of
smoking.
Moveover, maybe the act of quitting stresses people
out, and that's really
why quitters die faster in that first year
after quitti¬ng. Smoking is
just a marker for stress, you see©©
what you statist¬ics people 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 o f 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.
Because there are many intellectual steps which are not
perfectly
secure in any generalizati¬on, even the most detailed
inductive argument
only goes so far toward proof, as our fictional dialogue, which is based
on facts, demonstrates. It is also
u navoidable that the same evidence
will mean different things to
different people. In particular, it is more
difficult to induce
a person to follow a compli¬cated induct¬ive©reasoning
trail when
they dislike, or are threatened by, the conclusion at the en d.
In the medical sciences, assembling an irrefutable argument
for
causation is someti¬mes an impossible task for the same reason
it is in
astrono¬my or paleontology: the direct and definitive
experiment cannot be
done. Scienti¬sts 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
necess¬ary human
interventive experiments to perfectly assess
"risk factors" for harm may
be unethical, and so these risks
can not be studied directly by experiment
either [1]. How, then,
do we come to "know" (or confidently believe) 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 generatesÜj
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 knowle¬dge of simpler causal mech¬anisms
which we have
gained from similar systems in which experi¬men¬tation _is_
possib¬le. One of the most amazing things about the universe is
that this
kind of inference is possible at all, as Einstein once
commented.
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
pr ove to be surpris¬ingly sound (or
"robust," as scientists say). Why this should be true remains the deep
mystery that it was for
Einstein. We are only little more than re©stating
the mystery
when we note that the universe seems to have a certain degree
of
uniformity and symmetry at many levels, allowing us to correct ly
guess
at the structure of some levels of uniformity, on the basis
of knowledge
of others. Human intuition, trained by a core of
more secure direct
experimental knowledge, does seem often an
adequate tool for doing some of
this kind of guessing. On th e
basis of our past success, we expect (on
the basis of the
symmetry of past and future) that the present
inferent¬ial methods
of science will _continue_ to result in progress
toward truth in
many fields of knowledge. This progress in understanding
willo ccur even before final experimental "proof beyond all
reasonable
doubt" arrives in each case.
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 either side of the issues.
The HIV©AIDS Hypothesis, and Its Challengers.
Recently, several popular lay publications (Reason Magazine,
Spin
Magazine, the New York Native) have run articles calling
into question the
theory that the viral agent with the conclusion©asserting name, the
"human immunode¬fici¬ency virus (HIV)," is
the cause of the epidemic of
human acquired immune deficie¬ncy
disease, known as AIDS. Üj s
immune
respons¬e), 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 imp ortant. They
may in some
cases outweigh everyth¬ing else. Still, because the
smallpox virus is
necessary for smallpox (if not sufficient),
medical science still regards
it as "causal" in the sense that if
there is no microbe, there is no
illness. Elimi nate the smallpox
virus from the population and one
eliminates the disease, as was
in fact done in the 1970's.
Yet even this kind of "causal" connect¬ion 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
perhaps even that HIV is not
always necessary for AIDS, so 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 never even _contri
butes_ 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 i s 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,a nd the workings of the biomedical
scientific "establish¬ment" in
general? Or has science been completely
corrupted in working on
the cause and cure of AIDS, as many critics
suggest, so that with
this particular medical problem the scientific
method has c eased
functioning? Are we making any progress with AIDS, or
just
wasting billions each year chasing fantasies?
This essay will argue that we are not, and that when it comes
to
critics of the HIV/AIDS hypothesis, we have a practical case
in which
scientific skepticism has been taken too far. Science,
we are happy to
report, still works, and it is making progre ss
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 a certain extent) to
arguments over tast e.
This is not a thing which is taught about science
to students inÜj
What Is This Thing Called AIDS?
Scientific problem©solving begins with definitions, and in
choosing a
definition for AIDS we run immediately into the
HIV/AIDS contro¬versy.
Some of the difficulty is that definitions, even in science, are chosen
partly on aesthetic grounds.
There are utilitarian principles, too, of course. 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," (which gets promoted to a "disease" after it
stands
the test of time and we get used to it) we need to pick
our
defining ch aracteristics 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 isn't much
point
(other than pleasing some doctor's vanity) in defining a
new "disease"
which, when present, makes no difference in either
prognosis or treatment.
Nor is there any point in defining ad isease 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
charact eristics 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 intuit ive 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
infect¬ ion 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 be of little help in the question of whether
HIV
causes AIDS. Obvious¬ly, it would be nothing remarka¬ble if
we
"discovere d" that 100% of people with AIDS were infected with
HIV, if
we had previously chosen our AIDS definit¬ion to make sure
that it was so.
In re©opening the question of the cause of AIDS, what we need
then 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. Whe n we
have a suitable HIV©free
candidate definition for "AIDS," we canÜj bel, in
order to describe and
encompass in the first place? 2) If we
test our defined group, are 100%
of the people encompas¬sed 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 we are interested in.
Such a definition will
not be the standard one, of course, but
s ince the standard modern
HIV©containing AIDS definition is
unusable for this purpose, both we and
the HIV/AIDS critics are
required to construct special AIDS definitions
even to continue
to talk about the problem of causation. It's
unavoidable.
_AIDS Is An Acquired Immune Failure Syndrome_.
What is the best way to define AIDS without reference to HIV?
First,
the term "AIDS" stands for Acquired Immune Deficiency
Syndrome, but it has
always been understood (except by certain
critics, who we will come to
presently) that the amount of immun e
deficiency we are interested in, is
not a trivial one. AIDS is
the name historica¬lly chosen for a new
medical syndrome which is
essentia¬lly 100% fatal, and thus in defining
"AIDS" we are
looking for people with an immune deficie¬ncy in the range
whic h
is life©threatening, and which 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 šfunctional. In the early days of
AIDS, before
HIV was discovered, the syndrome was indeed defined
using such
opportunistic diseases (Fig. 1a), and people with
these infecti¬ons are
still included in the federal Centers for
Dise ase Control (C.D.C.)
clinical surveillance definition of AIDS
(but now only if they are also
HIV infect¬ed). We will not be
able to use this C.D.C. definition (Fig.
1c). Not only does it
assume HIV infecti¬on, but for historical,
political, and technic al 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 "oppor¬tunistic" infection.
Certainly there is a
good correla¬tion between immune function
and
what kind of opportunis¬tic infections occur, but the correlationÜj
ystem. 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 m anage
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.
When it comes to immune function, then (what we are interested
in with
AIDS), 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©lymphocyt¬e s." 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 lymphatic s).
The arm of the immune system which is control¬led most
directly by
T©lymphocy¬tes (the body's defense against viruses and fungi)
is
what is most defect¬ive in AIDS, and viral and fungal infections
are
(not surprisingly) the main opportunis¬tic infect ions which
appear and
cause death in AIDS.
AIDS is so specific in its attack that scienti¬sts eventually
found
that only one _subset_ of T©lymphoc¬ytes was initially
hardest©hit. This
was the so©called CD4+ or "helper" T©lymphocyte, which has the job of
stimula¬ting the immune system. Theo ther major type of blood
T©lymphocyte, the CD8+ or "suppres¬sor"
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.
[See appendix: "What is a CD4+ Lymphocyte"].
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+ lymphoc¬yte count of
800 to 1000, with a CD8+
count half of this. These are normal
v alues. 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
infecti¬ons might
be the result. A CD4+ count less than the CD8+ count
was once
use d as a crude marker for AIDS, but today with progress we
knowÜj he
problem.
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©threaten¬ing infectio¬ns begin to appear,
although approximately 95%
of AIDS patients survive beyond this
level of decline [2]. Another
feature of AIDS, however, is that
inevita¬bly the count grows worse over
time. Today, in the modern
era of antibio¬tics and more knowledgeable
care, 85% of AI DS
patients live to see their CD4+ lymphocyte count drop
below 50
[3]. Famous AIDS sufferer Kimberley 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 infecti¬on or other complication.
It is because of the implacable and more or less irreversible
loss of vital T©cells that AIDS remains a fatal conditi¬on, with
an average time of less than two years between the first
opportunis¬tic 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 simpl y
define "immune deficiency" as a 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. 1b).
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 definit¬ion all those
p eople who have one of the classic reasons
for a very low Tªlymphocyte count©© reasons which were well©known before
the AIDS
era (cancer, malnutr¬ition, tuberculos¬is, radiati¬on,
chemoth¬erapy,
etc). These people don't have AIDS, because the
historical
e pidemic of AIDS consisted of people with no T©lymphocytes for
no
other known reason. These people had appeared (more or less)
newly on
the scene in the 1980's with evidence of a fatal kind of
immune failure
which was _acquir¬ed_, meaning that it was an
e pidemic problem of
something "picked up" by previously healthy
people.
So let us simply collect all the people we can find with CD4+
counts
below 200 without known reason, and test them for HIV. When we do, we find
that essentially all are HIV infected, and
any who aren't don't 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 contra¬dict the simple
theoryÜj
_Enter the Critics_ Not everyone will agree to use the above
definition of
AIDS, of course. Before we go further, we will
introduce two major
critics of the HIV/AIDS hypothesis. Both are
scientists who hold Ph.D's.
Neither are physicians.
[See Appendix: "Two Critics: Duesberg and Root©Bernstein"]
The view that HIV plays no role in AIDS has been most notably
put forth
by Peter H. Duesberg, a molecular biologist specializing in a group of
vir¬uses which are related to HIV.
