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From: (Steven B. Harris )
Subject: Re: Alternative Treatment For HIV Infection
Date: 18 Sep 1995

In <43k5rj$> (MackayR) writes:

>Dr. Harris is right (although rude). We cannot draw broad conclusions
>based on this one tragic story. But I think this case history points out
>the dangers of western medicine run amok.
>Fifty-eight seperate medications! WOW! Has anyone done a double blind
>study on the interactions of these 58 meds? Is it possible? Who was the
>primary physician? Was any single physician in charge or was the patient
>shuffled from specialist to specialist adding to his medical cabinet as
>he went along? Fifty-eight medications! Is this clinically competent?
>Does it meet standards of practice? Is this kind of prescribing taught in
>medical school?
>While this one story does not erase the tremendous value and competancy
>of western medicine and all the good doctors out there, it brings to
>light the weaknesses of our current system of administering health care.
>I simply can't imagine one physician prescibing 58 medications to the
>same patient.

  Me either, but you can certainly see dozens used at the same time in
an AIDS patient.  It's hard to imagine AIDS unless you've treated it.
I can tell you, having lived through the epidemic as a physician from
beginning to present, that even veteran infectious disease specialists
have been totally shocked, and have completely changed the way they
practice.  With most diseases, you try one drug or antibiotic after
another.  With AIDS, you generally just keep adding them on (and if you
don't, your patient gets infected with something else, or dies).  And
yes, with this routine, survival is now better in AIDS than at any time
in the past.  In 1983, survival from onset of major symptoms (first
major opportunistic infection) was 7 months.  Today, it is in excess of
2 years.

   By the way, even with AIDS I simply don't believe that many
medications all at once-- although I've seen patients on half that
many, legitimately.  If somebody claims 58 at once, let them list them
here, or else shut up.  I really hate the spread of urban myths when
they are aimed at my profession.

                                      Steve Harris, M.D.

From: ((Steven B. Harris))
Subject: Re: Aids risk
Date: 23 Jun 1995

In <3se7pp$> (Todd Miller
) writes:

>(first quoting an earlier post of mine)
>>>All I was trying to say, which was an answer to the question
>>>originally posed in this thread, was that what comes over the
>>>news is quite different from what is published in the literature.
>>>When was the last time you saw on TV that the risk of transmission is
>>>about 1 in 1000 unprotected heterosexual contacts with an HIV
>>>positive person?
>>Since this is true only of a person who doesn't have another sexually
>>transmitted disease (something you cannot be sure of), it would be
>>wrong for the news to announce it as a general figure.  It applies to
>>monogamous married couples where one is HIV positive and doesn't know
>>it (as in hemophiliacs from 1982-1985), which is where the figure
>>comes from in the first place.
>Catch up on your reading Steve.  De Vincenzi (NEJM 331: 341, 1994)
>studied couples where they *were* aware of the partner's positive
>status.  Even though they were asked to wear condoms during the course
>of the ~2 year study, only half did.  Of these, 90% of the negatives
>remained negative; in the group wearing condoms none seroconverted.

Yes, I know this study.  That's NOT where the figure of 1 in 500 comes
from.  Yes, this study does show that some people are dumb (or maybe
didn't believe in the HIV/AIDS hypothesis).  If you figure out how many
times the average old married couple has intercourse in 2 years,
however, the figures are consistant with previous studies.

>>But such people now already know this figure from their doctors, and
>>don't need to hear it from Barney the Dinosaur.
>Why not?  My doctor never told me that anyway.

What, are you married to somebody who is HIV-positive?  Again, my point
is that the low probabilities apply to married couples, not people who
are (say) dating at lot in college.

>  Shouldn't everybody be
>aware of this, given that we've been told that sleeping with someone is
>equivalent to sleeping with all their sexual partners (implies 100%
>transmission, doesn't it?)

What medical publication did you read that crap in?  This is the kind of
thing people are told, but by their churches, not Dan Rather.  And
certainly not by the New England Journal of Medicine.  And hopefully not
their doctors, but you never know (there are some redneck doctors, sad
to say).

>>For the average heterosexual your odds of getting HIV from an HIV
>>positive person in a since act of intercourse can apparently be
>>anywhere from 1 in 1000, to 1 in 12, depending.
>I don't know where 1 in 12 comes from but maybe you could back it up
>with a reference.

Included in next message, about mycoplasmas.

>>These risks are not just published in the Scientific literature.
>>There was a discussion of AIDS risk in heterosexual intercourse in
>>SKEPTIC magazine (in many bookstores and newsstands) just 2 months
>>ago.  You know, that right-wing publication voted one of the year's 10
>>best by the well known fascist rag, _Library Journal_?  <g>.
>That's wonderful Steve, but I don't subscribe to SKEPTIC and the
>library is just across the street from where I work.  As long as we're
>advertising, I would also suggest the writing of Peter Plumley, F.S.A.,
>a member of the American Academy of Actuaries.  His material is free,
>and I would be happy to forward a relevant article of his to anyone who
>is interested.

Why not post it here?  Or has it been already?  I seem to remember it...

                                                Steve Harris, M.D.

From: ((Steven B. Harris))
Subject: Re: Montagnier (abstracts on mycoplasma; heterosexual transmission 
Date: 24 Jun 1995

From Steve Harris, M.D.

   Here are a few abstracts on the mycoplasmas "associated" with
AIDS.  They are as remarkable for what they don't say, as what
they say.  Mycoplasmas (particularly M. fermentans) have been
isolated from AIDS patients, though none is as nearly universal
in them as HIV.  These organisms seem to be more common in HIV-
positives than HIV-negatives, but the same is true of many, many
other organisms, especially if the "HIV-positive" group
considered consists of HIV-positive gay males.  So far as I can
see, no attempt has been made to look for mycoplasmas in any
AIDS group other than gay males, which is the classic way to test
infectious cofactor theories.  The important question of whether
mycoplasmas are associated with AIDS risk within the HIV-positive
group, which is necessary as a first step to establish them as
cofactors, has not been answered (in this, mycoplasmas are much like

    Acute Mycoplasma fermentans infection has been described as a
fulminating pulmonary disease is non-immunocompromised humans.
The organism may cause a nephropathy syndrome in AIDS.  Injection
of the pure organism produces a slow wasting disease in one type
of monkey, but without obvious other immune similarities to AIDS.
I have not been able to find a paper trying simultaneous M.
fermentans with SIV infection of monkeys, or HIV infection of
chimps.  Conclusion: Montagnier's mycoplasma theory is
intriguing in vitro, but like so many infectious cofactor theories,
so far remains without good epidemiologic or in vivo experimental

Sasaki Y; Honda M; Naitou M; Sasaki T.
Detection of Mycoplasma fermentans DNA from lymph nodes of
acquired immunodeficiency syndrome patients. Abstract: Biopsy
samples from seven patients with acquired immunodeficiency
syndrome were screened for Mycoplasma fermentans, M. pneumoniae
and M. genitalium infection by the polymerase chain reaction. M.
fermentans DNA was detected in four patients. Various tissues
were evaluated and the mycoplasma were mainly detected from lymph
nodes. Moreover, mycoplasma genus-specific DNA was isolated from
peripheral blood mononuclear cells of asymptomatic human immunod-
eficiency virus(HIV)-infected individuals (two of 31 HIV-infected
individuals). These data suggest that mycoplasma infection in
AIDS patients is not uncommon.
Microbial Pathogenesis, 1994 Aug, 17(2):131-5.

Blanchard A; Montagnier L.
AIDS-associated mycoplasmas.
Abstract: Previously, we hypothesized that mycoplasmas could act
as cofactors accelerating the progression of HIV disease. In the
present paper, we review the current knowledge on three
mycoplasmas (Mycoplasma fermentans, M. penetrans, and M. pirum)
that have been implicated as these putative cofactors. All three
mycoplasmas have been isolated from patients with HIV infection,
and serological studies have suggested that the presence of M.
penetrans could be associated with HIV infection. These myco-
plasmas share the capacity to hydrolyze arginine and ferment
glucose as well as to attach to and invade eukaryotic cells. The
possible mechanisms that could allow mycoplasmas to influence HIV
pathogenesis, specifically through the activation of the immune
system or the production of superantigen or by contributing to
the oxidative stress observed in HIV-infected subjects, are
discussed. These studies have offered and will continue to offer
major contributions to a better understanding of mycoplasmal
flora in humans and have begun to unveil some of the mechanisms
of virulence of these organisms.
Annual Review of Microbiology, 1994, 48:687-712.

Teel LD; Finelli MR; Johnson SC.
Isolation of Mycoplasma species from bronchoalveolar lavages of
patients positive and negative for human immunodeficiency virus.
Abstract: The rates of isolation of Mycoplasma species from
bronchoalveolar lavages of human immunodeficiency virus (HIV)-in-
fected patients and HIV-negative patients were compared. Mycopla-
sma species were more frequently isolated from HIV-positive
patients. In most cases, a known pulmonary pathogen was also
identified. All samples tested negative for Mycoplasma fermentans
by PCR.
Journal of Clinical Microbiology, 1994 May, 32(5):1387-9.

Tully JG; Shih JW; Wang RH; Rose DL; Lo SC.
Titers of antibody to Mycoplasma in sera of patients infected
with human immunodeficiency virus.
Abstract: One hundred sixty-seven sera collected from human
immunodeficiency virus (HIV)-negative blood donors (n = 41),
asymptomatic HIV-positive patients (n = 75), and patients with
AIDS (n = 51) were compared in a metabolism inhibition serologi-
cal test employing antigens to four distinct Mycoplasma species.
The proportion of sera with antibody titers of > or =
1:32 to Mycoplasma genitalium was significantly higher for
patients with AIDS than for HIV-negative blood donors. Serologi-
cal relationships between Mycoplasma pneumoniae and M. genitalium
as well as the possibility of increased susceptibility of AIDS
patients to infection with these two mycoplasmas might account
for this finding. Few sera showed antibody responses to Mycopla-
sma pirum or Mycoplasma fermentans.
Clinical Infectious Diseases, 1993 Aug, 17 Suppl 1:S254-8.

Montagnier L; Blanchard A.
Mycoplasmas as cofactors in infection due to the human
immunodeficiency virus.
Abstract: Results obtained in vitro suggest that mycoplasmas act
as cofactors with the human immunodeficiency virus (HIV) in the
development of AIDS. Mycoplasmas, including Mycoplasma fermenta-
ns, Mycoplasma pirum, and Mycoplasma penetrans have since been
isolated from HIV-infected individuals. In addition, M. ferment-
ans has been detected by different investigators in numerous
tissues and in the blood of HIV-infected patients. Higher titers
of antibodies to M. penetrans have also been found in HIV-infec-
ted patients as compared with noninfected individuals. These
mycoplasmas have been shown to have the capacity to invade cells
and to be potent immunomodulators. Although there is no doubt
that mycoplasmas are found in HIV-infected individuals and
eventually produce systemic infections, their pathogenic role in
association with HIV remains to be determined.
Clinical Infectious Diseases, 1993 Aug, 17 Suppl 1:S309-15.


Finally, here is a paper on HIV-transmission to Thai soldiers by
prostitutes, showing risks on the order of 1 in 18 to 1 in 30 per
act of heterosexual intercourse, with a broad range of risk.  I
have not been able to locate an earlier paper which found the
risk to be about 1 in 12 for Thai soldiers to contract HIV, if
they also contracted another classic sexually transmitted disease
during the same visit to a prostitute-- but no doubt the
bibliography of this paper lists the other.

AU  - Mastro TD ; Satten GA ; Nopkesorn T ; Sangkharomya S ; Longini IM
TI  - Probability of female-to-male transmission of HIV-1 in Thailand
      [see comments]
AB  - The epidemic of human immunodeficiency virus type 1 (HIV-1)
      infection in Thailand has allowed an estimate to be made of the
      probability of female-to-male HIV-1 transmission per sexual
      contact. In a study of 1115 21-year-old male military conscripts,
      of whom 77 (6.9%) were HIV-1 seropositive, sex with female
      prostitutes was identified as the principal mode of HIV-1
      transmission. With a mathematical model including data on
      conscript's age at first sexual contact, frequency of sex with
      female prostitutes, and province of origin; as well as
      province-specific HIV-1 seroprevalence of prostitutes, we
      estimated the probability of HIV-1 transmission per sexual
      contact to be 0.031 (95% confidence limits [CL] 0.025-0.040).
      Allowing for random error in the self-reported frequency of
      contacts, the estimate was 0.056 (95% CL 0.041-0.075). The
      transmission probability was significantly greater among men with
      a history of sexually-transmitted diseases. These estimates are
      substantially higher than analogous estimates made in North
      America. This high per-act probability of heterosexual
      transmission helps to explain the rapid spread of HIV-1 in the
      emerging epidemic in Thailand and perhaps in other countries
      where HIV-1 transmission is predominantly heterosexual.
CM  - Comment in: Lancet 1993 Jan 22;343(8891):186-8
SO  - Lancet. 1994 Jan 22;343(8891):204-7.