Duesberg's view, promulgated since
1987, is that HIV is harmless
and has
no causal role in AIDS, and that AIDS instead is caused
by drug use and
by immunosuppressive blood products (page
references to Duesberg's views
will be from his major 1992 paper
on the subject, and to a recently
published book by Ellison and
Duesberg [5
]).
At the other end of the skeptic spectrum are hybrid argume¬nts raised
by Robert Root©Bernste¬in, an associate professor
of physiology and author
of ¬¬_Rethink¬ing AIDS_ [6], the most
carefu¬lly©documen¬ted work to yet
assail the pre¬vailing medical
views on HIV and AIDS (Root©Bernstein
referen¬ces will be given in
the form of a page refere¬nce from this
book). Root©Bernst¬ein 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 Duesber¬g's original challenge, which has been the cause
of much
formal debate in the literature [7], a number of scienti¬sts, 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 an organizat¬ion called "The Group
for the Scie ntific 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
campaig¬ned to remove the requirement for HIV infection fro m
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 infect¬ed.
To be fair, there is some historical precedent for using a
definition
of AIDS which relies solely on the patient developingÜj efore HIV
testing
became available in 1985 (Fig. 1d). 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 announc¬ement of viral cause
was made the followi ng 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
suppress¬ion (higher CD4+ counts), who will _not_ progress
to
worse immune function, or quickly die. 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 critics, 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 critics
c an assemble, and these can in
turn be used as evidence to the
lay public that HIV cannot be the cause of
"AIDS."
Duesbe¬rg, for instance, 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, iss ynony¬mous with AIDS (Dues¬berg,
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 "3000 docu mented
HIV©free AIDS cases" [8]. Here again,
šDuesberg's chosen definition of AIDS is less than useful
šepidemiologically or clinically,
because people with such mild
immuno¬suppress¬ion as he uses to
define "AIDS" are not the people who are
dying, or a re shortly
destined to die (as will be made clear below).
AIDS is nothing
if not a fatal epidemic, and insist¬ing that mildly
compromised
persons who may or may not eventually get any worse be labeled
as
having "AIDS," as Duesberg routinely does, only se rves to confuse
the
issue (Fig 1e).
Perhaps following Duesberg, there is a general trend for
HIV/AIDS
skeptics to overdram¬atize levels of immune deficiency
which are not
clinica¬lly very significant. For example, RootªBernstein (p. 262), in
character¬izing a study of HIV©negative
(HIV
infection free) 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
šhe claims "represents extreme
immune suppres¬sion." It would take a
medically sophisticated
reader to k now that in AIDS 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 theyÜj
of immunosup¬press¬ion associa¬ted with a ratio of only 0.4 is
not
associated with significant risk of death by šopportunistic
infection.
Such a reader might wonder how we are justified in
calling a ratio of 0.4
"extreme immune suppres¬sion," if peopler arely die from it, as they are
known to do in AIDS. RootªBernstein does not say©© indeed, does not even
raise the issue.
Their overdrawn interpretation of the clinical
significa¬nce of
lab results is one of the places in which the absence of
medical
tra ining in the chief HIV/AIDS skeptics shows most clearly [9].
Indeed, Duesberg's paper [5] and Root©Bernstein's book [6]
each
contain descriptions of groups of HIV©free people who are
somewhat
immunosuppressed due to low CD4+ counts, but not
severely so, as defined
by our straightforward criteria of having
a sig nificant risk of
infectious death due to T©lymphocyte loss.
These immune deficient
patients in HIV/AIDS skeptic literature
are presented along with the
inference that perhaps somewhere
there exist people with these immune
suppress¬ive factors, or
šcombin ati¬ons of them, who are _severely_ are
permanently Tªlymphocyte immunos¬uppressed (as AIDS patients generally
are), and
yet still without having HIV. Duesberg and Root©Bernstein
only
have one difficulty in this argume¬nt©© neither has been able
to
actua lly _find_ any such people [9].
_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 aren't the only
ones who have been
looking for HIV©free people who are badly CD4+
lymphocyte
immunosup¬pressed without reason (i.e., good candida¬tes for
HIVªfre e 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
less than 300 (not
quite in the AIDS©class immunosuppression
range o f 200, but drawing
close). This syndrome was named "ICL"
š(idiopathic CD4+
lymphocyt¬openia), meaning "people with low CD4+
lymphocyte counts without
a medically©defined disease, or other
known immunosuppressive reason."
Why wasn't ICL simply called "HIV©free AIDS"? Critics have
darkly
suggested that the reason is politics, but in fact there
were problems
with consider¬ing these people as AIDS cases which
had nothing to do with
AIDS politics or the HIV theory. Oned ifficulty 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 produc¬ts, and
had no
evidence of sexual behavior which would have exposed them to
a
special
infe¬ction risk. Thus, as we will see, the most popular
alternat¬ive
AIDS hypo¬theses did not explain these people _either_ ©©© a fact which
did not keep them from being mentioned in nearlyÜj ot seem to
be
_acquired_ [10]. What justification was there, then, for
calling it AIDS?
Moreover, people with ICL were not only epidemiolog¬ically,
but often
immun¬olo¬gically distinguishable from AIDS cases: their
CD4+ lymphocyte
counts swung widely in response to infections and
were often much higher
than 300 (in contrast to people w ith AIDS,
whose CD4+ lymphocyte counts
tend to stay low and heading on an
ever©downwar¬d trend). ICL people also
often had low total
lymphocytes or low CD8+ lymphocyte counts, again
indic¬ating that
their immune failure did not make much distinction betw
een 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 suffering
from
opportunistic infections, did not even seem to share the implaca¬ble
death rate of AIDS [10].
Searches for HIV©negative people who have AIDS©type severe
immune
suppress¬ion have also been taken specifically within AIDS
risk groups.
Vermund reported in the United States Multicen¬ter
Cohort Study that of
the 2713 persiste¬ntly HIV©negative homos exual men in the study, who had
had a total of 22,643 blood tests,
only one significantly
immunosupp¬res¬sed man (CD4+ lymphocyte
counts persisten¬tly less than
300) was found. This man was
taking chemoth¬erapy and radiation for
cancer, and thus had a v ery
good reason other than his lifestyle to
explain his lab results
[11]. If this study is indicative, then most, if
not all, male
homosex¬uals with AIDS©range immune failure are
HIV©positi¬ve,
since it has proved very diffic¬ult to find any who are
HIVª negative.
Much the same seems to be true in IV drug users: in a study
of 1246
HIV©negative injecting drug users in New York City from
1984 to 1992, for
example, only 4 were found with CD4+ lymphocyte
counts less than 300 (if
IV drug use per se was a major caus e of
AIDS, the number should have been
far higher). In this small
group of 4 people, even though infected with
multiple other nonªHIV viruses, and with a history of heavy drug use,
immune
function was stable and without the steady decline in CD4+
lymphoc
¬yte 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
immunode¬pression, were _still_ not behaving
me dically like people with
AIDS.
So far as we know, then, so far in the United States ALL
people who
are a part of this new phenome¬non of permanently very
low (and
declini¬ng) CD4+s in high risk groups, have been infected
with HIV. This
does not prove that HIV causes AIDS, but it i s
surely an important clue.
Üj
Why Not Merely Use the C.D.C. Definition For AIDS, With HIV Taken
Out?
A persistent suggestion by critics is that it would be proper
to use
as an AIDS definition the current C.D.C. definit¬ion (which
includes all
HIV©infected people with a much expanded list of
infections and other
problems), but with the HIV criteria
re moved. 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 defin¬ition
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 peo ple
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.
Critics know that if "AIDS" is defined only in terms of
today's much
broader list of "AIDS©defini¬ng" diseases and
infections (which are meant
to be used only in conjunction with
HIV status), it is sure to be quite
true that the definit¬ion will
be fa r too broad to be prognostic. Such
opportunistic infections, as critics well know, someti¬mes happen in the
populat¬ion
occasionally even without the most severe CD4+
immunosuppr¬ess¬ion
which is characteristic of people who die with AIDS.
A study by Salvato illustrates this point [13]. In the
study, medical
records over 6 years for 1500 HIV©positive
patients were compared with
records for 1000 HIV©negative
patients who had Chronic Fatigue
Immuno¬deficiency Syndrome
(CFIDS) and evidenc e of immune suppres¬sion.
It was found that
the CFIDS patients had fatigue, lymphade¬nopathy
(swollen lymph
"nodes") and low grade fevers©© but that over the course of
6
years their problems were not severe. Only one of them developed
CD4+
lymphocyte co unts 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 v ery 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+ lymphoc¬yte count in these
patients
(not including the sin gle ICL patient) ranged from
500-1400, with an
average of 650. This was sign¬ificantly lower
than normal, but much
higher than typical for AIDS. Üj
in AIDS at
least as important as that of HIV, but this study
provides
evidence against this idea). Most inter¬est¬in¬gly, these
immunoªco¬mpromised HIV©negative patients were followed from 2 to 6
years,
and none experien¬ced progressive CD4+ lymphoc¬yte
decline
(except for the one patient with ICL, who, with treatm¬ent of
CMV
infecti¬on, showed increased CD4+ lymphocyte counts again). Such
CD4+
count stability is never seen in any random group of HIVªpositive people,
where average CD4+ count decline wi th time would
be inevitable. The
study authors' conclusi¬on:
"Even after a methodi¬cal 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 demonst¬rates that patients
with normal CD4 counts can
develop AIDS defining opportunist ic
infections [...] Upon long-term
follow-up these patients do not
appear to experie¬nce progressive CD4
depletion."
Most importan¬tly, 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,
without crossing into the deadly long term
immune fa ilure 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 (by any
good definition) 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 CD4+ lymphocyte loss) and death by opportunistic
infectio
n which is characteristic of AIDS; and it is only these
people who are
_always_ HIV infected.
How and Where AIDS First Appeared
The story of the detective hunt for the cause of AIDS is told
with wit
and clarity by Randy Shilts (an author who in 1994, at
the age of 42,
ultimately became a casualty of the šdisease
himself), in the best©selling
book _And the Band Played On_.
Oth er good histories of the early AIDS
epidemic are also available [14].
Historical¬ly, what happened in the U.S. in 1981 was that
homosexual
men began presenting to physicians in increasing
numbers with very, very
low CD4+ lymphocyte blood counts (but not
lowered counts for other
subtypes of šlymphocytes), a de¬stroyed
im mune system with lymphatic
tissue destruction, opportunis¬ticÜj n an
increasingly large scale in the
early 1980's.
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 federa¬lly©run Centers for Disease
Control (C.D.C.) in Atlanta
(more on this below). It was in the Summer of
1981 that alert
physicians brought to the attention of the C.D.C. a
mini©epidemic
of immunodefic¬iency and pneumonia caused by unusual
organisms (A
fungus called _Pneumocy¬stis 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 sexªstimu l¬ant©chemical use or illicit
narcotic use, both very common
among the first cases of AIDS, might be
somehow causing immunosuppr¬ession. Perhaps sexual contact was a red
herring©© or merely
a marker for a small and fairly tight©knit
sub©community of
peo ple who shared common interests in non©sexual
activities which
might be damaging their immune systems.
Those physicians treating infectious diseases in homo¬sexual
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 promisc¬uous as to make
contact©tracing impossible;
Weisman observed that promiscu¬ous 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 immunod¬eficie¬ncy were
e
ventually found to form sexual contact networks, of the kind
that have
always been seen by researchers using the classic
epidemiol¬ogic 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,
9 had direct or indirect (one
intermediate partner) sexual
contact w ith a single French©Canadian
airline steward, a man who
was also sick with immunode¬ficiency.
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
trans¬fusions. Soon also came reports that an
iden tical immune
deficiency of a new severe variety was now being
seen in men with
hemophi¬lia, a genetic disease in which sufferersÜj people with
hemophilia
and AIDS emphasized that, in these people, none of the
same drug or
male©homosex¬ual behavio¬ral factors were present that
had been seen in
the first group of AIDS sufferers [15].
Further, the same was true of those with "transfusi¬on©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 connect¬ion with
anyone else with an immune
problem, EXCEPT for a history of a blood
trans¬fusions years in
the past, during the time in which transfusions
were associated
w ith AIDS.
In late 1982 all this worried epidemiologi¬sts as the
reports
continued to come in. They knew that another viral disease
called
hepatitis B ("serum hepatitis") was also transmi¬tted 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
historica¬lly also
shown up early in people with hemophi¬lia, who because
of their
large pooled blood©product exposure have historica¬lly 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
contamina¬nts in donated blood for general
transfusion. Thus, the same 3
groups of people who had historica¬lly been infected with hepatitis B in
the 1970's, 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 componen¬ts that
went into those people who had later
de velo¬ped 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 homosex¬ual behavior. On
the
ot her hand, matched case©controls who had been transfused
identically
from the same blood bank but had _not_ develo¬ped AIDS
after transfu¬sion,
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
statist¬ical association of transfu¬sion©associa¬ted 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 some¬thing about normal
transfu¬sion
blood itself, or perhaps some other factor unrela¬ted t o
transÜj The remarkable fact©© from which there was no escape©© was
that
AIDS in a transfusion recipient PREDICTED the lifest¬yle of
a
blood©donor he or she had never met (a donor which generally
turned out
to be a promiscuous homosex¬ual man who had thought
himse lf to be
perfectly healthy). Nothing but an infecti¬ous
agent (or more than one)
could explain a statisti¬cal connect¬ion
between a blood donor's sexual
habits, and risk to the person
receiving the blood. As for drugs or
immune toxins, it was
impossi¬bl e 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 quantit¬ies to cause
total
immune failure in the recipient, and do it years after the
transf
usion.
Eventua¬lly, with many cases like Arthur Ashe's on record (but
showing
up in the early 1980s, earlier than Ashe's did), AIDS
looked
epidemio¬logically _very_ much like hepati¬tis B. The hunt
was on for the
microbe, or microbes, which caused the new
s yndrome. 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 wa y 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 b ut
the
most die©hard skeptics [14].
[See Appendix: "What is an Antibody? and What Does HIV©positive
Mean?"]
The Skeptics and the History of HIV and AIDS
But what if AIDS and immune failure are not really new©©
perhaps (as
some critics suggest) we just look harder for them
now that we recogn¬ize
them? Could our new theories be warping
our views so completely that by
now that we have made a new
"plagu e" out of something that was here all
the time? Epidem¬iol¬ogically, 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 infect¬ion with immune failure h ave
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
de¬ficiency and HIV infection in 1959, the
earliest pro ven case of
modern AIDS. The diagnosis was made by means of
preserved
autopsy tissue specimen HIV testing, 30 years after the factÜj
This man's death alone provides good evidence that HIV is
not a
product of deliberate genetic engineering, for in 1959
biologic science
was simply too unsophisticated to work with
lymphotropic
(lymphocyte©infecting) retroviruses like HIV, let
alone e ngineer them
[103]. HIV is an accidental infection of
humans with an African primate
virus, if it is anything at all.
The genetic material of the most common
HIV©1 strain is most
similar to that of a virus known to naturally infect
chimpanz¬ees,
and it m ay be that HIV's ancestors have been present in
Africa,
perhaps even in humans, for a very long time©© perhaps
thousa¬nds
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
indigen¬ou
s African monkey viruses, and almost certainly has been
derived from them
quite recently in virus evolutionary time (less
than several centuries).
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
homosex¬ual male, who died of strange opportunis¬tic 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
We stern Hemisphere in 1968. In corro¬bora¬tion, 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. Ap¬parently HIV
viral infection
has been present in small con¬tingents 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
1980's, with HIV infection quickly rising to 50% in some
risk©groups? The
answer may be that if it was not the simple
presence of HIV virus in the
United States that changed, perhaps
it was the social milieu.
In the late 1960's drug use became far more widespread in the
U.S.,
and the invention of the disposable plastic infection
syringe about 1970
made IV drug abuse possible for the first time
on a large scale. Also
be¬ginning around 1969 (the date of th e
New York Stone¬wall riots),
homosex¬uals in the U.S. began to take
open political power, and
concomi¬tantly one faction of male
homosexu¬als began to engage in the
high©infection risk "bathho¬use
lifestyle" chronicl¬ed by Shilts. In
addition, the Ameri can
homosex¬ual©male commu¬nity was apparen¬tly many
times re©infected
by many world©traveling disease "vectors" from other
countries in
the 1970's, including the previously mentioned 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]. Üj
What happened in the late 1970's in the U.S. is that when a
large
enough fraction of the American homosexual©male popula¬tion
became
infected with HIV, the U.S. blood supply, maintained with
volunteer
donations only, finally became contami¬nated with t he
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 forh emophilia treatment became HIV contaminated, no doubt
primarily
by IV drug users selling plasma to support a drug habit.
The
dates are not coincidental©© a crossover between initial HIV
infected
groups occurred as some homosexual men experi¬mented with
I V drugs in the
late 1970's, and male IV drug users in large
cities turned to homosexual
prostitu¬tion in order to obtain
drugs. The resulting new epidemic of
transfus¬ion and hemophi¬liaªassociated AIDS, beginning in 1982 and rising
sharply in 1984,
help ed to bring the acquired nature of AIDS into focus.
The small, but not zero, incidence of AIDS in the
American
homosexual©male and IV drug©user communities before the
late
1970's in no way subtracts from the reality of the dramatic
increase
in AIDS which took place in the early 1980's on the
heels of e xploding
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. The HIV/AIDS skeptic Root©Bernstein documents a few
cases of unexplained opportunistic infection deaths
from the medical
literature before 1980, but clearly an epidemico f immunosup¬pressive
deaths cannot be seen in the historical
record before 1980 by any act of
imagina¬tion.
By contrast, at present "AIDS" (a new epidemic of immunodefici¬ency
deaths) 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
prematu re 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 categor¬ies of mortal¬ity remain
stable.
If mere re©labeling of deaths into different categories
was a proble m,
these "newly recog¬niz¬ed" AIDS deaths would come
out of other previously
defined mortality categori¬es, and this
clearly isn't happening [21].
AIDS, the disease, may be old, but
AIDS, the epidemic, is indeed something
new.Üj [See Appendix: "Hemophilia and Life Expectancy in the 80's"]
People with hemophil¬ia, unlike homosexual men, represent
a
well©defined group with long©term docume¬nta¬ble changes in
morbidity
and mortali¬ty, since they had been well©studied as a
group before the era
of AIDS. This research shows that people
with hemophili¬a began to die of
dramatic¬ally differ¬ent things,
starting about 1982 [22] See Fig 2. A
recent check shows little
evidence of a special incidence of
opportunis¬tic diseases in
people with hemo¬philia in the U.S from the
turn of the century upt o 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 immunos¬uppres¬sed enough to be somewh
at
more suscepti¬ble than normal to bacterial infections.