From: ((Steven B. Harris))
Subject: Re: Aids risk
Date: 24 Jun 1995

In <3sgohr$>
(Goh Yong Wah) writes:

>James Scutero ( wrote:
>> Elizabeth Glaser was infected by HIV through a blood transfusion while
>> she was pregnant. She passed HIV on to her children through childbirth.
>> Her husband did not become infected because HIV is very difficult to
>> transmit from a female to a male. No conspiracy here, sorry.
>> -James M. Scutero, original proponent of
>> WWW homepage:
>HIV is very difficult to transmit from a female to a male?????!!!????
>How is this possible????
>I thought the chances are equal between male and female....
>care to explain?
>either via post or email....Thanks!
>yong wah

Apparently it's about twice as difficult to pass from female to male
with vaginal intercourse.  If you add any anal intercourse, in which the
receptive partner is also known to be at considerably more risk (from
studies of gay men) the risk goes up for women as well. (This assuming
hetero anal intercourse is like gay anal intercourse, which is maybe a
big assumption).

                                         Steve Harris, M.D.

From: ((Steven B. Harris))
Subject: Re: Why won't the anyone address this ???
Date: 28 Jun 1995

In <3sl1vo$> (Jerry
Bostick) writes:

>Hi all, *again*, this is a repost which *no one* addressed.
>I really wan't to know if i'm screwed up here ??  (Email, or
>post). But i really think this is an important aspect of this
>problem (as i think it's true and can't understand why it's so
>surpressed by the media).
>------------------ previous post --------------------------
>Hi all,
>I seem to be suffering under a notion (which i've picked up
>from sporadic medical sources) that AIDS (read HIV) is really
>hard for a man to contract through vaginal intercourse.  I've
>heard that the virus is really weak in a hostile environment
>(i.e. needs warm, moist environment at all times) and that
>climbing up a man's urethra and infecting him is almost impossible.
>And, that hetro guys only get AIDS from vaginal intercourse if they
>have an open sore on their penis.
>Please, don't flame me, i'm only wondering if anyone else has
>heard this kind of thing???

Jerry, we've been addressing this in quite a few posts, just none
specifically to YOU.  Lurk awhile and learn.

It is thought from studies of married people that that the chance of man
getting HIV from an HIV-infected woman with no other diseases, is about
1 in 500 to 1 in 1000 per act of intercourse.  However, there is
indirect evidence that the chance is much higher if she is actively ill
with HIV-- either in initial infection (where it could be mistaken for
flu), or else in the last stages of HIV, when a person can become
markedly more viremic (more virus in the blood and secretions) months
before they fall apart, or even start to look very ill.  If you get the
wrong person your odds probably go way up.

There is also evidence that people infected with other "venerial"
(sexually transmitted) diseases (and not necessarily with sores on
penises-- urethritis may serve as well) are at much higher risk to get
HIV from an infected woman.  For Thai soldiers seeing prostitutes, the
HIV risk varied from 1 in 12 acts to 1 in 30 or so.  HIV spreads
heterosexually quite easily in the "VD belt" in subsaharan Africa, for
probably the same reason.  Since "VD" is common in some populations in
the US (visit a college student health clinic sometime), there is
absolutely no justification for inferring that condomless heterosexual
sex is safe under any circumstance.  It's probably fairly low risk for
"discriminating" and/or "not-too promiscuous" heterosexual men (you know
who you are-- folks who've never had any OTHER kind of sexually
transmitted disease).  But, as with anything, even low risk things can
kill you if you're unlucky.  That's part of life, in my view, and is no
reason not to *ever* ride a motorcycle or skydive.  It's just a reason
not to do such things a lot.

                                              Steve Harris, M.D.

From: ((Steven B. Harris))
Subject: Re: Found casual prejudice
Date: 13 Jul 1995

In <3u252v$qfp$> Ken M
<102225.1412@CompuServe.COM> writes:

>I've been working as a volunteer with an AIDS support group.
>Recently, two incidents of bias through public misperception
>1. In the post office, I was standing next in line wearing my
>AIDS-support T-shirt. The clerk wouldn't call me over to his
>window; but as soon as another clerk was free and I headed for
>her window, the first one called "Next" loudly, and continued to
>do so as I conducted my business. Obviously, he didn't want to
>touch a package from a person wearing an AIDS shirt.
>2. One of my people died, and his significant other called the
>hospital equipment rental company to come and retrieve the bed
>and other equipment he'd rented from them for the duration. They
>refused to take it back, or even remove it from the house, and
>the S.O. had to deal with it himself.

Comment: this is misperception, and needs to be dealt with by public
education.  However, calling it "prejudice" puts it in the same general
category of people who don't want to drink at the same waterfountain as
a person of color.  But people's actions here may reflect genuine fear
for their lives, however scientifically wrong they are, so this isn't
just run of the mill bigotry.  You have a right to be indignant, but
please remember 1984, when the suggestion was made that gay men not
donate blood, and they took it with just about the same political
attitude as if they were black people being told their blood wasn't
wanted, or good enough.  And they said so quite vocally, and many
refused to stop donating, and some in fact continued donating as a
political act.  And this without doubt caused the deaths of some people.
 Let those dead people cool your anger: "prejudice" and irrationality,
when it comes to diseases, goes both ways.

                                          Steve Harris, M.D.

From: B. Harris)
Subject: Re: Help! Need info on Hepatitis C
Date: 20 Oct 1996

In <1996Oct20.170409@mcrcr6> (ROBERT S.
HOLZMAN) writes:

>In article <>,
> (himself) writes:
>> In article <5473gr$> "James Scutero"
>> writes:
>>> [...]
>>> I found this quote from a guy who says that injection drug users share
>>> needles and spread infectious disease. I thought you might be
>>> interested, since you asked for evidence that injection drug users
>>> share needles.
>>> "Hepatitis B also result from a virus (discovered in the 1960s) and is
>>> transmitted mostly between heroin addicts sharing needles, among
>>> sexually active and promiscuous people, or in the Third World from
>>> mothers to their children around the time of birth." - Peter Duesberg
>> To what extent? And does this constitute a "Global Epidemic"?
>Yes, actually globally endemic, especially in the far east, and an
>epidemic in the members of the selected populations mentioned above that
>have not yet been vaccinated.
>Perhaps if you were better informed on Hepatitis B you would be better
>informed about HIV/AIDS.

   No kidding.  In 1980 hepatitis B was not a general heterosexual
epidemic in the US, but was largely confined to gay men and IV drug
users.  But it WAS a heterosexual epidemic in Africa.  Dispite this odd
epidemiology, nobody, not even Duesberg, suggests that hepatitis B is
not an infectious disease.  The really weird thing, however, is that in
the face of these facts (which both Duesberg and Root-Bernstein are
well aware of), both men go on to suggest that the relative confinement
of AIDS to gay men and IV drug users in the US, but not in Africa,
suggests that AIDS *ISN'T* an infectious disease.  Go figure.  Are
these people stupid, or what?

   I have one gay friend in particular who is considerably smarter.
In the early 1980's he read _Plagues and Peoples_, a book he now
credits with saving his life.  That book tells how in the late 19th and
early 20th centuries we stopped most of the major plagues of previous
centuries well before the advent of antibiotics, by the simple
expedient of breaking the chain of infection between strangers.  No
more spitting on the streets. No more communal well dippers.  Good
sewage treatment.  Public health laws with teeth, and quaranteen
enforcement. Separate water glasses and silverware, with washing
between uses.  An entirely new set of social mores, based on the germ
theory of disease.  My friend, who was and is exuberantly gay, realized
that in the late 1970s this kind of isolation between strangers had
entirely broken down for many gay men.  Physiology will not support a
culture in which young men with money and time can vacation to Mykinos
or New York, or San Francisco, and stay in YMCAs or baths, and have sex
with several strangers whereever they go.  He realized that the
consequence would inevitably be the return of global plagues in gay
men, and with AIDS he realized he was seeing one of the first ones
(after hepatitis B).  He plotted the first couple of years of numbers
of AIDS cases, and drew it on a log graph for himself, and saw the
straight line, indicating an exponential growth phase.  He remembers in
particular one night at a San Francisco hamburger diner in about 1983,
he was sitting with 8 gay friends, who were all intending to go out for
a night at the baths.  He told everyone what he had realized, and
warned them what they were facing.  They laughed at him.  Of the nine
people there that night, he tells me that only two are now alive (the
rest now dead of AIDS), and one of the two survivors is HIV+ with
declining T-cells (I know this man also).  My friend, who decided to be
celibate from 1982 to 1985, and who met his current lover in a safe-sex
class, is still healthy, and HIV-negative.  And he still reads science
books.  You never know what you might learn.

                                         Steve Harris, M.D.

From: B. Harris)
Subject: Re: Help! Need info on Hepatitis C
Date: 22 Oct 1996

In <> (Bruce
Stephens) writes:

>>>>>> "himself" == himself  <> writes:
>> To illustrate the truth of this tale, consider the way "Aids" never
>> happened in the UK because British gays never have sex of any kind.
>I thought we had all agreed that AIDS had happened in the UK---just
>not on the same scale as in the US?  I don't see anything surprising
>about this (assuming, as I do, that it's true): sexual activity is
>surely a social thing which varies from culture to culture, just as
>drug use does.  Claiming that the sexual behaviour of homosexual men
>in the UK is similar to that in the US strikes me as plausible
>(somewhat similar general culture), but I'm also happy to accept that
>it might well be false.  And that's ignoring possible differences in
>how HIV got to the two countries: perhaps it got to the US first, and
>perhaps in more significant numbers.
>Bruce Stephens			| email:
>Utrecht University              | telephone: +31 30 2534630
>Department of Mathematics       | telefax:   +31 30 2518394
>P.O. Box 80010, 3508 TA Utrecht, The Netherlands

   As has been pointed out, the UK has not had the large group of IV
drug users infected by sharing needles, since clean needles have always
been easier to get in the UK.  Nor did the UK never ever have the open
"gay bathhouse" culture of the late 1970s and early 1980's which spread
AIDS so effectively though large parts of the gay culture in San
Francisco and New York.  And though John snidely points out that
British gays have all the same kinds of sex that US gays had in the
1980's, he forgets under what kinds of circumstances they had it.  Anal
intercourse, for reasons that must be obvious even to John, is
associated with easy availability of showers and baths, and is more
often not the standard stuff of back alleys, public bathrooms, gay
bars, or whatever it is that passed for gay meeting places in most of
the UK when AIDS was getting started (I have this on authority from my
gay friends, and John is welcome to dispute it).  UK gays certainly had
anal intercourse, I'm sure, but without the baths it was generally at
home or in some hotel with their lovers.  It wasn't public, and not
nearly as promiscous.  They didn't anal sex with 5 or 10 strangers in a
row (sometimes literally), night after night, in a giant bathhouse orgy
of travelers.  Precisely that kind of thing DID happen in baths in many
large US cities in the late 1970's and early 1980's, however (a
description of a real-life scene which I'd like to have seen, and which
might have been titled "Conga Line of the Damned," was reported to me
with one man saying: "If our mothers could only see us now....")  The,
ah, botton line is that UK gays DIDN'T do it like the Yanks.  For an
epidemic like AIDS, that makes (and did make) all the difference.

                                      Steve Harris, M.D.

From: B. Harris)
Subject: Re: Ho, Harris & Hitler
Date: 28 Dec 1996

David Pasquarelli <>
(Subject: Ho, Harris & Hitler)
writes: Message-ID: <> (Steven Harris) wrote:

> That CD4 turnover is as high as viral turnover is a much less
> secure hypothesis, since there are possible ways that virus
> particles might be produced without killing cells.  So Ho might
> be wrong about this particular hypothesis (which needs to be
> differentiated from the viral production findings).  But he
> might be right also.  Time will tell.

>>What the good doctor fails to acknowledge is that while we
are waiting for "time to tell" if Ho's theories are correct,
asymptomatic, HIV-antibody positives are being dosed to death
with profitable, toxic chemotherapies. If Ho is incorrect, if HIV
does not cause an acceleration in the turnover of CD4 cells and
if, in fact it's not "the virus, stupid" but rather "the immune
system, idiot" that should be our focus, then many, many
individuals have suffered needlessly and died prematurely because
of Ho's "hit early and hard" soundbite antiviral advice.<<

    Comment: So?  And if you're wrong and a lot of people listen
to you and take no drugs, and Ho is right, then YOU'VE killed
them.  It behooves us to take a look at the evidence on either
side, and see whose advice is based on wishful thinking, and
whose on the evidence.