Significan¬tly, however, in the years before AIDS, people with
hemophilia
had never been noted to be partic¬ula¬rly susceptible to the
more
obvious _fungal_ infections, such as candida esophagiti s, common
to
AIDS patients and others with low©lymphoc¬yte type immune
deficienc¬y.
After 1984, however, this type of AIDS©associa¬ted
opportunistic
infect¬ion and immune failure rapidly became the
single most common cause
of death in people with hemophi lia 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
increa se in raw numbers of deaths
was consis¬tent with an epidemic, or some new very toxic contami¬nation
of the clotting factor
supply. It is not consist¬ent with slower social
changes, slower
toxin or immune suppress¬ion models, multifactor¬ial
causation
mo dels, 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©labelin¬g in response to
AIDS hysteria).
Mortality figures in hemoph¬ili¬a 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 mortali¬ty, it could be inferred
that
the mortality rate for HIV©negative people with hemophilia
did not
increase much in the 1980's, if at all.
How significant was the increase in death rate for HIVªpositives in
this group? In one _Journal of the American Medical
Association_ study it
was found that in a cohort of 111 people
with hemoph¬ilia infected with
HIV in the early 1980's, one third
ha d died by 1992 [26]. The reader is
asked to 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
th e early 1980s in the United states, a quarter had been reportedÜj
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 hemo¬philia had risen as
clotting factor
treatment became available through the 1970's,
until by 1980 it was
nearly normal [23]. After 1984, however,
life expectancy in this group
began a steep decline, and by the
early 1990's was at a lower level than
at any time since before
World War II [24]. In the 1980's, total
mortal¬ity for hemophi lia
increased in all age groups above 9 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 1987-1¬989 [27].
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% progressi on to AIDS in this group) caused
death rates to rise for long
after the window of new HIV infection closed
(they are still
rising as of this writing, although clinical AIDS or
severe
lymphocyte loss (ICL) has yet to be reported in children
with
hemophilia
born after 1986).
The fact that there was a massive and silent HIV infection of
half of
the people with hemophilia in the early 1980's is beyond
question. The
HIV/AIDS skeptics' quest to divorce this event
from the epidemic of deaths
by AIDS in this same group over th e
next decade has resulted in some
remarkable and curious statements about hemophilia mortality. Duesberg,
for instance (p. 216)
quotes only older statist¬ics for hemophilia
patients from the
pre©1986 period, before AIDS deaths became very large.
His
pr actice of using randomly reported AIDS and mortality data
for
people with this disease (which is often notoriously unrelia¬ble
in
the best of circumstan¬ces [29]) instead of the much more
reliable cohort
study data, also results in figures which
minimize the impact of AIDS.
Cohort data shows mortal¬ity 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
communi ¬ty. Root©Bernstein does no
better than Duesberg at
providing updated informa¬tion in this area,
offering one paper's
1979 pre©AIDS statistics [23], without update and
without qualifica¬tion, to represent _contem¬por¬ary_ life expecta¬ncy in
people
with
hemoph¬ili¬a ¬in 1993 (p. 247). This repres¬ents very sloppy
scholarship
(something which stands out parti¬cularly in RootªBernstei¬n), but the
oversi¬ght does allow the author to skip
discussion of the pronounced and
otherwise awkward peak in life
expe ctan¬cy for hemophilia in the middle
1980's. Üj hemophi¬lia have suffered no mortality increases in the age
of
AIDS, does suggest that people with hemophi¬lia live longer than
ever
due to recent factor concentrate developme¬nt, and thus live
long enough
to die of immunosupp¬ression caused by longer tre atments with clotting
factor concen¬tra¬te, instead of from hemophilia
(Duesbe¬rg, p. 220).
Although clotting factor does indeed appear
to be mildly
immunosuppre¬ssive (albeit in a different way than
AIDS©© see appendix
hemophilia section), the main pro blem with
the hypothes¬is that clotting
factor itself causes AIDS is that
two studies of HIV©positive people with
hemophi¬lia have found
that HIV infection and not clotting factor use is
the critical
risk for AIDS. These studies found that once a person is
HIVªpositive, risk of AIDS is _not_ related to amount of clotting
factor
used or severity or type of hemophi¬lia©©©effects that
would have been
expected if clotting factor carried a significant
immune risk independent
of its HIV content [31]. Availabl e
statistics thus strongly suggest that
the known associat¬ion of
clotting factor use and AIDS risk is merely due
to the increa¬sed
risk of being infected with HIV the more clotting factor
has been
consumed; once HIV infection has occurred, it doesn't mat ter
how
much clotting factor is used.
Can a Viral Epidemic Explain the Historical Timing and Epidemiol¬ogy of
AIDS?: 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 "strawªmen." 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
opp osite 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 understand¬ing the opposing
si
de's position (straw man arguments may also, of course, be
used
deliberately solely for rhetorical purposes©© a practice generally
considered beneath respect in scientific debates). In the
HIV/AIDS
debate, straw men set up by heretics have most often
be en medical
hypothe¬ses 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
import¬ant corollar¬ies necessarily
deduced from the idea that HIV causes
AIDS, or were in other any
o ther way central to it. Other straw men are
ideas that the
orthodox scientific "establi¬shm¬ent" never put forth
seriously at
all, though they may be attacked vigorou¬sly by heretics as
though
they are current medical dogma. We will presently see sample s
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 US, and argues
th at these data are anomalo¬us (p. 2)
if the virus was transferredÜj tran¬sferred
much earlier than 1978 to the
new world, and remained at low
levels in male homo¬sexuals and inject¬ing
drug users in America
until changing social factors in the 1970's
encoura¬ged its spread
(exactly as Root©Bernstein himself indirectly sug
gest¬s), 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 epidem¬ic©© namely that
AIDS has (at least so far)
shown no clear inclination to spread
rapidly by a complete
heteros¬exual©sexual©transmis¬sion mechanism
in th e 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
inf ection in mates of HIV©positive men with
hemophi¬lia, or the
nearly zero rate of infection in U.S. heteros¬exual
prostitu¬tes
(unless they are drug users). If AIDS is an infecti¬ous
disease,
ask the critics, then why doesn't HIV infect very well?
All these arguments are against straw men, so far as the
cause of AIDS
goes. There is nothing in the HIV/AIDS theory
which demands that any
particu¬lar transmission mechanism be the
chief cause of the spread of HIV
infection in any given place, or
wh ich demands that the HIV virus be as
infectious in one locality
as another. For example, it now seems likely
from many studies
that efficient sexual transmiss¬ion of HIV 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
require¬ment(s) for efficient HIV sexual transfer eas ily
explain the
difference between spread of HIV in tropical Africa
vs. the developed
counties. They also adequately explain why a
disease which spreads well
sexually only in popula¬tions with an
extreme level of both promiscuity
and rectal mucosal traum a
(i.e., one sub©segment of Ameri¬can homosexual
men) has not yet
become a generally spread¬ing epidemic in the U.S.
It isn't that the HIV/AIDS heretics haven't come across
such
explanations. Root©Bernstein, in a good discussion of
the
epidemiol¬ogy of AIDS, admits that there is nothing especially
strange
about a sexually transmitted disease which spreads easily
in homosexual
males but not heterosexuals. Both syphilis and
hepatitis B in the 1970's
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
differen t¬ial _behavi¬or_ in the homosexual and
heterosexualÜj
Thus, Duesberg argues that a disease which restricts itself
to classes
of people in America, but not in Africa, cannot be
explained by a
micro©organi¬sm. But while he is doing so, fellow
heretic Root©Bernstein
(pp. 281©303) is noting that infectiouse pidem¬iol¬ogy in one group of
American homosex¬ual males (who may
have ulcerative sexually transmitted
diseases and in addition be
sexually infected with giardia, parasites,
amoebas, hepatitis A,
and B, shigella, salmonella, etc.), may resemble far
more t he
disease epidemiology of some African countries than that
of
heterosexuals living next door (p. 290). In this, an AIDS caused
by an
infecti¬ous agent such as HIV may behave as just as AIDS
statist¬ics
suggest it does, and yet merely follow a pattern
al ready amply
demonstr¬ated before AIDS, with many another
infectious disease.
Root©Bernstein is someti¬mes too competent a
scholar for his own good:
his Chapters Eight and Nine©© which
address the epidemiol¬ogic differences
and commonalities of U.S.
homo sex¬ual men and African heterosexuals due
to sexual practices
and social changes which appeared newly in the 1970's
and 1980s©ªnot only believa¬bly explains and refutes most of
Duesb¬erg's
epidemio¬logic problems with AIDS (Duesberg, p. 209), but
also
doe s the same with many of Root©Bernstein's own epidemic proble¬ms,
raised in Chapter One.
Unfortunately, Root©Bernstei¬n is willing to let lifestyle and
habit
differe¬nces explain epidemiol¬ogic differences when it suits
his
argumen¬t's needs, but much less willing to consider them when
they don't.
An illustrative example occurs as Root©B ernstein discus¬ses the rectal
traumas and infections which occur during
certain male homosexual
practic¬es, writing of these (p. 283©4):
"It is now accepted that such injuries and infections greatly
increase
the risk of con©current infecti¬ons (HIV or otherwise)
and of semen
gaining access to the immune system following anal
interco¬urse."
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 pos¬sibility 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
discr imination, unless some
other factor is involved."
Here, unfortunately, Root©Bernstein is wrong, and wrong for
the very
reasons that he himself dis¬cusses in the quote precedi¬ng the last. Much
like HIV, hepatitis B infection in
homosexual men _also_ correlates with
rectal trauma and receptive
anal intercou¬rse [32], and there is little
reason to believe that
the "other factor" is anything other than the
fairly straigh tforward mechanical injury that Root©Bernstein has
alreadyÜj infecti¬on). It is a chara¬cteris¬tic of Root©Bern¬stein'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.
Here is another example of Root©Bernstein's difficulties with
simple
explanations: The known fact that HIV is difficult for an
asymptomatic HIV
carrier to transmit to another person by needle
stick, or by heterosexual
contact between married couples, does
_not_ necessa¬rily argue for the
need for additional unknown coªfactors or immune suppression in the more
common cases of HIV
transmission. Low infection rates for needle sticks
may just as
easily be explained by the known fact that virus blood leve ls
in
"healthy" HIV©infected people are low. Similarly, the known fact
of
low HIV infect¬ion risks during some kinds of heterosexual
intercourse
similarly admits to several interpret¬ations, but one
which requires no
additional hypotheses is surely (and simply)
that certain kinds of
_homosex¬ual_ behavior are more dangerous
from an infection trans¬mission
standpoint (as discussed above) by
their very _mechanical_ nature, without
need to resort to the
dubious and insupportable idea that the individuals
wh o practice
them must also be grossly immunologically compromised for
HIV
infection to occur.
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 diff icult
to transfer to a healthy
individual." In fact, existing studies
establish no such thing. Studies
quoted by Root©Bernstein never
demonstra¬te that only "unhealthy" people
in known risk groups
contract HIV, only that certain traumatized risk
groups
(promisc¬uous 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 (immunologicall y)
are capable of contracting
HIV. Although men with hemophilia and
homosexual men are on average mildly
immunosupp¬ressed 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
he alth)
shows that those who seroconvert to HIV (demonstrating
HIV
infection) may initia¬lly (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 diseas e in
every sense of the terms; and
moveover that since Dept. of Health
and Human Services Secretary Margaret
Heckle¬r's dramatic announcement in 1984, most scientists have
conside¬red HIV to play thisÜj uch 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
(at worst) occasionally when some
scientist expresses a rash
opinion without consider¬ing his formal
training.
(Dr. Robert
Gallo, official co©discoverer of HIV, must by now badly
regret
his remark about HIV being able to cause AIDS in Clark Kent
[35];
but this is hardly the N.I.H. official position). The
subtitle
warning of Root©Bernstei¬n's book is _The Tragic Cost of
Pre¬mature
Consensu¬s_, and it appears from the book that it is upon
the
"HIV©only" theory of AIDS that the "premat¬ure consensus" of
the
establishment is in dire danger of settling, if it hasn't
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 import¬ant implica¬tions of the HIV©only
theory of
AIDS are that all the risk groups should develop AIDS
at approxi¬mately
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 opportu¬nis¬tic 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 t he
biological _age_ of the
HIV©infected person, scientists have
never, even at the beginning,
seriously conside¬red such a theory
as Root©Bern¬stein here lays out.
"One logical implication [continues Root©Bernstein] is that
the
immunological status of an infected person should be irrelev¬ant to
susceptibil¬ity to contagion or to the progression
from infection to
disease. Acquisition of the retrovirus should
be the sole factor
determin¬ing whether an individual develops
AIDS. Everyone should be at
equal risk for AIDS, just as
eve ryone 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©Bernste¬in's book with the impression
that the
author has single©handedly discove¬red that infecti¬ous
disease risks
depend partly on host immune defenses and host
behaviors and
environments. The reader might well decide further
that the biomedical
commun¬ity today does not in general think in
terms of individuals having
differ¬ing resis¬tances to various
disease¬s, and is accept¬ing 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 microbeÜj
xposed
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
"causali¬ty" in infecti¬ous disease in merely the sense of
"necessi¬ty"
(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 that
"The
seed is nothing, and the soil is everyth¬ing." Thus, RootªBernstein
spends many chapters assailing an idea that physi cians
have not held
since the late 19th century, and certainly have
never genera¬lly held in
the case of AIDS.
No infe¬ctious agent is usually "sufficient" to cause disease
in a
natural host, although in a laboratory (or perhaps very
occasiona¬lly in
nature) it may be sometimes true that inoculum
(microbe "dose") may be so
high as to make host resista¬nce alm ost
irreleva¬nt.
Naturally©occurr¬ing 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 succe ssfully
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 read er of
Root©Bernstein
might be surprised to learn of it after RootªBernstein 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 unprecedent¬ed.
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 pr oduce 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.
Once again, medical science has long assumed that there must
exist
host factors and other factors which explain why some
people die of (say)
tuberculosis or serum hepati¬tis 3 months
after infection, and others not
until after 3 decades©© but again
th ese factors have nothing to do with
our standard way of
speaking of infectious disease "causation." The
question of
whether eventual liver failure from chronic infectious
hepatitis
is "caused" by the viral infection, is medically simply
anotherÜj way of asking whether or not it would occur _without_ the virus.
It does not mean that other causal elements in the chain are
being denied
by medicine©© only that for very practical and
necessary reasons they are
being ignored at present (we will
return to these reasons later in
discussing polio).
"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 infecti¬ous disease know n,
including other infectious diseases
which may have latency times
to death fully as long as those for HIV. Too
much of RootªBernstein's _Rethinking AIDS_ consists of arguments that the
HIV
hypothesis needs to be re©thought because HIV infection has
str ange
properties©© properties which on close examination turn
out to be broadly
similar to those of many other infectious
diseases.
What Are the Alternatives to HIV? Early Causal Theories of AIDS.
The dissection of the disease phenomenon of AIDS illustrates
the
workings of medical epidemio¬logy as few other epidemics have.
For a time
in 1982, a number of causal theories of AIDS competed,
including several
which did not involve infectious agent s. The
fact that the first AIDS
cases were homosexual men who were heavy
illicit drug users engende¬red a
drug©use theory of AIDS which
lasted for mainstream investigators only
until it became clear
that non©drug using recipients of blood products
from m any walks
of life were develop¬ing the same immune problems. A few
skeptics, however, refused to consider the drug theory falsified by
the
finding of many non©drug using AIDS patients, but instead began
to
postulate _additio¬nal_ causes of immune failur e for each
additional
"AIDS" group identified.
This group included Peter Duesberg, who believed that drug
use caused
AIDS, but postulated additionally that people with
hemophilia had began to
suffer immune failure in the early 1980's
from long time clotting factor
use, just at the same time as gay
men and IV drug users began to suffer
from a similar immune
problem©© and that the timing was purely
coinci¬dental. The fact
that HIV infection was proved (by later stored
blood sample
testing) to have spread silently and largely concurrently
though
bot h gay men and people with hemophi¬lia a few years before
the
AIDS epidemic, was explained as being merely an early warning
of
impend¬ing immune failure in these groups. (In HIV/AIDS skeptic
lore,
HIV is a harmless bellwet¬her virus which can tell when
ce rtain members
of modestly immunosu¬ppressed groups are headed
for future immune failure,
and rapidly infects them ahead of
time).
The process of multiplying causal theories in order to
minimize HIV
responsibility for AIDS has finally cul¬minated inÜj s to
be
epidemiologically unfalsifiable, even in Root©Bernstein's view
(see his p.
92, quote below©© we will turn to this theory later).
At the time of the early drug/toxin theories of AIDS, the
leading toxin
candidates were the inhaled amyl and butyl nitrite
street drugs
("poppers") used heavily and almost univers¬ally as
sexual©experience
enhanc¬ers in the 1970's and early 1980's by t he
same fraction of
homosexual men who indulged in high risk,
promiscuous sexual practices
causing injuries to mucosal tissue,
and who also historica¬lly were the
first U.S. group to develop
AIDS as an "epidemic" [14].
Since this group was the one that suffered the first major
impact of
AIDS, a number of early studies found high statistical
correla¬tions
between AIDS risk and nearly everything to do with
this group's lifestyle.
Later, after the HIV virus was
šident ified, the C.D.C. found that HIV was
universally present and
active in such men who developed AIDS. Almost as
prevalent were
a number of other chronic viruses, such as CMV
(cytomegalovir¬us),
HZV (Herpes Zoster virus), EBV (Epstein©Barr virus),
and HSV©1 ,
2, and 6 (Herpes Simplex viruses 1,2, and 6). Many of
these
chronic viruses were found to be replicat¬ing actively in
homosexu¬als with AIDS. This state of "viral re©activat¬ion" (a
product
of immune suppression) was less common in AIDS sufferers fro
m
other risk groups, mainly because other groups had not been
infected
with as many chronic viruses in the first place.
Sorting through the drug
and infection variables among promiscuous homosexual men with AIDS was a
statistical nightmare,
although it became easier to separate out important
AIDS risks
when AIDS in other groups with different lifestyles was
considered.
Epidemiologists fought it out in scholarly journals. After
the main
battle was over, they even tried to decide who hadn't
guessed from the
beginning on epidemiologic grounds that the
problem might be infectious,
even before a specific causal virus
wa s proposed©©© occasionally
lambasting each other's past methods
in print with words like
"Neander¬thal" [37,38]. Before HIV was
identif¬ied, however, the basic
problem for epidemiologists was
that statist¬ical methods could not by
themsel¬ves suggest whi ch
lifestyles or practices (if any) were causal
for AIDS, and which
were merely an associative marker for some other
causal factor
which (perhaps) had not been measur¬ed. _After_ HIV was
identified, however, a second statisti¬cal appraisal could be take n
using
HIV status as a statistical factor, in an attempt to see if HIV
had
a closer associational (and therefore presuma¬bly more likely
causal)
relations¬hip with AIDS, than other previously identif¬ied
factors [39].