    >>Of course, the HIV-negative Harris has on more than one
occasion demonstrated that he doesn't give one ripe FUCK about
those of us who have tested HIV-positive. To him and a multitude
of other "concerned scientists" we are just this month's lab
experiment on which to test previously-shelved poisons and launch
a career.<<

   Comment: Now, now.  Yes, I'm HIV-negative.  If you yourself
are positive, how come you haven't observed the inexorable fall
of CD4 cells in yourself and your HIV-positive friends, even
while living a clean and drug-free life?  Or don't you look?  Or
maybe you and all the other people at ACT-UP SF tell yourself the
numbers are meaningless.  Sorry, but they aren't.  Acute changes
with nucleoside therapy may be meaningless, but the rate of fall
of lymphocyte count while off therapy is very meaningful, and
prognostic.  Believe it.

   As for what I care about, I have two HIV+ friends who are both
on combination therapy, including nucleosides, protease
inhibitor, and IL-2-- all with my blessing, thank you very much.
Both are doing fine in every respect, BTW.  One of them should
have AIDS by now, based on the rate his CD4 counts were falling
for years without any treatment at all (he had become a
therapeutic nihilist after the death of a lover from AIDS).
Today, his CD4 counts on full treatment are in the normal range.
Perhaps that's not worth much, but his viral load is also very
low, and he clinically completely healthy.

   It is true that I personally no longer have any formal
doctor-patient relationship with anyone who has HIV; but then
I've recently moved to Salt Lake City, where I'm a geriatrician
in private practice, and I don't expect AIDS to burn through the
community of elderly Mormons anytime soon.  With regard to that,
please understand that this entire discussion is so tangential to
the concerns of the career I have, or any I have yet to launch,
as to be laughable.  I'm here on this newsgroup because I'm
interested in how science works (for which you need to understand
non-science and superstition), and because I'm also dedicated to
putting some of that knowledge into practice.  I do my best to
stamp out dangerous foolishness wherever I find it, and the AIDS-
heresy war is a pretty good place to work in (I've also had my
share of debates with missionaries and Creationists, however).
That doesn't mean I'm not also involved in a myriad of other
political and scientific causes; it's just that here is where YOU
see me.

   >>To those HIV-positives presently being pressured to initiate
life-long regimens of potent chemical concoctions, it's
important to realize that:
--> Ho's theory of HIV pathogenesis is WRONG and the
subsequent administration of chemical agents based upon this
flawed hypothesis is unwarranted and dangerous.<<

   Comment: Sez you.  But that's your guess, because neither nor
I has any direct evidence at this point.  Ho's theory that a lot
of virus is produced in most HIV infected patients, and that
antiviral drugs (specifically protease inhibitors) stop this, is
obviously correct-- it's very nearly a direct and simple
observation, with Q-PCR.  As to whether stopping this production
does any good early in infection, vs. waiting until later, it's
hard to say.  That's why we do clinical studies, don't you know.
Clearly, antiviral drug therapy with nucleosides does some good
in later stages of HIV infection (CD4 counts below about 300 or
so) so long as the virus does not develop antiviral resistance.
Why shouldn't it be the same for other antivirals?

  >>Drugs like AZT, 3TC and protease inhibitors merely
interfere with cellular metabolic processes to manipulate
dubious blood-borne measurements like viral load & CD4
counts so as to suggest actual benefit from the agents.<<

   Comment: Sorry, but there is quite a lot of evidence that they
do more than this.  For instance, early in the course of AZT
therapy in "virgin" late state HIV patients who still have AZT
responsive virus, the AZT patients experience weight gain and
improved Karnofsky scores, and many patients even regain skin
test responsiveness (see the original Fischl study of AIDS/ARC
patients).  These are the same kinds of things that your Mr. Fred
Shaw argues are markers of genuinely effective immune therapy,
rather than simply meaningless markers.  So how, now?  How soon
you forget your own criteria, when you don't want to believe

   In addition, people with AIDS/ARC treated with AZT don't *die*
as quickly as people untreated, again until the virus becomes
resistant.  Is being dead vs. alive a good enough clinical
outcome for you?  Nor are these isolated results.  In addition to
the results of the original Fischl study, three other studies in
patients started on AZT at an earlier stage of HIV infection
(ACTG 016, ACTG 019, and the European Cooperative study) have
found that AZT delays progression to symptomatic infection or
AIDS, as compared with placebo.  Only one of these three was by
Fischl's group.  This is not just fooling around with lab tests
or esoteric markers.  Finally, ACTG 19, as you may know, showed
that low doses of AZT did as well at delaying AIDS as higher
doses, with much less toxicity.  These results demonstrate that
AZT toxicity is separable from even its positive effect on AIDS.

    Finally, studies of combinations of drugs, like ACTG 175 and
Delta, agree that people on combinations of nucleosides have
fewer deaths than on monotherapy with any single agent at the
same dose-- a finding which (even if we didn't have the placebo
controlled studies) is pretty difficult to explain unless many of
these drugs somehow mitigate the toxicity of each other,
something that seems wildly unlikely for a bunch of what you are
claiming are general immune suppressives.  What-- ddC, ddI, and
protease inhibitors ALL decrease AZT toxicity, and AZT in turn
decreases the toxicity of ddI and ddC?  Sure they do.  And even
if you believe THAT, it's rather hard to explain why (for
instance) people given ddC + AZT survive better than people given
AZT alone, *except* if they've already been on AZT, where there
is no difference between groups.  This makes sense in terms of an
already AZT resistant virus rapidly mutating to escape what is
effectively ddC monotherapy-- but makes no sense at all from the
viewpoint of toxicology if you believe nucleosides are the

   >> These touted markers, in fact, do not correlate with
improved cellular immune system functions, improved health or
delayed onset of opportunistic infections. Rather, these markers
are used as a form of psychological terrorism to market and
sell exorbitantly priced drugs. Don't buy into it!<<

    Comment: You really do not know whether reduction of viral
load by means of antivirals correlates with health or not (I
expect this question to be answered in 1997, however-- with a
vengeance).  However, in view of the drastic effect of
combination nucleoside therapy and protease inhibitors on viral
load, and the drastic effect of nucleosides and protease
inhibitors on clinical well-being when the virus responds, it
seems reasonable.  You must be living on Mars, not San Francisco,
if you haven't observed the effects of protease inhibitors on
ordinary signs of health in people in the last stages of HIV
disease.  You may believe that these people who get protease
inhibitors and get out of the hospital, gain weight, and go back
to work are "zombie people" filled with zombie CD4 cells, but I
think the most intelligent way to bet is that they are actually
doing better than if they hadn't elected to be treated.  *Not* to
assume that they just look better and think they are better, but
in fact are all going to turn to dust and wither away, like
Dracula in the sunlight, real soon now (any minute now....)  Of
course, if you want to wait to take antivirals, that's up to you.
Just don't expect that really sick people are going to look at
the (apparent) health of people taking protease inhibitors, and
follow you.  Hardly anybody is THAT dumb.

   And if some people who aren't sick want to try suppressing
their viral production, that's not dumb either.  Viral production
correlates very well with rate of progression to AIDS, and it's
not unreasonable to try to change it.   There is, believe it or
not, some very modest evidence that effect on viral load, but not
on peripheral lymphocyte counts, correlates with effectiveness of
an antiviral, at delaying clinical decline.  In the original
Fischl studies conducted in 1986 it was noted that rise in CD4
cells did not correlate at all with reduction in opportunistic
infection, and also it was noted that rise in CD4 cells was
immediate in the AZT group, while decreases in
opportunistic infection in the AZT group (over placebo) didn't
start until a month into the study (this dissociation suggesting
that AZT suppression of infection, because delayed, is immune
mediated, yet has nothing to do with peripheral CD4 numbers).  So
all this was known from the beginning and is discussed in
standard texts (no-- ACT UP SF didn't discover it).  However,
Fischl & Co ALSO found in the original study and ACTG 016 that
suppression of p24 antigenemia (a very crude viral load index)
was improved up to 500 mg of AZT a day, but not between 500 and
1500 mg per day.  And this is also exactly what the clinical
studies showed: Higher doses of AZT didn't decrease progression
to AIDS any better than did 500 mg/day. Both were equally good,
with respect to placebo (and they WERE better than placebo, by
quite a bit).  So there is crude agreement here between clinical
efficacy of an antiviral, and efficacy at changing a test value,
of the sort that gives me a lot more hope for viral load as a
marker of antiviral drug effectiveness, than I ever had for
changes in CD4 counts.

    Not that I think this is going to change your mind, but it's
how I think.  Please save this conversation, however, because
we're going to come back to it after the protease trial results
come in over the next year, and see who was right.  Be
interesting to see if you apologize, or if you take the easy way
out, of claiming that the drug companies cooked all the results
you don't like (the Lauritsen maneuver).  I, of course, has no
such way out, because I'm not crazy.

   >> These drugs damage the already depressed
cellular immune response and destroy vital organs like
the liver, kidneys and gastrointestinal tract of otherwise
healthy HIV-antibody positives.<<

   Comment: This is B.S., the product of your fevered
imagination.  I've already noted the return of skin test
responsiveness when patients with AIDS are given AZT.  And the
reduction in opportunistic infections in these patients speaks
for itself.  So does the weight gain and improvement in Karnofsky
scores.  All studies which have suggested that people on longer
courses of nucleosides do worse, are of people started on high
dose monotherapy AZT quite early in the course of HIV infection,
and continued on it long after the virus is expected to become
resistant.  Big deal.  All these studies tell you, is not to do
this.  They don't say a thing about combination therapy or
protease inhibitor use.  We have no studies, please note, of
people started on AZT as compared with people started on placebo
and kept on placebo.  It's not ethical to continue a placebo
controlled study when the placebo group is clearly dying faster.

   >>> Countless HIV-antibody positives very well may live LONGER
and with a HIGHER quality of life if they avoid being pressured
into taking these drugs on the basis of Ho's flawed theory of HIV
pathogenesis. A theory, mind you, that is unproven, under attack,
yet still hyped across the globe by TIME magazine at the behest
of powerful AIDS organizations funded by large contributions from
drug companies.<<

   Comment: A theory which has the results of half a dozen
clinical trials behind it, each with endpoints like AIDS or
death.  Sorry, but the observational evidence trumps your
theories.  And agrees, so far, with Ho's (at least so far as the
virus goes-- not necessarily so far as CD4s go.  But I said

   >>Yes, Dr. Harris is correct about hindsight's revelation of
truth. History certainly will bear witness to the atrocities that
are presently being committed on the basis of a heavily-hyped yet
tragic mistake. A mistake that is deliberately being kept in
place to support a multi-billion dollar pharmaceutical and
biomedical industry.<<

   Conspiracy mongering.  <yawn>.

   >>It is quite appropriate that a third-rate scientist like
David Ho shares the "Man of the Year" title with history's other
mass-murderers honored by the reactionary Time/Warner
conglomerate. David Pasquarelli/ ACT UP San Francisco<<

   Comment: Right.  TIME/Warner clearly has it in for the Jews,
and that's why they picked Hitler in 1938....

   For the record, TIME's Man of the Year is the most influential
man of the year, not who everybody is supposed to like.  During
the Kuwait invasion crisis, you'll remember that TIME's Man of
the Year was Saddam Hussein, and TIME made the point about
influence over and over.  Ho is influential.  However, I also
think the evidence suggests that he's basically right.  It's the
virus, stupid.

                          Steve Harris, M.D.

From: B. Harris)
Subject: Re: For John himself: Women and AIDS
Date: 01 Jan 1997

In <> Randolph Richards <>

>Still trying to help with young Johnny's education, here's a bit from
>AIDS Daily News (27 Dec):
>"Women Overrepresented Among Young Persons With AIDS"
>Reuters (12/27/96)
>     An analysis of the more than 37,000 AIDS cases diagnosed in
>New York City between 1984 and 1993 found that most of the young
>people diagnosed with AIDS were women and that women developed
>AIDS at a higher rate than young heterosexual men.  Dr. Marcelo
>Pagano and colleagues at Harvard's School of Public Health
>reported that by 1993 the majority of AIDS patients under 30 were
>women, and that most of these young women had contracted the
>disease heterosexually.  The researcher also noted a
>"youth-gender effect among black persons with AIDS," leading him
>to conclude that "women are overrepresented among younger persons
>with AIDS, particularly persons of color."