It did [40].
Much the same thing happened with other viruses, especially
when
statistics were extended across different risk groups.
Infectious HIV was
finally found to be present in essentiallyÜj
than
was seen with any other virus [41]. Furthermore, although
the
prevalence of HIV was high (as much as 50%) in certain risk
groups,
such as homosexual males in some cities, or in people
with hemophil¬ia,
the difference in HIV status for a risk group,
and those who actually
contracted AIDS within the risk group, was
by far the largest _change_
associated with any virus, increasing
from 50% to 100%.
Furthermore, as noted, most of the change in HIV infection
status had
occurred before 1984 in people with hemoph¬ilia [28],
long before the
worst incidence of immun¬osu¬ppress¬ion and increased death rate in this
community, proving at least that HIVp ositivity was not derivat¬ive of
_severe_ immunos¬uppressi¬on,
since it preceded it. As judged by CD4+
lymphocyte counts in
people who were followed over time, most of the loss
of immune
function in _individual_ HIV©positive people with
hemo¬philia,
came
after HIV infection, as well [42].
Finally, it was found in several studies that while HIVªnegative
homosexual males might be mildly immunosuppressed, their
immune function
was never seen to drop as low as AIDS©classªimmunosuppression (immune
failure), as defined by CD4+ lymphocyte
cou nts below 200. Moreover, when
followed over time, HIVªnegative homosexual men did not become MORE
immunosupp¬ressed, but
HIV©positive ones did, and in prospective studies
when men were
followed by blood tests as they actually contracted HIV,
this sam
slo w and steady decay in immune status happened to the
newly
infected group after contrac¬ting HIV infection, starting
immediately after infection. HIV, when contracted by men being
followed
in studies, was generally contracted during a time when immune
st
atus (CD4+ lymphocyte count) was reasonably good [43]. Men who
were
severely immunosuppressed (CD4+ lymphocyte counts below 200;
essentia¬lly
immune failure) with no other explanation (such as
cancer), invaria¬bly
had become HIV positive already, or in o ther
words, had become
HIV©positive _first_ [44]. Such tight correlat¬ions between timing of
immune failure and time of infection do
not hold for any other known viral
infecti¬on in immunosuppressed
people.
Lifestyle factors such as non©injected drug use and exposure
to blood
products (as in transfusions or hemophilia treatments)
did correlate with
risk of developing AIDS, but this association
could be completely
explained in the statist¬ics by the fact t hat
these behaviors (including
even perhaps nitrite ("popper") use
[45]) also increased risk of
contrac¬ting HIV. To discover which
was most importa¬nt to risk, HIV or
drug use, epidemiolo¬gists
statistic¬ally "controlled" for HIV status
(i.e., compared people
with each other only within HIV status groups),
attempting to
discover if drug use or blood product exposure was important
to
AIDS risk AFTER the HIV virus was contracted, or independently of
it.
The answer, it turned out, was generally no. By an d large,
drug use and
promiscuity were not independent variables after HIV
infect¬ion was taken
into account (with two exceptions, to beÜj
* With regard to risk of AIDS in homosexual men, Susan Buchbinder
followed
588 men in the San Francisco Men's Health Study who were
infected with HIV
at well documented times in the early 1980's
(this is known because their
sera was being stored for use i n a
hepatitis study). Of 588 men, 51% had
developed AIDS by 10
years, and 69% had developed AIDS within 14 years of
becoming HIV©positive. The San Francisco study also found that
HIVªnegative controls (both homosexual and heterosexual) had stable
immune
status, and did not develop AIDS, nor AIDS defining
diseases.
Of 538 men who became HIV©positive before 1983 in this
study, only 8%
were "healthy" HIV©positives as of Jan 1, 1993.
This group of 1 person in
12, who for reasons still not understood possibly will be long term
survivors of HIV infection, was
foun d to be quite time©stable in immune
function, though mildly
abnormal in immune status with respect to
HIV©negative controls.
[Italics]: _Significantly, the long term healthy
HIV©positive men
were as likely to have had sexually transmitted diseases
or bee n
users of illegal drugs as the other HIV©positive men in the
study
who became ill_ [46]. Those who progres¬sed to AIDS and those
who
remained healthy, reported equal and signifi¬cant use of
marijuana,
nitrite inhalan¬ts, and ampheta¬min¬es. Both group s had
similar herpes
and hepatitis B infection immunity on lab testingª© objective markers for
risky sexual behavior [46]. Regarding
people already infected with HIV,
there is no support from this
study for the idea that either of the two
possible outcom es
(eventual progression to AIDS, or the long term health
which may
be possible for a small subset of HIV©infected people)
has
anything to do with non©injected drug use or sexual habits
_after_ HIV
infection, within a fairly wide range of behavior.
A specific re©analysis of non©injected illicit drug use in
this study
[40] showed that 3 stratifications of drug use groups
into low, moderate
and heavy use, had NO statistical effect on
risk of progression to AIDS in
groups (even if done imperfectly,a s Duesberg contends, some effect should
still have been seen).
[Fig. 2]. All 3 HIV©positive drug©use groups over
several yearsªtime lost CD4+ lymphocytes with equal rapidity and developed
AIDS
with equal probability; and all 3 HIV©negative drug use group s
did
not lose CD4+ lymphocytes at all, and did not develop AIDS
defining
diseases. Crude death rates in groups agreed with CD4+
loss rates and
AIDS diagnosis rates, suggesting no bias problems
with any of these
markers, as has been suggested by critics.
Statistical association of nitrite use with AIDS disappeared when
only
homosexual men, or only HIV©positive men, were examined, and
thus nitrite
use was seen to be merely a marker for homosexual
behavior or HIV risk in
San Francisco men, not an independ ent
AIDS risk. Previous investiga¬tors
in this study had also examined
the statist¬ical effect on AIDS risk of
reported recrea¬tio¬nal nonªinjected drug use, and certain sexually
transmitted infecti¬ons,Üj
also found no association [47].
* In the Multicenter AIDS Cohort Study following a group of
1835
HIV©positive homosexual men, it was found that the 59 men
who
developed AIDS over 15 months during the course of the study were
no
more likely to have used inhaled nitrite "poppers" in the
p revious two
years than were 295 matched controls picked from the
same group, who did
not develop AIDS [48]. In another paper from
this study entitled "No
evidence for a role of alcohol or other
psychoactive drugs in accelerating
immunodef¬iciency in HIV- 1-positive indivi¬dua¬ls..." Kaslow and
coworkers found that the
proportion of HIV©positive men at enrollm¬ent who
developed AIDS
during the follow¬ing 18 months ranged from 5% to 8%, and
that
among HIV©posit¬ive men with low CD4+ lymphocyte counts, thos e
who
continued to use drugs showed no significantly higher 18-month
risk of
AIDS than non©users. No other manifest¬ati¬ons of immunode¬ficiency were
posi¬tively associa¬ted with substance use
prior to enrollment in this
study. Prior use of non©injected
drugs was not associa¬ted with low mean
CD4+ lymphoc¬yte counts at
enrollm¬ent, and continued drug or alcohol use
after enrollm ent
was not associated with greater subsequent decline in
CD4+
lymphocyte counts. The authors conclude that as used in a
large
cohort of homosexual men, psychoactive substances did _not_
enhance
the progression of HIV infection to lower CD4+ counts or
AI DS [49].
* Like¬wise, the Vancouver Lymphadenopathy-AIDS Study (VLAS)
comparing
HIV©negative to HIV©positive men found no sexual
behavior variables which
correlated with CD4+ lymphocyte counts
independent of HIV status, and for
the 25 men who developed AIDS
during
the study found no significa¬nt differen¬ces in sexual
behavior or
illicit non©injected drug use as compared with 80
controls who were
HIV©positive but remained AIDS free [50]. These studies included 78
HIV©negative men who were heavy users
of many drugs who did not lose CD4+
lymphocytes or develop AIDS
defining diseases, and also 19 HIV©positive
men who reported no
recreational drug use of any kind (and who were
followed,
incid entally, before AZT became available, yet lost CD4+
lymphocytes steadily [51]).
Again, AIDS risk in all studies correlated highly with the use
of both
intravenous and also certain non©injected drugs in
homosexual men, but
just as highly with promiscu¬ity and high©risk
sex in such men. If
non©injected drug abuse (particularly nitri te
use) was simply part of the
lifestyle which caused one to
contract the HIV virus, we would expect the
correlation between
non©injected drugs and AIDS to be high, without being
causal. To
separate out any independent effects of orally
administe¬red,
in haled, or intraven¬ous illicit drug use, it is necessary
to look
at only men who had been infected with HIV while still
showing
reasona¬bly good immune function (CD4+ lymphoc¬yte count), and
ask
the question of whether drug use THEN, after infection, had any
effect
on the risk of later AIDS (which in most cases, appearedÜj
The statistical answer was that after HIV infection, continued
inject¬ion of narcotics did seem to increase risk of AIDS, but
that use of
no other drug had any effect at all. Specifica¬lly,
several early
(pre©HIV) studies found connecti¬ons between nitrite
use by male
homosex¬uals and Kaposi's sarcoma; but (in addition to
the many studies
cited above) later studies found that this
associat¬ion between nitrite
use and AIDS disappeared after
controll¬ing for HIV status [52]. If
recreatio¬nal nitritei nhalants or oral drugs caused AIDS or Kaposi's
sarcoma, and HIV
was harmless, there should be some continued statistical
association between AIDS risk and nitrite or other drug use, even
when
looking only at HIV©positive men, or only at HIV©negative men.
No such association has been found in more than half a dozen
studies
[37©40, 46©52].
Illicit drugs did not cause AIDS, with the qualification
that
injection of drugs was implicated as a cofactor (see below). In
the
end, the "drug©only" hypothesis of AIDS pathogene¬sis failed
all careful
epidemio¬logic scrutiny. Even among IV drug us ers,
although short term
overdose deaths tend to swamp any necessarily
long©term consequences of
HIV infection [53], studies have
generally shown that HIV infection is an
additional risk factor
for IV drug users [54©56].
Injected or IV drug use, of course, proved an excellent way
to
_contract_ HIV, if needles were shared. There was no
evidence,
however, that injected drugs themselves ever led to severe
AIDSªtype immunosuppress¬ion (CD4+ lymphoc¬yte counts less than 20 0),
in
the absence of HIV. There was some evidence that IV narcotic use
could
be quite immunos¬uppressive (leading at least in part to
fatal
infections), and a co©factor for rapid AIDS development in
people
HIV©positive. Some studies found that continue d IV
inject¬ion of heroin,
but not use of other drugs, hastened
progres¬sion to AIDS in HIV©positive
people [57], but other
studies have suggested that heroin does not
decrease CD4+ counts
as AIDS does, so the immunosuppression of heroin
users is not duet o the pure drug [22]. One study [58] suggested that
HIVªpositive IV drug users who switch to methadone (an oral
heroin
substitute) may have slower progression to AIDS, but there was
no
mortality difference between using methadone and quitting
narcotics c
om¬pletely, so IV injection per se, rather than
narcotic use, was possibly
the offending practice. Studies of IV
drug users who continued IV drug
might be implicat¬ing not drugs
themselves in the rapid production of
AIDS, but rather simply
continued need le©sharing leading to acquisition
of more virulent
strains of HIV. The same was possibly true of extreme
promiscuity, which also continued to be a risk factor after
HIV©infection,
in one study [59]. Acquisition of CMV was also a
possible
consequence of
risky behavior, although the role of this virus as
cofactor was limited
at best [60].
In summary, the search for controll¬able cofactors in developÜj 't
by
much. Nor was there any evidence that avoiding these behaviors
led to
significant delays in AIDS, as compared with risk groups
such as
HIV©positive hemophiliacs, who still had a 50% chance of
death from AIDS
over 15 years.
The Critics Don't Give In
The above results have not convinced those who champion the
drug
hypothesis as the cause of much of AIDS.
Duesberg, for example, accepts a causal role for drugs in
AIDS (and
for that matter, also for smoking in the causation of
lung cancer:
Duesberg, p. 213) on much the same grounds which he
rejects for assigning
a causal role to HIV©© namely, epidemiol ogi¬cal correl¬ati¬ons and
suggestive lab experime¬nts. The irony of this position is that the
correlations are not
nearly as good statistic¬ally for drug use and AIDS
as they are
for HIV infection and AIDS, and lab animal experime¬nts
with
retroviruses mimic human AIDS immunodefi¬ciency far more
precisely
tha n lab animal experiments with drugs have. Nitrite
recreational drugs, for instance, do not cause lymphocyte
abnormalities,
lymphadenopathy, or CD4+ lymphocytes to disappear almost
completely at the same time CD8+ lympho¬cytes rise, as in AIDS©©© yet
ch
ronic retrovirus infection of experimental animals routinely
causes these
odd and specific phenomena. Nor have opportunistic
infections or
lymphomas ever been seen in a nitrite treated
animal, and yet these are
hallmarks of lentivirus infections.
Appa rently, Duesberg's standards of
evidence change greatly with
the hypothesis he likes.
Duesberg actually accused a group of scientists of data
fabricat¬ion
[61] after a paper in _Nature_ reported findings not
in line with
Duesberg's drug hypothesis [40]. Duesber¬g's letter
to _Nature_ calling
some results of the paper from the San
Fran cisco Men's Cohort study less
than honest, was refused print
by _Nature's_ editor, with an
accomp¬any¬ing edi¬torial [62]. An
independent institutional review board
cleared the researchers of
Duesberg's charges, which have been answered in
print by the
a uthors [63].
In the study printed in _Nature_, the authors had found in
the San
Francisco cohort men no connec¬tion between the four most
commonly
reported kinds of illicit drug use and later progression
to AIDS, after
results were controlled for HIV status (i.e.,
heavy drug users had the
same likelihood to progress to AIDS as
light users, if HIV©positive, but
HIV©negative men did not
progress toward immune failure, no matter what
their drug use).
[See Fig 3]. Moreover, these results held also for the
1985©1986p eriod before the drug AZT (the use of which Duesberg
has
suggested may cause AIDS to develop in HIV©positive people) wasÜj
Duesberg's objections were that the study had not controlled
carefully
enough for drug use between HIV©positive and HIVªnegative groups in the
study, but Duesberg did not address the
obvious question of why such
considerable controlling for drug
use a s _was_ done, had absolutely no
effect on differential AIDS
risk seen. Duesberg also complained after
seeing the raw data
that supposedly "AIDS©defining" diseases in the
HIV©negative
group had not been counted as "AIDS," despite the author's
denial
that this had happened. Here apparently much depends on
a
disagreement between Duesberg and others as to what constitutes
clinical
AIDS. A recent article in _Science_ suggests that one
difficulty is over
the question of whether mild opportunistic
conditions such as oral candida
(thrush) constitute clinical
"AIDS." Duesberg, ever ready to define AIDS
broadly, argues they
should [22]. In any case, the specifics of
Duesberg's reanalysis
of the Nature paper have never been printed, and
death rates in
this stud y again underscore the fact that Duesberg's
broadly
defined "AIDS," which strikes HIV©negative people, somehow
does
not kill nearly as well as the standard variety.
As for worsening immune failure in groups over time (seen as
declining
CD4+ counts in the HIV©positive men, independent of
drug use, but not in
HIV©negative men, no matter how much drug
use), Ellison and Duesberg have
noted that this phenomenon isn'ts o clear before the data is reduced to
averages. This, however,
seems a trivial complaint (making group trends
clear is _why_
scientists calculate group averages).
The bottom line is that, for now, the drug hypothesis of AIDS
has no
epidemio¬logic associational evidence behind it which is
independent of
HIV infection. HIV infection, by contrast, is
heavily associated with
AIDS risk, independent of drug use.
[See AZT Section in Appendix on the question of whether AZT
contributes to
AIDS]
Previously Known Viruses
Because Duesberg does not regard any virus as being capable
of causing
a fatal disease long after the body has generated an
antibody immune
response to the microbe, he rejects a causal role
for any virus in AIDS.
The evidence for multiple viral infec tions in many of the early victims
of AIDS, however, has caused
many such "non©HIV virus" theories to be
generated and tested.
For example, though Root©Bernstein does not regard
HIV as always
a šbystander virus in AIDS, he does regard other viruses in
A IDS
to be just as important as HIV. Are the other viruses (CMV,
EBV,
Herpes, etc.), or at least their antibodies, present as often in
AIDS
as those of HIV? Üj
true only
in homosex¬ual men with AIDS (where co©infection with EBV and
CMV
along with HIV is nearly univers¬al). In science, situati¬ons
in
which several possible causes are all nearly 100% associated with
a
particular effect do not help us to differen ¬tiate causali¬ty, a
point
that Root©Bernstein makes (p. 279©280) without taking the
next logical
step. What are needed with viral studies and AIDS,
obviously, are AIDS
cases where some of the putative viral causes
are present less frequently
than 100% o f the time. Such cases
are available. In both hemophilia and
transfusion©associated
AIDS, HIV infection is universal, whereas infection
and reªactivation with other viruses, such as CMV and EBV, is variable
[64]. In short, some people with AIDS in these groups have never
been
infected with CMV or EBV viruses at all in the past©© but
all have been
infected with HIV.
Much the same is seen to be true when people in AIDS _risk_
groups are
examined for antibodies to various viruses. EBV or
CMV antibodies alone,
in themselves, are not predict¬ive for
development of AIDS in risk groups
where exposure prevalence of
CMV
and EBV is much less than 100% [60,65], a fact that
eludes
Root©Bernstein, who writes šwith too much generality that CMV
and
EBV šantibodies are "synonym¬ous with AIDS" (p. 103). In fact, as
we
have noted, CMV and EBV antibody are not unusually common i n
either
HIV©positive people, or AIDS patients, from groups such as
štransfusion
recipients, and people with hemophili¬a, in some
countr¬ies [66]. Nor are
antibodies to these viruses a clear
extra risk factor for development of
AIDS, even in HIV positive
people [60]. Cases of people multiply
infected with many chronic
viruses, but not HIV, are also well known, and
such people are
easily differentiable from AIDS on clinical and
laboratory
grounds (see the study of Salvato [13] above). Despite
RootªBerns tein's suggestions, statistical associations
clearly
differentiate HIV from other viruses in AIDS.