   Yep.  All this is not exactly today's newsflash, however.
Heterosexual AIDS in the US is almost entirely a disease of women.  In
fact, so close to entirely, that there is cause to wonder if the few
men aren't lying about their homosexual encounter history (as men are
known to do).  In AIDS education in the US we ought to be concentrating
on 1) IV drug users, 2) Boys who are homosexually active, and 3)
girls-- telling them that their chief risk is from boys in category 1
and 2.  And probably from anal sex, in particular.   HIV is NOT spread
in the US like your ordinary garden-varieties of V.D.(STD) (the far
East is a different matter, of course), and it's high time we stopped
pretending in AIDS education that it is.  In the US, if we had clean
needle programs everywhere, and could get people to use condoms
religiously for anal sex alone, we could probably pretty much stop AIDS
in its tracks.

                                              Steve Harris, M.D.

From: B. Harris)
Subject: Re: HIV's base sequence?
Date: 06 Jan 1997


  >>3) Never in the history of human illness has a viral
epidemic so precisely targeted specific risk groups.  This is a
white flag if I've ever seen one.<<

    What kind of a white flag?  The problem is, there are all the
same risk groups targeted by hepatitis B.  And they really don't
relate to each other, otherwise, despite Duesberg's fantasies.
According to Duesberg, not only do illegal drugs and AZT both
have to do something no chemical has done before, but hemophilia
factor does also.  And that's not even addressing the transfusion

   >>Could this be why the CDC does not track tertiary
heterosexual AIDS transmission (CDC, July 10, 1995, response to
US Congressman Gil Gutknecht)?<<

   No, they don't, because they can't think of any reason to.
Gil Gutknecht, BTW, wishes he'd never heard of AIDS heretics.
He's since fired the member of his staff who got him to put his
name on such cheap and silly questions.

   >>4) Glaxo Wellcome has indicated that adverse events
associated with AZT is 'indistinguishable' from HIV disease.<<

   No, it's indicated that some are.  This is not to say that AZT
causes AIDS.  Many of the events indistinguishable are not AIDS
defining, such as weakness, wasting, low platelet counts, etc.

   >>5) The precise mechanism of cell death following HIV
infection as of July 10, 1995, was sloughed off as a 'a topic for
research' by the CDC. This is a pretty big piece of evidence to
ingore considering AIDS is characterised by a depletion of

   When animals are given lentiviruses they lose there T-cells
also.  We don't know the mechanism.  Does this mean it doesn't
happen?  No.

   >>6) The life expectancy of hemophiliacs has increased; from
11 years in 1972 to 27 years in 1987 despite the fact that 75% of
this group had been infected years before 1987.<<

    Incorrect.  The median age of hemophiliacs increased between
1972 and 1987, but the life expectancy decreased.  They are
different things.  Life expectancy reflects instantaneous current
risk, while median age reflects a sum of effects of medical
advances over many decades.   Understand the difference?

    And by the way, while median age increased, obviously it
didn't increase 16 years in 15 years.   Hopefully it will be
obvious that it is impossible for any population to age 16 years
in 15, even if nobody dies and nobody is born.  It could be done
by adding old people (immigration), but it seems unlikely that
enough hemophiliac emigration could happen to make up for the
effects of birth and death.

    >>7) The incidence of recreational drug use in the US
correlates perfectly with the number of AIDS cases to date
(see/read the Duesberg Phenomenon).<<

     Incorrect.  The fact that both rose hardly makes for a
"perfect correlation."  Note also that no graph in the number of
AIDS cases or AIDS deaths, shows any change in slope or effect
whatever around 1987, when AZT began to be given to HIV
patients.  Thus, there is NO correlation there.  And yet this is
one of Duesberg's main theses, and AZT causes most modern AIDS.
Apparently, you see correlations where you'd like them, and
ignore the lack of them, where they fail to appear.

   >> And make no mistake about it; Peter Duesbergs' drug/AIDS
hypothesis was the original hypothesis proposed by the NIH and
CDC in 1984, until Gallo stole the Frenchs' viral sample and
proclaimed his victory. <<

    There is no evidence Gallo stole anybody's sample.  The
French sent Gallo a number of samples, and one of them wound up
where it wasn't supposed to, in Gallo's other cultures.
Specifically, one fast-growing isolate of the French virus
contaminated and "took over" many of the cultures in Gallo's lab.
But then, we must remember that the same isolate took over all
the cultures in Montagnier's lab also, without them realizing it
any more than Gallo had.  So the French didn't have the virus
they thought they had, and neither did Gallo.  And the same
strain (just for good measure) accidentally contaminated and took
over all the cultures in at least one lab in the UK.  Sloppy
technique, but the French can hardly blame Gallo for having
happen to him what happened to them and the English also (are we
to assume that in Gallo's case it was theft, while in everybody
elses it was an honest mistake?).  The NIH saw it that way also,
because when this new evidence was presented, they cleared Gallo
of all charges.

   >>In real science however, let us remember we are seeing the
repercussions of long term drug use (still going on today), of
the largest demographic mass of people in the history of the
world (76 million Americans)- the baby boom.  Conversely, the
number of HIV infections has remained a constant as reported by
the CDC at one million in the US since 1985.<<

    CDC estimates for HIV infections in 1985 of necessity were
rough estimates only, and highly insecure (do you have a source,
by the way?).  The test came out commercially only that year, if
you will remember.  There is no reason to believe any numbers
based on very small population sampling, were accurate. There are
many reasons to believe drugs do not cause AIDS, and I've
detailed them in my article.  Read it.

> What evidence would you like?  There is lots of virus, there is
> lots of damage to the body.  What more do you want?

>>Proof, that HIV causes cell death and immune suppression.<<

   What sort of proof would satisfy you, short of deliberately
injecting people with it?  And why would it?  We have proof that
SIV and FIV cause cell death and immunosuppression in animals,
but you don't believe that.  Why would you, if we had the same
caliber of evidence for HIV-1 and humans?  If you don't want to
believe it, you're not going to, no matter what the evidence is.

>      Again, PCR is quite capable of being used quantitatively.
>This is not a matter of debate.

>>According to its' inventor, Kary Mullis, it is.<<

Too much LSD, I'm afraid.  Too bad.   However, the studies are
irrefutable.  Quantitative PCR is real.

> >If I'm so far from the truth, why did we begin using this
> >diagnostic in the first place?  Why is there no current prospective
> >intervention study based on viral load????
>     Such trials are underway-- they simply haven't been published yet.
> When they are (I expect one in the next few months) what are you going
> to say about it?

>>Please send it to me, unless of course Abbott Labs authored it.

Dr. Holzman has already provided at least one cite, which I
hadn't seen.  I don't know why funded it or authored it.  Who
would be acceptable to you?  I mean, you seem to believe the
government and all academic institutions are in on the

                              Steve Harris, M.D.

From: B. Harris)
Subject: Re: So What Is That Red Stuff?
Date: 06 Jan 1997

In <5apd2r$> (James Scutero) writes:

>Go ahead and scan in the picture and enlarge it. Please point out the
>distinctive lentivirus morphology. I see bleb-like particles of various
>shapes and sizes. I don't doubt that the picture is supposed to be of a
>some retroviruses budding from a cell, but without knowing the procedures
>used to obtain the electron micrograph, and what tests were done, I can't
>say I know what I'm looking at. I certainly wouldn't take TIME's word for

   For the record, you can't see lentivirus morphology well in scanning
electron micrographs, because they only look at the surface of the
virus (and the surface of cells, as well).  To see morphology you need
stained viral cross sections of the sort you get in good transmission
EMs.  Scanning EMs aren't great for identifying cells, either, for this
reason.  To the scanning EM, cells and viruses are just little balls,
pretty featureless except for external shape differences and sizes.

>	I think HIV may be a human endogenous retrovirus which may be
>broken from latency by herpes viruses or by other factors. Harris
>seems to believe otherwise.
>	Harris does not give satisfactory reasons why HIV is not a
>human endogenous retrovirus. The behavior of HIV-RT is one reason why
>he seems to think that it is not endogenous to humans:
>	"...Also present along with the RNA in the FIV viral
>	core are molecules of a particular variety of reverse
>	transcriptase enzyme peculiar to several previously known
>	lentiviruses, including HIV. This reverse transcriptase
>	functions best with a particular concentration of magnesium
>	ion, and does not work (as this enzyme from other retroviruses
>	sometimes does) with ions of the chemically somewhat similar
>	mineral manganese..."
>        REFERENCE: Harris, SB, Skeptic, Vol. 3, No. 2., p. 65 (1995).
>Later he writes:
>Subject:      Re: magnesium dosage???
>From: B. Harris)
>Date:         1997/01/01
>Message-Id:   <5ad7sd$>
>X-Netcom-Date: Wed Jan 01  2:39:41 AM CST 1997
>>[...]That RT enzyme in lentiviruses like HIV is a lot more like the
>>normal cell polymerases in this regard (which need Mg+2), than those of
>>other retroviruses.
>>                                             Steve Harris, M.D.
>	If HIV-RT is like normal cell polymerases, why can't it be part
>of a human endogenous retrovirus? Many animals have their own kind of
>lentiviruses, why not humans?

   No reason why we couldn't.  It's just that the retroviruses found in
all human cell lines up to now have been C-types which use Mn2+.  I
have no idea why this is, but it's the same in animals also: endogenous
retroviruses use Mn2+ RTs.  Lentiviruses all use Mg2+, and so far as I
can tell, there are no endogenous lentiviruses in any animal (by which
I mean viruses found in every nucleated cell in every animal, passed
though the germ line).

   The reason I don't think humans have lentiviruses is that you can
carve up human DNA and look for lentiviral sequences (lentiviral RT
sequences, for instance), and they aren't there.  Except in
HIV-positive people, of course.  But they are a very small minority.
There is no way a virus can hide from a restriction digest and probe of
a genome.  Any more than a gene for a hereditary disease can, once its
sequence is known and probes are constructed.  You can hide an elephant
in a house, but not after the house has been reduced to kindling by a
tornado, and passed though the mesh screens of a hundred archeologists.
 That's what modern techniques do to cells.  No HIV genes, or parts of
HIV genes, are there in the DNA of the cells of the average person.
They simply aren't.  No place they can hide.

   It is partly for this reason why Lanka deserves the horse laugh in
claiming that "HIV" is just a bunch of misidentified normal gene
products from normal cells.  Sorry, but in normal cells from HIV
negative people, those genes simply ARE NOT THERE.  Forget the

                                                 Steve Harris, M.D.

From: (Steven B. Harris)
Subject: Re: CMV Retinitis Despite High CD4 Lymphocyte Counts
Date: 22 Feb 1997

In <>
(himself) writes:

>In article <5egcm6$> "James Scutero"
>>    [...]
>>    Another report from France also noted the onset of acute CMV
>>    infections among 8 patients with low CD4 counts (mean = 37) who were
>>    started on combination therapy including protease inhibitors. Acute
>>    CMV infection (retinitis, submaxillitis, pseudotumoral colitis,
>>    pneumonitis, CMV viremia) occurred despite clinical improvement of
>>    the patients and an increase by more than 5 fold in mean CD4 counts.
>>    The average time from the first administration of protease
>>    inhibitors and the onset of the CMV event was 37 days.
>What do they mean by "clinical improvements", in view of the way
>the combinations are wrecking the health of these people? Is this
>just shorthand for some insane mumbo-jumbo about cell counts?
>Thanks for these reports, Giacomo.
> John

No, "clinical improvements" means, by definition, improvements in
something more than just lab numbers.  Patients feel better, look
better, gain weight, experience remission of opportunistic infections,
etc, etc.

The paper J. Scutero quotes does have an interesting observation, which
is that for CMV retinitis, the raised CD4 counts brought about by PI
treatment are not as protective as such counts when they occur
naturally.  However, the paper does NOT say that there is no
improvement in CMV protection at all.  And the improvement in multiple
other opportunistic infections with PI treatment demonstrates that real
increases in immune response are taking place.  That's what we really
are about.  In the end, it doesn't matter if this improvement is due
only to cells being moved from here to there (nodes to blood), or not.
Although I don't think for a minute that it's entirely the latter,
since lymphocytes work mostly in the lymphatic tissues, and simply
moving them would be highly unlikely to cause such improvements in
clinical response (again, clinical means improvement in health status
that can be measured "at the bedside", not just with fancy lab tests).

   Quite frankly, I'm not surprised that patients whose immune system
is reconstituted by PIs, might not go back to perfect function even if
their peripheral counts go back to normal-- anymore than healing in any
other organ system which is damaged by a disease, is necessarily
perfect.   You can cure TB, but you can't always restore a lung, for
instance.   You liver enzymes my go back to normal if you are a
cirrhotic who stops drinking, but that doesn't mean your liver is now
fine.   Nodes are seriously disrupted by HIV-- the very structure of
them is destroyed, in somewhat the same way that the structure of the
liver can be destroyed by alcohol.  All this suggests that perhaps if
you have quite severe immune compromise already, the later you start on
PIs, the less well you're going to do (much independent support for
that also, from doctors who are treating AIDS patients).  A message
which Scutero, of course, does not want to hear.