It is necessary for heretics to come to grips with the
crucial point
(hard to explain if HIV has no causal role in AIDS)
that the utility of
HIV antibody screening is _exactly_ that a
positive HIV screen, found in
only 0.3% of the population, is
predi ctive of risk for development of
severe immunodef¬iciency,
i.e., 50% risk of developing severe,
life©threatening immunodeficiency within less than 15 years. By
contrast, EBV and CMV
viral immunity and antibodies are acquired by most
(well over
50%) of a ny normal, healthy population of humans during
a
lifetime, and thus are not predictive of future severe
immunodeficien¬cy and death, except to the extent that they are
markers
for membership in particular risk©groups (such as gay men). Like
many other factors, the association of viral antibodies with
AIDS across
risk groups disappeared when people were compared
within groups©© except
for HIV, where the association persists. Üj
most simple
test of prognostic value. As any life or medical
insurance
company knows, HIV infection status (HIV©positivity status)
is
more surely predict¬ive of future death due to future severe
immune
failure than any other known piece of medical infor It is necessary for
heretics to come to grips with the
crucial point (hard to explain if HIV
has no causal role in AIDS)
that the utility of HIV antibody screening is
_exactly_ that a
positive HIV screen, found in only 0.3% of the
population, is
predi ctive of risk for development of severe
immunodef¬iciency,
i.e., 50% risk of developing severe, life©threatening
immunodeficiency within less than 15 years. By contrast, EBV and
CMV
viral immunity and antibodies are acquired by most (well over
50%) of
a ny normal, healthy population of humans during a
lifetime, and thus are
not predictive of future severe immunodeficien¬cy and death, except to
the extent that they are markers
for membership in particular risk©groups
(such as gay men). Like many other factors, the association of viral
antibodies with
AIDS across risk groups disappeared when people were
compared
within groups©© except for HIV, where the association persists.
Üj ¬mat¬ion
related to viral infection. In science, if one has a list
of
factors which are independently statistica¬lly associated with
an
effect (such as AIDS), this does not prove that any of them are
causal.
If one of these factors (such as HIV infectio n) is far
more highly
associated than any of the others, however, it
becomes difficult to argue
convincingly that it is no more
important than the others are. We will
return to this point
later.
Why Did Medical Science Historically Implicate HIV?
The standard method of trying to identify a new virus in a
new disease
suspected of being caused by a new virus, is to
attempt to culture a new
virus from an infected person, then show
that antibodies to this virus are
present in all people with the
d isease, but less often in people who are
not ill. It is also
helpful to show that persons develop antibodies to
the virus
during the acute illness.
Sometimes viruses can be very difficult to culture in lab
glassware.
This is especially true of viruses which grow in
human T©cells©© cells
which could not be grown well without
certain growth factors only
discovered in the 1970's. In 1980,
Dr. Robe rt Gallo of the NIH formally
reported isolating a virus
he named "Human T©cell Leukemia Virus," (HTLV)
which infected Tªcells and which was thought to cause some cases of
T©cell
leukemia in humans. This virus was a retrovirus (a virus
type
associated wit h cancer causation), and it was a distant relative
of
the "Feline Leukemia Virus" (FeLV) which caused leukemia in houseca¬ts.
Because the transfusion results had shown that AIDS could
be
infectious, and because AIDS patients had abnormal©looking Tªcells
which looked something like those from retrovirus©infected
animals, or
T©cells in cultures infected with retroviruses, earl y
AIDS researchers
began hunting a T©cell retrovirus. In early
1983, a team of French
scientists led by Dr. Luc Montagnier
isolated a new retrovi¬rus which they
reported in May of that
year, calling it eventually
Lymphadenopathy©Associated Virus
(LAV), b ecause it had been isolated from
tissues of a French
patient with enlarged lymph tissues, or
"lymph¬adenopathy" (this
man died of AIDS in 1988). The French had been
alerted to the
possibility of a retrovirus in AIDS patients by an American
team,
led by G allo, which was convinced that the AIDS virus was
another
variety of HTLV. It wasn't. Üj [See appendix: "Montagnier,
Gallo, Slip©Ups and Wrong Paths"]
The new virus discovered by the French was a tiny,
spheric¬al,
membrane©coated, protein©studded virus 1/100th the diameter of
a
lymphocyte, with an inner protein viral core shaped like a
truncated
cone, with a dense base. Under the electron microscop e
it didn't look
like the feline FeLV or the human HTLV leukemia
viruses (Fig 4), which had
no distinct cores. Eventual¬ly, the
LAV virus was correctly understood
that Summer by the French team
not to be a leukemia virus as they had
thought, but rather t o be
the first human "lenti¬vir¬us." This
hypothesis was first formulated when Montagn¬ier, at a suggestion from a
colleag¬ue, began
reading about "lentiviruses" or "slow viruses" ©© a
class of
animal retroviru¬ses he'd never previously heard of. In on e
book
was an electron microgr¬aph of the "equine infectious anemia
virus,"
a virus which sometimes produced a familiar©sounding
immunodefi¬cie¬ncy
and lymphadenopathy disease, after long latencies, in horses.
Montagn¬ier found himself looking at a tiny
membrane©coated virus shaped
like a sphere, containing a protein
viral core in the shape of a narrow
cone [67]. Antibodies
against the horse virus cross©reacted with
Montagnie¬r's new
virus, but not with Gallo's HTLV.
Most importantly, coded AIDS patient serum provided by the
C.D.C.
contained antibodies to LAV, but not HTLV©III, and
Montagnier proved his
lab could easily pick out AIDS samples from
normal samples in the C.D.C.
material, without knowing the codes.
T hus, Montagnier had his answer,
but nobody would believe him for
almost a year.
Lentiviruses and Latent Diseases
Most readers will remember that viruses in some sense are not
complete
living organisms. Animal viruses when outside cells
don't metabolize, and
cannot reproduce or grow by themselves.
Instead, most viruses are little
more than tiny floating package s
of genetic material, sometimes without
much other equipment.
Viruses can šreproduce themsel¬ves only by entering
a living cell
and commande¬ering the cell's synthetic machinery to subvert
it
into making more virus particl¬es, which are then, in turn,
re leased
to infect more cells.
A metaphor for a virus would be a truck©load of blueprints
which rolls
into a completely automated factory, and once there,
is somehow able to
use the bluep¬rints to control the factory's
machinery to cause it to make
more sets of blueprints and moret rucks to carry them, all of which are
then assembled and sent
out to take over more factori¬es.
[See appendix: "How Do Viruses Hide From the Immune System?" and
"What is
a Retrovirus?"]Üj
Members of one class of viruses use RNA as their genetic
material, and
are called "retrov¬iru¬ses," because their synthesis
of DNA from RNA
proceeds retrograde, in the opposite direction to
what is "normal" in the
rest of biology. Retroviruses avoid the
body's immune system by inserting
themselves into the DNA of the
host cell.
Most retroviruses cause no major disease, but not all are
harmless. A
sub©class of retro¬viruses, called "lentiv¬iruses" is
capable of slow
infec¬tio¬ns resulting in death. Lentiv¬iru¬ses
typica¬lly spend lengthy
waiting periods in hiding in the c ell
nucleus (music lovers will
recog¬nize the same root as in _lento_,
meaning "slow"), and even
lentiviruses may never cause overt
disease in their natural hosts.
Sometimes, however, the lentivirus disease produced after a latency
period can be devasta t¬ing,
though sometimes diffic¬ult to detect
epidemi¬ologically due to the
delay between initial infect¬ion¬ and death.
Lentivi¬ruses were named in 1954 in honor of several very slowªacting
brain infecti¬ons of farm animals. The classic example was
a sheep
disease with a latency as long as a decade, called
"visna" (an Icelandic
word for "shivering"). Visna wiped out
m ost of the sheep populat¬ion of
Iceland in 1939 because it had
not been realized in 1933 that
apparently©well sheep brought to
the island from Germany had actually been
carrying a latent
disease. The ability of visna to cause disease many
years after
inf ection has since been demonstrated in a series of
controlled
experiments with sheep [68]. The visna agent proved
eventual¬ly
to be a retrovirus and a lentivirus, and the ominous pattern
of
the visna epidemic will become familiar to the reader during thec ourse
of this essay, as we discuss other better©known viruses in
this unique
class. HIV, our main subject, is a lenti¬virus. It
is clearly related to
the visna sheep lentivirus in struct¬ure and
genetics, and even more
closely to "equine infecti¬ous ane mia
virus" and several other
immunosuppressive lymphoc¬yte©infecting
(lymphotropic) animal lentiviruses
the reader is shortly to meet.
How To Dismiss All Laboratory Animal/Virus Experiments
Before we meet these viruses, we should note that molecular
biologist
Peter H. Duesberg's scientific heresies do not only
extend to his views on
HIV. Duesberg, for instance, is unable to
believe that any disease which
confines itself relatively rigid ly
to classes of susceptible people, can
qualify as a genuine
communicable disease caused (in any sense) by a
treatable
microbe. In these diseases, Duesberg tellingly prefers to
focus
entirely on the host, refusing to consider the role of the
microbe
at all (as we will see, the issue of "causation" is a
difficult one for
HIV/AIDS skeptics). Thus, Duesberg and Ellison
dismiss (for example)
Legionnaire's disease and hepatitis C as
fantasy diseases made up by the
biomedical establishment forÜj ses of profit and self©aggrandizement (pp.
35©38, 57©59).
Duesberg also does not believe in slow infections in general. The
modern physic¬ian perusing Ellison and Duesberg's AIDS book
will be
astounded to read that syphilis | | |