                                                Steve Harris, M.D.

From: B. Harris)
Subject: Duesberg and "Wheeeer's the Virus?"
Date: 30 Mar 1997

In Message-ID: <> writes:

   >>Doesn't all of this prove that a retrovirus doesn't kill
cells directly?  Also, when Dr. Harris says "the retrovirus
genetic information is hidden from the immune system, which would
otherwise destroy the virus inside the cell, or destroy
the entire cell."  Doesn't this disprove the theory that HIV
puts the immune system into a "suicidal" autoimmune attack,
since when HIV infects a cell, it is hidden?<<

   Comment: perhaps I didn't make myself clear.  Retroviruses can
hide from the immune system quite well, by inserting themselves
into DNA, and staying quiet.  It's sort of like a bankrobber
hiding out in somebody's basement or attic, until the "heat" is
off.  He can stay that way pretty safely, but obviously can't
stay that way forever.  Life goes on, even for criminals.

   Retroviruses are sneaky, and the lentiviruses like HIV are
sneakiest yet.  Lentiviruses can insert themselves into the DNA
of cells which aren't dividing, unlike the tumor retroviruses.
But life goes on, and even lentiviruses have to reproduce
sometime (particularly if they are stuck in a non dividing,
differentiated cell which isn't going to divide for them).  To
reproduce in such a cell they have to come out of hiding in the
DNA, and make RNA and protein.  When that happens, the immune
system sees them.  To continue the crime metaphor, foreign RNA
inside cells triggers interferon, which chops up viral nucleic
acids inside the cell, like a pit bull that has finally been
awakened by a burglar who has made too much noise, and begun
chomping burglar.  Or viral replication inside cells activates
apoptosis mechanisms, and the cell commits suicide, like owners
razing a rat-infected building.  Or foreign viral proteins inside
cells get chopped up by enzymes and transported and presented on
the outside of the cell--- sort of like pieces of dead people in
Jeffrey Dahmer's garbage cans-- and that brings the "cops" (in
the body, these are other immune cells-- NK cells and cytolytic
T-cells).  These kill virally infected cells, which are
identified by the chopped up and presented pieces of virus stuck
to their surfaces.  Like John Wayne Gacy's house, the community
of cellular neighbors razes such infected cells.

   Finally, it is, despite what you've heard from Duesberg and
his crowd, quite possible for retroviral infection to kill cells
directly.   Instead of going through the nuclear chromatinic
clumping that characterizes programmed cell death (apoptosis)--
which is sort of like the family turning out the lights and
cleaning up before leaving a house which has been condemned--
it's also possible for cells infected by HIV to simply blow up
without any preamble, like an arson in the middle of the night,
as the virus wrecks the membrane structure of the cell during
reproduction (see Proceedings of the National Academy of
Sciences, USA  85:3570, 1988).  Nature is not as simple as
Duesberg wants to make it.  HIV doesn't simply destroy cells, or
not.  Some HIV *strains* destroy lymphocytes, and some don't.
Worse still for complexity, as a given strain mutates in the body
it can acquire a taste for a different cell type (lymphocytes
instead of macrophages), as well as the ability or propensity to
destroy cells in culture.  Such cytolytic strains are most often
isolated from people in the later stages of HIV disease (AIDS),
perhaps not surprisingly.

   Some viruses in culture even cause cells to merge with each
other (which is fatal for reproduction), but it's not clear if
this happens much in the body at all.

   Which of all of the rest of the mechanisms of killing of cells
named above is most important in AIDS, hasn't been decided yet.
Perhaps all are involved, and they change at different stages of
the disease, and between one person and another.  What is known
is that as HIV infection goes on, the lymph nodes, which have
been keeping most of the virus out of the blood stream, begin to
fail.  During the low symptom time of HIV infection, viral levels
in cells in nodes are 10 to 1000 times what they are in blood
cells, but in the last stages of the disease, viral levels rise
in blood to the same high level as in the nodes.  Clearly the
nodes have stopped working, and when they are removed and tested
for ability to trap virus, they don't.  Microscopy shows that
centers of dividing lymphocytes which trap HIV and deal with it,
have been replaced by fibrous tissue.  Lymphocytes in the blood
(which originate in the nodes) continue to decline, until finally
they are gone also.  There isn't any "re-trafficking" by this
time-- the whole cellular immune system by this time is gone.

   And now we come to my problem with Peter Duesberg.  To put it
bluntly, the man is dishonest in his arguments.  Duesberg says
flatly that retroviruses do not kill cells.  When reminded of
experiential evidence that they do (the paper cited above, for
instance) he retorts that they may kill cells in the artificial
medium of a culture, but not in animals.  When reminded of
experiments in which retroviral (lentiviral) injections kill
animals (and how could they not without killing cells-- a point
that Duesberg himself makes), Duesberg objects that these are
animals "too young to have immune systems," or in ill health
because of captivity or inbreeding.  Okay, another qualification.
Retroviruses kill cells in weak animals, Duesberg admits.  The
problem now is that by this time, Duesberg has forgotten what
groups get AIDS, groups which he has insisted that HIV is
harmless for.  See if you can follow the logic below.

    Crack babies have undeveloped immune systems, and Duesberg
even posits that they have additional immune problems because of
their mother's drug use.  Certainly enough to give them all the
other opportunistic infections of AIDS.  Are they not, then,
exactly the type of compromised "young" which Duesberg has
admitted that retroviruses can kill in animal experiments?  Of
course they are-- but for Duesberg, admitting this logical and
inescapable conclusion to be drawn from his beliefs and prior
statements would weaken his overall case, and he knows it.  So he
abandons intellectual integrity here, and simply denies.  Read
Duesberg's book-- young monkeys have no immune system, so SIV can
kill them.  But crack babies with no immune systems cannot be
harmed by HIV, because HIV is a harmless virus.  We know, because
with one exception (Duesberg's bird tumor virus) all retroviruses
are harmless.  Duesberg says so.

    What is different about experimental animals supposedly dying
of retrovirus infection only because (in Duesberg's arguments)
they were kept confined in cages--- and prison inmates with AIDS?
Well, according to Duesberg, the difference is that the prisoners
have HIV, which we know is harmless because all retroviruses are
harmless.  So they must be dying of something else.   Or what is
the difference between the supposedly poor previous health of
retrovirus infected experimental lab animals (which Duesberg
never documents), and the poor health of chronically malnourished
drug users who suffer from ill effects of every other disease in
their environment?  Yet Duesberg insists that HIV is the ONLY
microbe which can play no role in these problems of drug users,
because HIV is harmless.  Because all retroviruses are harmless.

   Except when they aren't.

   Shorn of his argument the retroviruses never kill cells and
never kill animals, Duesberg is basically left only with the idea
that HIV activity, even if it did kill cells, is not enough to
cause the loss of cells seen with AIDS, and that the immune
response seen in AIDS should be enough to keep the virus from
causing any problems, anyway.

    Yet here again, Duesberg has a little problem with the bite
of reality.  Duesberg would have us believe that the
establishment decrees that AIDS has a latency period of 10 years,
during which almost no virus is detectable, and during which
antibody response is good.  How, then, he asks, can the virus
during this time destroy the immune system and cause AIDS?

    The problem here is that the establishment never said any
such thing about AIDS.  AIDS happens on many time scales, and
some of them are quite soon after HIV infection.   Cohort studies
have demonstrated AIDS as little as 3 months after initial HIV
infection, with steady immune decline from normal to severe
immune failure documented throughout that time.  Such rare cases
are simply the tail of the group of "rapid progressors" in cohort
studies-- the 10 to 20% of men who develop AIDS within 2 or 3
years after initial HIV infection, and who (again) show steady
immune decline from normal to AIDS, during the period from
initial HIV infection to clinical AIDS.  Such men have high viral
levels, and high fractions of mononuclear blood cells infected
(just the way Duesberg said it would have to be if HIV caused
AIDS), and they also (as a rule) often show poor antibody res-
ponses to the HIV virus, and poor neutralization antibody titers-
-also just the way Duesberg said it would have to be if HIV was
causing the illness.  But does Duesberg acknowledge at least THIS
group as a possible group of people in whom AIDS is being caused
by HIV infection?

   He does not!  He doesn't, because this would weaken his case
badly.  The problem for Duesberg, you see, is that there isn't
any good bright dividing line between rapid progressors, and the
average progressors who get immune decline and finally AIDS, at a
more leisurely pace after HIV infection.  For every man who gets
AIDS two years after HIV infection and has a high peripheral
cell-infection percent all that time, and weak antibody response;
there is somebody *else* who progresses in 2.5 years, and has a
slightly lower virus level, and slightly better antibody re-
sponse.  And another who does the same in three.  Or Four.
Decline of immune function in people with HIV is shades of gray,
with immune decline progression correlating with viral load and
immune response, and obviously, it's all ONE process (just on
different time scales) if it's a process at all, and Duesberg
must sense this.  So he refuses to get on the slippery slope,
even at the beginning of it, which is where he said he'd be as a
regular "virologist" who believed diseases where real when they
were active.  Once again, his integrity is the loser.

   So where IS the HIV in people who progress to AIDS more slowly
with HIV infection?  It's in the lymph nodes, as noted above.
The very limiting dilution titer culture and limiting dilution
PCR tests which Duesberg applauded when they showed low levels of
HIV burden in peripheral mononuclear cells, later showed much
higher levels in lymph nodes where 99% of the body's T-cells
live.  Following this result, Duesberg said he didn't trust this
kind of testing anymore.  Worse still, when a new test called
quantitative competitive PCR (QC-PCR for RNA) showed relatively
high levels of free HIV virus in the blood even in people with
slowly progressing disease, corresponding (surprise) to the high
numbers of infected cells in their lymph nodes which were making
virus, Duesberg refused to believe the test at all, saying that
it put out numbers which were thousands of times the real values
(which Duesberg was sure he knew, because they were the ones his
theory demanded).

   That the tests were wrong, of course, was flatly impossible,
since the tests had been standardized against known quantities of
the cultured and counted HIV virus, which even Duesberg acknowl-
edged to exist and been well characterized.  And QC-PCR had also
been compared and validated using another test, the branch chain
DNA test (bDNA) which used a different, non PCR method, but still
gave the same results.  Under the circumstances, Duesberg's
insistence that a pair of different standardized and controlled
tests (in which known controls were run along side every set of
unknowns) were giving identical wrong answers, was irrational.

    And that's where we are with skeptics of the HIV-AIDS theory.
At some point, they find it necessary to simply deny the
evidence-- for instance accusing a perfectly good and well-
controlled test of not giving the right answers, even though they
cannot give a plausible reason why it shouldn't (if it works to
successfully quantitate known controls, there can't be anything
wrong with the test, even though some misguided skeptics have
even tried to argue this;  there is no sense arguing that the
theory of a test is faulty is the test is known to correctly read
control samples).

    Or else, skeptics must accuse one group (usually many groups,
who have replicated each other's work) of participating in a
great conspiracy to publish false data.  The mark of a
revolutionary scientific theory, is that it seeks to explain
known observations in a new way.  The mark of a quack theory is
that it discards known observations if they don't fit, and simply
calls them lies and conspiracy.  HIV/AIDS skeptic theories are
generally of the latter kind.

                               Steve Harris, M.D.

From: B. Harris)
Subject: Re: Heterosexual AIDS halved on re-analysis
Date: Thu, 20 Nov 1997

In <650651$> (George M.
Carter) writes:

>Granted, it does not appear so frequently in middle class white
>suburbia. But it is there. Among straight kids. Is it any less
>heterosexual when a woman gets infected from her husband? Is it any
>less heterosexual because it is a person of color? Or in a poor

   Frankly, yes.  If the "heterosexual epidemic" is entirely an
epiphenomenon of women who get it sexually from IV drug-using or
bisexual males, then obviously what you do about it is different than
if these women had gotten it from men who'd gotten it from women.  It's
sort of like rabies: if all humans get it from animals and hardly ever
from each other, then you direct your quaranteen and vaccination
efforts toward animals, and vaccinate and quaranteen humans rarely.
Vaccinating most people against rabies is a waste of resources.  Ditto
teaching heterosexual men they need to use condoms for all new
partners, when statistically their chance of getting AIDS from such an
encounter is about 1 in a million (about the same chance as dying on a
commercial jet).   And if they avoid crack prostitutes, higher yet.

>This is the one area where I think you are correct to a certain extent
>but potentially blind to the possibility that the expression of AIDS
>in Europe and North America could take a rapid shift.

   I think if it "could", it would have already.  Sorry.

>And given the
>clinical latency, it may be more than we realize if the so-called
>"low" or "no-risk" populations are practicing unsafe sex, passing
>infection but not getting tested. I don't think that is too
>likely--but certainly it underscores the need for a sound public
>policy that teaches safer sex practices and so forth.

    No, for these resources aren't free.  All resources you spend
teaching young straight men to use condoms, you could use to teach
young bi or gay men to use condoms.  A job which isn't getting done as

    Sorry to be politically incorrect, but the way we're treating this
disease in America makes no medical sense at all.

                                    Steve Harris, M.D.

From: David Rind <>
Subject: Re: ELISA test for HIV - False positives?
Date: Wed, 04 Feb 1998 15:52:03 -0500

Robbie wrote:
> I am wondering if any in the group have heard of false
> positive results for the ELISA HIV test?  Have been told of
> an interesting case where a young male with no known or stated
> risk factors was told he was rejected  by the blood bank due to
> the HIV test being inconclusive (I believe they use the ELISA test
> but it may of been the Western Blot).  As an aside to
> this, the result was sent by mail to this person's address!
> I would of thought that something as sensitive as this would
> *not* be sent by  mail!  Can anyone here imagine being sent a
> letter saying that they are  found to be HIV positive after
> donating blood?

The ELISA test for HIV has a fairly low false positive rate compared
with most tests, but fairly high for such an important screening
test.  The way it is performed in most settings, the specificity
is around 99%, or a false positive rate of 1%.  For this reason,
at least in the US, a Western Blot is *always* performed for
confirmation of a positive ELISA, before the results are released.

However, an "inconclusive" result is almost certainly from a
Western Blot, and not from an ELISA.  This is not a false positive --
the test was not positive, it was inconclusive.  Long term follow
up of people with repeatedly inconclusive Western Blot results
show that people like this, who do not have risk factors for HIV,
generally never turn out to be infected with HIV.

I would hope that the letter did not say that they were infected
with HIV.  However, again in the US, the Red Cross will not
accept blood from someone with an inconclusive Western Blot,
to try to make the blood supply as safe as possible.

David Rind

From: B. Harris)
Subject: KSHV Antibodies in SF in 1985, and KS with AIDS (was: A few questions 
	and observations for both sides)
Date: 8 May 1998 07:58:11 GMT

In <>
(DieStanDie) writes:

>>Has there ever been a good study that took fecal matter into
consideration as a major contributory factor to certain AIDS diseases?
I can't remember having seen it anywhere.<<

    Statistically, it's been known for a very long time (earlier than
HIV) that various anal activities put one at much higher risk to get
HIV, mainly because rectal mucosa is more fragile than vaginal, and
bleeds.  It's full of macrophages, also, ready to take up HIV.  The
connection between receptive anal sex and poppers and AIDS is what put
the popper people onto the popper hypothesis.  Except that (duh) the
evidence was just as good that the receptive anal sex was the part that
was the problem.  There is actually a paper where the authors tried to
calculate a "rectal trauma index", and found that it correlated very
well to HIV infection risk.  Surprise.

     HHV-8 (also known as KSHV), the virus that almost certainly causes
KS, has all the epidemiology of a fecal-orally spread agent.  Think of
hepatitis A for the epidemiology of KSHV, whereas HIV has the
epidemiology of hepatitis B.  KSHV is not generally in blood (though
see evidence below), so it doesn't contaminate transfusions and
hemophiliac aids patients.  Or children.  But the virus is everywhere
where there's poor sewage control (most of Africa), and also it's a
silent epidemic in gay men.  Or was, until HIV brought it out in 1980
or so.  In Africa, where everybody has KSHV in the poor equatorial
countries, it's generally a sporadic and not very agressive disease.
But when HIV swept through these countries it caused epidemic KS with a
vengence in children, women, everybody.  And THAT form looked like the
gay KS of America.  HIV was the difference.

    Again, in the absense of HIV, KS is a slower and more sporadic
disease in Africa, and in America before HIV, KS was a disease of renal
transplant patients, and elderly men of mediterranean and semitic
descent.   And it wasn't particularly aggressive.    In countries with
higher than normal KSHV infection rates, like Italy, even women IV drug
abusers get KS much more often than expected when they get HIV.  In the
US, female IV drug users get KS much more rarely because they don't
have KSHV.  Sanitation.

   The incidence of KSHV in American men was examined in the NEJM this
April 2, 1998 issue, and it explains a lot.  The study was undertaken
as part of the San Francisco men's health study, where they basically
went from block to block in 1984-5 and recruted unmarried men ages
25-54 to be part of a prospective study to look at risk factors for
AIDS.  They got about 1034 men this way, almost at random, of which
about 80% turned out to be homosexual or bisexual.  They've been
following all these men for years.  It's a fantastic study which has
told us much about the natural history of HIV.  For example, of the 822
men who were homo or bi sexual, 400 were HIV-positive in late 1984.  By
contrast, in 1985 not a single one of the 212 men who reported no
homosexual contacts was found to be HIV-positive.   Since the baseline,
though 1994, AIDS has developed in 63% of the 400 homosexual and
bisexual men who were HIV-positive when the study began.   There has
been no AIDS in any of the 200 heterosexual HIV-neg men.

   The April 2 study looks at KSHV (HHV-8).  They went back and looked
for antibodies to KSHV in the 1985 initial baseline samples.  These
included the 400 who were HIV-positive, a random 200 samples of the 422
homo or bisexual men who were HIV-negative at that time, and finally,
200 of the 212 HIV-negative exclusively heterosexual men.

   Results are fascinating.  In 1985 sera, 37.6% of the bisexual and
homosexual men were positive for KSHV antibodies (223 of 593 men).  48%
of the HIV infected men had KSHV, but only 17% of the HIV-negative homo
or bisexual men did.   In the 195 exclusively heterosexual men tested,
NONE had KSHV antibodies.  Probability of being KSHV infection went up
linearly with number of male sexual-intercourse partners.  Probability
of infection with KSHV was not associated with infection with asthma,
diabetes, hayfever, or infectious mononucleosis (a marker for
non-intimate contact, or contact of the mouth to mouth sort).  However,
infection with KSHV WAS associated with incidence of infection with
several STDs (urethritis, gonorrhea, syphilis, genital or anal herpes
and (most interestingly) with incidence of infections with giardia and
shigella/salmonella.  These data suggest both sexual and fecal-oral
contact risks for KSHV, something which has been suggested indirectly
from the epidemiology for many years, but is here seen more clearly
than in any previous paper.  Interestingly, risk of being infected with
KSHV almost made a significant association with a history of
transfusion (uivarient p .06), suggesting that this mode does
occasionally occur, but is more rare than other modes.

   The link between KSHV and subsequent KS risk is also very clearly
seen in this paper.  For those men infected with both viruses (HIV and
KSHV) in 1985, probability of KS developing in the next 10 years was
49.6%.  Half!   KS was not seen in HIV-negative homosexual men at all,
even if KSHV positive .   Importantly, KSHV antibody not only preceeded
KS development and predicted it, but also early KSHV antibody was an
*independent* predictor of subsequent KS, independent of CD4 count or
number of sexual partners.  This is again indirect evidence against the
notion that KS is a caused by poppers or many sexual contacts.  As is
the case with HIV, such things were found to increase the chance of
getting KSHV, but once the virus was aquired, numbers of partners did
not affect risk of getting KS (as they should have if this was entirely
an environmental exposure disease, or if KSHV was merely a marker for a
yet unfound sexually transmitted agent which caused KS).

    Readers will remember that once men were infected with HIV,
subsequent use of poppers, and subsequent numbers of partners, made no
impact on future risk of developing AIDS.  That is one important way
epidemiologists know they have the cause of a problem.  If many things
correlate with risk of getting a diseases, but all things stop
correlating after one of the variables changes, then that is likely to
be the causal variable of interest.  We now have studies showing such a
relationship between HIV and AIDS, and between KSHV and KS.

                                           Steve Harris, M.D.

From: B. Harris)
Subject: Re: The New AIDS disease
Date: 9 May 1998 08:05:54 GMT

In <> George Lagergren
<> writes:

>     I believe in Africa that AIDS was spread thru hetrosexual action.
>     Big question:  Why is AIDS a "new" disease beginning about 1980?
>     Have not people had immune system problems throughout history?

     Think of the new Ebola and Hanta virus outbreaks.  Think of the
new strains of flu virus that sweep the Earth periodically.  Where do
new viral diseases in humans come from?  Animals.

     HIV-2, which causes AIDS in West Africa, is basically the same
virus called SIV in monkeys.  It's just SIV that has been transferred
to humans, and now causes disease in them.  It doesn't hurt monkeys,
but it causes AIDS in baboons and macaques.

     HIV-1, the main AIDS virus, and the one which causes almost all
the disease in Africa and America, is closest in structure to a virus
found in chimpanzees.  It probably came from chimpanzees, sometime
before 1959, spreading slowly in humans at first because of slow human
movement in equatorial Africa before industrial development.  Not
surprizingly, HIV-1 causes a very mild disease in chimps.  They lose
the same cells in their immune systems that humans do, but only a few
chimps given HIV-1 have lost enough to become ill enough to be classed
as having AIDS.  From what we can see, however, the process of
infection of HIV-1 in chimps, and HIV-2/SIV in baboons and macaques, is
identical.  The same part of the immune system is destroyed.

    The worldwide outbreak of AIDS is apparently related to the
Kinshasha highway, which connected the main AIDS regions in equatorial
Africa (endemic areas for chimps) with the coast.  From there it spread
to France in the early to mid 1970's.  Starting in 1976, a French
Canadian homosexual airline steward who had been in France spread the
disease to many gay men on both coasts of the United States.  HIV was
recovered from serum specimens stored from vaccine tests in gay men in
the US, starting in 1978.  It wasn't seen before then.  The first AIDS
case in the US showed up in 1980, and a number of cases caused the
problem to be recognized in 1981.  The maximal rate of silent HIV viral
infections in gay men, in transfusions, and in hemophilia products was
in 1982, all before the clinical disease itself (which takes at least
several years to incubate in most people) had shown up more than a few
hospital cases.   There wasn't a test for HIV until 1985, and by then
it was too late for hundreds of thousands of people in the US, who had
already been infected.

                                       Steve Harris, M.D.

From: B. Harris)
Subject: Re: AIDS statistics
Date: 19 Aug 1998 07:16:00 GMT

In <> tbone55@hotmail<SPAM>.com
(Buddie) writes:

>what is the current number of people who are estimated to be infected
>with the HIV virus and with full-blown AIDS?
>>   HIV virus-- 20 million.   Full blown AIDS-- maybe 2 million.
>Is this world wide or in the US.

World wide

From: B. Harris)
Subject: Re: More important information on AIDS in Africa
Date: 28 Dec 1998 23:46:19 GMT

In <> (Richard A. Schulman) writes:

>On 21 Dec 1998 19:40:35 GMT, B. Harris)
>>   No, almost all of the AIDS in Africa is caused by HIV-1, exactly as
>>                                        Steve Harris, M.D.
>What hypotheses have been developed in an attempt to explain why the
>percentage of females afflicted with AIDS in Africa is approximately
>50% of the total afflicted population (in contrast to the
>male-weighted epidemiological profile for the Americas and Europe)?
>Is receptive anal intercourse more common among female prostitutes in
>Africa? Is bisexuality more common? Are there diseases or cultural
>practices common to the affected African areas that might make females
>highly susceptible to HIV-1 infection even in vaginal intercourse?
>(posted and emailed)


   The short answer is that nobody knows for sure.

   I think the last hypothesis is presently the leading one.  Africa
has a lot more other (untreated) STDs which cause ulcers and
inflammation, and facilitate heterosexual transmission.  Also, lack of
circumcission with respect to America does not help.  Others hypotheses
are that people with African heritage simply have an increased genetic
susceptibility to HIV infection (this is seen even in the US), and that
helps heterosexual transmission (this is not that novel an idea-- for
example, people with black African heritage are known to be more
susceptable to cryptococcus, but less to other infectious diseases.
Your heritage determines your immune weaknesses and strengths).

   Other possibilities:, the strains of HIV-1 are a bit different in
Africa, and that may contribute.  Prostitution is more common in
Africa, with large workforces of men living in cities away from
families in the country for months or years at a time, for economic
reasons.  And no good public health system to keep the prostitutes
(semi) "clean."  I'm betting that it's the other kinds of STDs that
contribute here, since in the US, prostitutes have a surprisingly low
incidence of HIV infection, even those who don't use condoms with
"regular" customers.  But their surveilance and treatment for other
curable STDs is a lot better than in the third world.

   Finally, the difference between the African plague and the American
plague looks less impressive when you subtract a lot of the American
gay male plague which was caused by the unique American bathhouse
culture in the early 80's.  No other country had that, and in
consequence no other country had our very large gay plague.  They
probably would have, but we found out about it here first (after just
about every susceptable gay man had been infected silently circa
1981-4), and other countries learned from us to prevent it before the
experience could be copied to them.  And, of course, the test
availability in 1985 helped that effort enormously.  In America, we
didn't have the test during the worst years of spread among gay men and

                                        Steve Harris, M.D.

From: B. Harris)
Subject: Re: Origin of AIDS -- What ISN'T Reported...
Date: 21 Feb 1999 15:38:20 GMT

In <7akheg$m5$> "John"
<> writes:

>But they still make polio vaccines on monkey kidneys

   The only problem is that monkeys can't even be infected with the
most common strain of human HIV.  Ergo, it didn't come from monkeys.

                                       Steve Harris, M.D.

From: B. Harris)
Subject: Re: Origin of AIDS -- What ISN'T Reported...
Date: 21 Feb 1999 17:37:05 GMT

In <bK6U9GXuMZNp@mcrcr6> (ROBERT S.
HOLZMAN) writes:

>> But they still make polio vaccines on monkey kidneys
>> "Is it only a coincidence that HIV infection manifested itself at the same
>> time as the introduction of vaccines that are now known to have been
>> contaminated with simian viruses?" --Dr Strecker

    Well, maybe, no.   It was mass vaccination which was at the root of
the population explosion in equitorial Africa, which forced humans into
the last chimp habitats, made them run roads though there to the coast,
and then screw up the aggrarian economy so that massive numbers of men
left their wives and families in villages and went to work in cities
where there were prostitutes.  So it may be all connected.  Just not
the way Strecker thinks.

    Public health the quick and dirty way has been a disaster for
Africa.  You can't just suddenly double or triple the number of
surviving children, without providing some kind of technological
infrastructure to support them when they grow up.  Which is what
happened.  Not doing so is an invitation to all kinds of
epidemiological disasters later on, very much like preventing natural
forest fires, only to build up kindling later for the mother of all
blazes.  Mother nature bites back.  AIDS just happens to be one of the
bite-backs we got for messing with the ecological balance in Africa,
without doing it carefully and properly.  But TB, malaria, mass
starvation, and all the other miseries of Africa, are not far behind.
Attitudes in Africa in the 50's all kind of remind me of the hubristic
American Park Service's "conservation" attitudes during the same time.
And the disasters which resulted are strikingly similar in both cases.
Except in Africa we had piles of human bones instead of piles of deer
bones.  And Idi Amin, instead of Grizlies, attacked people and ate
them.  Otherwise it was just another day in Yellowstone.  What else,
really, could we expect?

                                      Steve Harris, M.D.

From: B. Harris)
Subject: Re: Right-Wing Congress and Free AIDS Drugs for All ! (was Re: HIV 
	vaginal load?!)
Date: 15 Apr 1999 09:28:46 GMT

In <> (fred)

>Gee, Richard. From my vantage point I see NO difference between
>yourself and those you demonize as "right wing".
>After all, YOU and the rest of the pharmaceutically-bribed
>mainstream establishment are in bed with the right-wing conservative
>element of Congress that has, WITHOUT protest and IN EXCESS of
>Clinton's annual budget requests, approved and increased funding
>for FREE drugs for those with HIV.
>While there is NO other FREE disease treatments coming out of
>Congress, one must wonder why these Bible-thumpers are so generous
>towards homosexuals, the sexually promiscuous ethnics and the
>needle junkies.

   Great lobbying.  World's best.  Hundreds of thousands of unusually
articulate Left liberal men in their 30s with lots of disposable income
and time and social consciousness, who know they're probably dying, but
won't be too ill to lobby for years and years yet.  It's a disease
researcher's dream.

    Contrast with Alzheimer's where the people who get it are usually
very elderly and ill with other things, and by the time anyone is
reasonably sure they have it, can't remember who the president is, much
less take part in an effective political campaign.   And whose kids
have mixed feelings about having them live forever anyway.  I somehow
doubt we'll see the assult on dementia arrive with quite the same force
in congress.  And yet, give this congress, it's so much more

From: B. Harris)
Newsgroups: sci.physics
Subject: Re: How can we use this gene theory to cure.
Date: 9 Jan 2000 14:06:42 GMT

In <> Uncle Al <>

>AIDS is your stndard RNA virus.  It incorporates into the host genome
>and is thereafter incurable.  Ditto Herpes zoster, chicknpox and
>shingles.  RNA viruses are HORRIBLE examples because they suffer on
>the average one mutation every reproduction.

   Ahem.  AIDS (more properly, HIV infection) is not your standard RNA
virus.  It's merely your standard retrovirus (a small subset of RNA
viruses).  It mutates far more quickly than viruses without a reverse
transcriptase.  Retroviruses go through part of the life cycle in which
they make DNA and insert it into yours. The vast majority of RNA
viruses (the flu, for instance) leave your DNA alone, and copy their
RNA directly from RNA, using enzymes they bring along, and which have
high fidelity.   A retrovirus is thus with you forevermore, rather like
the fly genes in Seth Brundle.  As for the flu-- two weeks later if
you're better, it's gone from your system.  The major mutations in flu
are not from what happens inside you, but from crossover from different
viral stains when they infect the same host (as when swine flu infected
pigs in Chinese rice paddies each droppings from avian flu
infected water fowl, and then pass the hybrid onto the family they live

  A few DNA viruses (Hepatitis B) go through an RNA intermediate, but
don't insert DNA into your genome-- they just stay around near your DNA
permanently in some people.  And a few (8 known) other DNA viruses get
DNA very closely associated with your DNA, where it always hangs around
in your cells permanently.  And causes cold sores, genital herpes,
chickenpox, CMV, and so on.  Also the virus that causes Kaposi's
sarcoma, interestingly.

From: "Steve Harris" <>
Subject: Re: HIV transsion via (inorganic) needle; not mosquito?
Date: Sat, 23 Mar 2002 17:53:55 -0800
Message-ID: <a7jbhe$7h8$> wrote in message ...
>Can any one provide a better explanation than this garbages 'explanation'?
>-- Chris Glur.
>Subject: <URL:>
>    Scientific American: Ask the Experts: Medicine
>If a used needle can transmit HIV, why can't a mosquito?
>P. Smith,
>Masclat, France

The basic answer is that there's far more blood on a used needle than on a
mosquito's mouthparts (which are far smaller and finer). Studies using
radiolabeled blood for quantitation have proven this conclusively.

BTW, your chance of getting HIV infection from a simple needle stick is only
1 in 500 (depending of course on the viral load of the person the needle
came from).  Even the amount of blood on a needle is pushing it.  Most HIV
infections in drugs users were not from 'needle sharing" per se, but rather
from needle+bulb or needle+syringe ("works") sharing.  Not the same at all.

I welcome email from any being clever enough to fix my address. It's open
book.  A prize to the first spambot that passes my Turing test.

From: "Steve Harris" <>
Newsgroups: za.politics,,
Subject: Re: HIV transsion via (inorganic) needle; not mosquito?
Date: Mon, 1 Apr 2002 11:09:53 -0700
Message-ID: <a8a87b$lsk$>

<> wrote in message news:a8a5im$5td$
> <> wrote:

> A proper analysis requires considering the size of HI virii.
> Which I understand (perhaps wrongly) are thousands of times
> smaller than malaria pathogens.  Perhaps if a 'few' virii are
> transfered via the mosquito's lance, they are 'killed' by the
> imune system ?   A properly answer is required


HIV viruses are 1/10th micron in diameter- so maybe 1/20th or 1/30th the
size of malarial parasites being injected by a mosquito.

Most HIV in the blood is non-functional and non-infective (the virions have
lost the knobs that allow them to attach to immune cells).  And yes, I'm
sure that even functional ones "die" (become nonfunctional; lose the knobs)
after being injected, and before they can hit a cell that has the right
receptors.  It takes thousands of HIV virions to be infective-- how many
thousands isn't known precisesly, because it requires knowledge of how
"sick" (or functional, if you will-- or "fresh") the little machines are
(thinking of viruses as "alive" or "dead" is not a very productive effort,
any more than it is for your automobile).  Again, the knobs on HIV are
coming off continuously, and after that they're pretty harmless (or perhaps
NEARLY harmless).

As for whether or no the immune system is able to "kill" or somehow
inactivate even HIV virions in working-order before they have the chance to
infect, my guess is that some of this takes place (as with all viruses). I
don't know the mechanism.  Some antibodies bind somewhat non-specifically.


From: "Steve Harris" <>
Subject: Re: HIV doesn't cause AIDS, drugs do.
Date: Mon, 13 May 2002 12:00:39 -0600
Message-ID: <abov7e$u4t$>

"Bob" <> wrote in message
> In article <YSRD8.7656$>, M
> Tools <> wrote:
> > Seems that if a person takes drugs that weaken the immune system, then
> > they would be more susceptible to diseases than folks who did not.
> > So........ If a person uses antibiotics a lot, they would have a
> > weaker immune system? If so, then it could be said that the drugs
> > cause Aids, etc.
> Only if it could be shown that such antibotics actually had a cause and
> effect.  Considering how many HIV- people are taking antibiotics over
> years long periods for various conditions ranging from acne to chronic
> abcesses and don't suffer any noticable immune impairment, there isn't
> much to support this hypothesis.

More than this, the epidemiological controls were run with the high risk
groups (IV drug users and hemophiliacs) who were HIV-neg.  In thousands of
people they failed to find anybody with AIDS-level depression of the immune
system (though it is true that mild immune depression with HIV routinely
DOES occur in both hemophiliacs and IV drug users).

AIDS is immune FAILURE (ie, you go down to almost no CD4 cells at all), and
that simply doesn't occur in risk groups without HIV (though there are many
people in risk groups who don't have HIV, so it's easy to find controls).
Moreover, in both hemophiliacs and IV drug users, the immune systems (CD4
counts) of HIV+ people were found to decay over time as the groups were
followed, whereas this did NOT happen in HIV- people, no matter how many
drugs they used, or how much factor concentrate. Nor was there a dose
response seen any longer in hemophiliacs and drug users, ONCE HIV status had
been controlled for-- the users of lots of factor concentrate and illegal
drugs progressed no faster than the users of small quantities, if they were
HIV-positive. So HIV was main effect.  Any gross correlation with AIDS and
drug or factor use is seen to be a spurious one-- a confounder, in
statistical terms, due to the fact that the more people shared needles or
used factor concentrate for hemophilia, the more likely they were to become
HIV+.  But once infected (once HIV status was controlled for) all
dose-effects for drug or hemophilia factor use disappeared completely from
the statistics.

How much more clear can this be?

Okay, let me add another touch. Let us note that there is no model of animal
AIDS which employs antibiotics or drugs of abuse.  No matter what you do to
animals with drugs, you cannot get all their lymphocytes to disappear, while
their other white cells look fine (the routine finding in AIDS). If AIDS was
caused by poppers or antibiotics or drugs of abuse as the critics contend,
it should be easy to show that you can selectively destroy nearly all of an
animals lymphocyte system with these, and keep it destroyed once the drugs
are stopped.  But nobody has ever been able to do this. The hypothesis that
it is possible is pure moonshine.

But there IS a good animal model for AIDS, involving retroviruses.  The few
remaining lymphocytes of humans with AIDS look beaten up in the same funny
way as those in cats with feline leukemia virus (FeLV), and that caused the
first investigators to suspect a retrovirus infected lymphocytes in people.
Eventually, such a class of virus was found-- the lenti-retroviruses or
lentiviruses. These are 9 kilobase 9-gene retroviruses with often a somewhat
cone-shaped core and always a mangesium-dependent RT, or reverse
transcriptase (the natural RT in normal cells and other retroviruses prefers
manganese, which is not the same stuff as magnesium).  These lentiviruses
infect lyphocytes are known to cause deadly immune destruction by lymphocyte
loss, when they cross the species barrier into closely related species.
Thus, in cats, feline immunodeficiency virus (FIV) doesn't hurt lions and
tigers (which carry it naturally), but it makes housecats lose their
lymphocytes and come down with opportunistic infections of the sort that
lymphocytes surpress. In primates, SIV doesn't harm african monkeys (which
carry it), but it causes Asian monkeys (rhesus and macaques) to lose their
lymphocytes and come down with opportunistic diseases (including many that
human aids victims get). Experimentally infected cats with FIV and macaques
with SIV lose their lymphocytes slowly (starting with the CD4+ kind)-- they
go down and they STAY down. Nothing much happens to their other white cells.
This awesome selectivity is seen with no other animal model for immune
destruction. Again, you can NOT do it with drugs. Those who wish to argue
this point are invited to post countering studies (good luck).

Finally, today we know that HIV-1 from human AIDS patients is very close in
structure to a retrovirus found in chimpanzees (SIV-cpz), and which is
naturally carried by chimps. It is (surprise!) 9 kilobase 9-gene
lenti-retrovirus with a cone-shaped core which carries a Mg dependent
reverse transcriptase. It doesn't usually make chimps ill. However, it was
ominously first isolated from humans who had lost their lymphocytes and
begun to suffer opportunistic infections, after having intimate contact or
fluid exposure from other humans with the same problem. And we know this
disease had its origins in Africa,  because historically the first cases
were described there in the 1970's, and stored HIV+ serum samples from
Africa are older than anyplace else in the world.  In fact, HIV and AIDS
historically come from just those countries in which chimps are still to be
found in the wild, and these countries have the highest HIV infection rates
in the world today.

And there you are.


From: "Steve Harris" <>
Subject: Re: Polio vaccine not resposible for HIV transmission
Date: Fri, 16 May 2003 13:35:03 -0700
Message-ID: <ba3i40$a7g$>

"Roger Schlafly" <> wrote in message
> "Vaccine-Man" <> wrote
> > A paper in the _Proceedings of the Nat'l Academy of Sciences (USA)_
> > will be published shortly that shows HIV-2 was present in humans no
> > later than 1945. ...
> Your statements don't even make any sense. Of course it was present
> later than 1945. When the paper is published, post the URL and we can
> read it for ourselves, and we can see what it really says.

He probably means no earlier than 1945.

HIV-2 is essentially identical with SIV from African
monkeys. It hasn't been in humans long, since it has mutated
almost not at all.

HIV-1, the major cause of AIDS, by contrast has quite a few
differences from SIV-cpz, the chimp version of SIV from
which it is apparently derived. It's obviously been in
humans for longer.

Why did HIV-1 it start to spread out of Africa only in the
early-70's? Probably because it was confined to isolated
equatorial African populations. When the Kinshaha highway
was built, the virus had a way to get out, to the coast
cities, and then onto jets. It got to France where a gay
promiscuous Canadian airline steward picked it up and took
it across the Altantic starting about 1976. From then on, it
was off and running.

From: "Steve Harris" <>
Subject: Re: Polio vaccine not resposible for HIV transmission
Date: Fri, 16 May 2003 17:48:21 -0700
Message-ID: <ba40uu$qb8$>

"john" <> wrote in message
> Bullshit said with Authority is the best.  Those viruses sure like
> modern transport!  That monkey to man transmission sure looks likely
> with your polio vaccs grown on monkey tissue.
> That beats the trans Atlantic Airlines

There's no evidence for it. HIV-1, which causes 99.9+% of
AIDS in the world, is a chimp virus, not a monkey virus.
Most of AIDS certainly cannot have come from green monkey
derived polio vaccine. That kind of epidemic would be HIV-2
or nothing.

From: (Steve Harris
Subject: Re: Why HIV is so Prevalent in Africa
Date: 10 Oct 2004 17:58:06 -0700
Message-ID: <>

James Michael Howard <> wrote in message
> Why HIV is so Prevalent in Africa:


One problem with your hypothesis is that it runs up severely into some
nasty facts.  We know testosterone cannot be a very important factor
in development of HIV infection into AIDS, because risk of people who
seroconverted to HIV after transfusions of tainted blood (in the mid
1980's before the HIV test was available to screen the blood supply)
have been examined. There's a big age effect in such data (the older
the person, the sooner they develop AIDS after HIV seroconversion from
a transfusion), but there is no sex effect. Women take about the same
average time (10 years) to develop transfusion-related AIDS as do men.


From: (Steve Harris
Subject: Re: Why HIV is so Prevalent in Africa
Date: 11 Oct 2004 19:55:38 -0700
Message-ID: <>

James Michael Howard <> wrote in message

> On 10 Oct 2004 17:58:06 -0700, (Steve Harris
> wrote:
> >One problem with your hypothesis is that it runs up severely into some
> >nasty facts.  We know testosterone cannot be a very important factor
> >in development of HIV infection into AIDS, because risk of people who
> >seroconverted to HIV after transfusions of tainted blood (in the mid
> >1980's before the HIV test was available to screen the blood supply)
> >have been examined. There's a big age effect in such data (the older
> >the person, the sooner they develop AIDS after HIV seroconversion from
> >a transfusion), but there is no sex effect. Women take about the same
> >average time (10 years) to develop transfusion-related AIDS as do men.
> >
> Thanks, Steve.  Please provide citations to support your remarks.  I
> had a lot of trouble finding support for you remarks.  I need this in
> order to better respond.


This should be interesting.

There are many such papers. Here are 4 off the top. You can also look
at any good textbook of AIDS, and I suggest you do so..

1. Epidemiology. 1998 Nov;9(6):605-12.

Comment in:
    Epidemiology. 1998 Nov;9(6):590-3.

Effect of gender, age, transmission category, and antiretroviral therapy
on the progression of human immunodeficiency virus infection using
multistate Markov models. Groupe d'Epidémiologie Clinique du SIDA
en Aquitaine.

Alioum A, Leroy V, Commenges D, Dabis F, Salamon R.

INSERM U330, Universite Victor Segalen, Bordeaux, France.

This article illustrates the use of time-homogeneous Markov models with
covariates to estimate the AIDS incubation period distribution from
prevalent cohorts and to evaluate the effect of factors such as gender,
age, human immunodeficiency virus (HIV) transmission category, and
antiretroviral therapy on disease progression. We applied this
methodology to the analysis of data from a cohort of 3,027 patients
enrolled from a hospital-based surveillance system of HIV infection in
the Bordeaux University Hospital and four secondary public hospitals in
southwestern France. A total of 998 individuals (33%) progressed to AIDS
during a median follow-up period of 34 months. Based on a progressive
three-state Markov model, the estimated mean and median incubation
periods were 9.1 years [95% confidence interval (CI) = 8.7-9.6] and 7.5
years (95% CI = 7.2-7.9), respectively. Our analyses showed a similar
disease progression in men and women {please note, Mr. Howard]; we
observed a more rapid progression for older subjects compared with
younger ones and for homosexual men compared with heterosexuals,
intravenous drug users, and transfusion recipients, who had similar
disease progression rates after adjusting for age. The use of
antiretroviral therapy appeared to slow disease progression. Moreover,
the results indicated that a combination therapy of zidovudine with
another antiretroviral drug may be more efficient than zidovudine

PMID: 9799168 [PubMed - indexed for MEDLINE]

2. Ann Intern Med. 1990 Nov 15;113(10):733-9.

Comment in:
    Ann Intern Med. 1990 Nov 15;113(10):729-30.

Infection with human immunodeficiency virus type 1 (HIV-1) among
recipients of antibody-positive blood donations.

Donegan E, Stuart M, Niland JC, Sacks HS, Azen SP, Dietrich SL, Faucett
C, Fletcher MA, Kleinman SH, Operskalski EA.

University of California, San Francisco.

OBJECTIVE: To assess the incidence of human immunodeficiency virus type
1(HIV-1) transmission by antibody (anti-HIV-1)-positive blood components,
and to determine the immunologic and clinical course in HIV-1-infected
recipients.  DESIGN AND SUBJECTS: We retrospectively tested approximately
200,000 donor blood component specimens stored in late 1984 and 1985 for
anti-HIV-1, and we contacted recipients of positive specimens to
determine their serologic status.  They were compared with both
recipients of HIV-1-negative transfusions and healthy (untransfused)
controls. Subjects were seen at 3- to 6-month intervals for up to 4 years
for clinical and immunologic evaluations.  MEASUREMENTS AND MAIN RESULTS:
Of 133 recipients, 9 had other possible exposures.  Excluding these
cases, 111 of 124 (89.5%) were anti-HIV-1-positive (95% CI, 84.1% to
94.5%). The recipient's sex, age, underlying condition, and type of
component did not influence infection rates [Please note, Mr. Howard].
The cumulative risk for developing the acquired immunodeficiency syndrome
(AIDS) within 38 months after transfusion was 13% (CI, 7.5% to 21.6%). At
36 +/- 3 months after the index transfusion, seropositive recipients had
lower counts of CD2+CDw26+, CD4+, CD4+CD29+, and CD4+CD45RA+subsets and
more CD8+I2+ lymphocytes than did recipients of anti-HIV-1-negative
transfusions. The CD4+ and CD2+CDw26+subsets changed the most rapidly.
The absolute CD8+ count remained normal. CONCLUSIONS:  Transfusion of
anti-HIV-1-positive blood infected 90% of recipients. The rate of
progression to AIDS within the first 38 months after infection was
similar to that reported for homosexual men and hemophiliacs. Although
most lymphocyte subset counts changed over time, CD8+ counts were

PMID: 2240875 [PubMed - indexed for MEDLINE]

3. AIDS. 1992 Oct;6(10):1187-93.

Women and HIV infection: a cohort study of 483 HIV-infected women in
Bordeaux, France, 1985-1991. The Groupe d'Epidémiologie Clinique
du SIDA en Aquitaine.

Morlat P, Parneix P, Douard D, Lacoste D, Dupon M, Chene G, Pellegrin JL,
Ragnaud JM, Dabis F.

Centre Hospitalier Regional et Universitaire (CHRU) of Bordeaux,

OBJECTIVES: To study the epidemiological trends, clinical patterns,
evolution and prognosis of HIV infection in women. DESIGN: Cohort study
of 1816 HIV-infected patients. RESULTS: Up to 1 January 1991, 483 (26.6%)
of the patients reported to the Groupe d'Epidemiologie Clinique du SIDA
en Aquitaine surveillance system were women. The male-to-female ratio has
decreased progressively (3.4:1 in 1985; 2.7:1 in 1990) over time. Fifty
per cent of HIV-infected women are or have been intravenous drug users
(IVDU). The proportion of heterosexually acquired HIV infection increased
from 11.6 to 34.6% over the last 5 years; 46.9% of the women infected
through heterosexual intercourse reported sexual contacts with male IVDU.
Excluding Kaposi's sarcoma, no significant difference was observed
between men and women in the overall distribution of AIDS-defining
events. The observed trend of a slower progression to AIDS in women,
compared with men, disappeared when controlling for prognostic variables.
However, female sex significantly enhanced survival after AIDS diagnosis
in multivariate analysis (relative risk, 2.7; 95% confidence interval,
1.1-6.2). CONCLUSION: Early diagnosis of HIV infection in female patients
and prevention of HIV infection among women is now a priority for public
health interventions, both in industrialized and in developing countries.

PMID: 1466851 [PubMed - indexed for MEDLINE]

Comment: Note that the enhanced survival of women here after AIDS
appears, is by comparison to homosexual men. This is not a fair
comparison since homosexual men are known to have multiple other
coinfections. When HIV-infected heterosexual women are compared with
**heterosexual men of the same age,** the difference in outcomes
generally disappears.

4. J Acquir Immune Defic Syndr Hum Retrovirol. 1998;17 Suppl 1:S13-6.

Determinants of progression to AIDS in HIV-infected individuals: an
update from the Italian Seroconversion Study.

Rezza G.

National AIDS Unit, Centro Operativo AIDS, Istituto Superiore di Sanita,
Rome, Italy.

The Italian Seroconversion Study (ISS) involves 16 major HIV-treatment
centers across Italy and about 1,200 individuals. These individuals were
HIV-negative less than 2 years before the first positive test and
seroconverted between 1980 and 1994. The majority were infected through
i.v. drug use (56%), male-to-male sex (25%), and heterosexual contact
(7%). For each end point, crude and adjusted relative hazards were
calculated using standard survival techniques such as Kaplan-Meier
curves, log-rank test, and Cox proportional hazards regression models.
Autoregression models were used to describe CD4 cell reductions.
Objectives were as follows: to estimate HIV disease progression rates; to
assess whether there are differences in the rate of development of severe
immunosuppression, AIDS, and death according to age, gender, and exposure
category; to identify co-factors and predictors of disease progression;
and to evaluate the clinic-based population "effect" of antiretroviral
treatment. The risk for developing AIDS among individuals in the ISS
cohort was less than 50% by 10 years after HIV seroconversion. Using
univariate analysis, more rapid progression was found for older
individuals than for younger individuals and for homosexual men compared
with those in other exposure categories. No difference between men and
women was observed. [Please note, Mr. Howard] After adjusting for age,
differences among exposure groups disappeared. Individuals with a history
of acute HIV disease were more likely to develop AIDS than other
seroconverters.  Co-infection with HCV and HTLV-II did not accelerate
progression to AIDS. The cumulative incidence of receiving pre-AIDS
therapy within 7 years of seroconversion was 49.2% (95% CI 45.3-53.0).
The relative hazards of developing AIDS in patients who started treatment
with zidovudine (AZT) monotherapy was 0.57 (0.36-0.91) and 0.92
(0.64-1.33) within the first year and after 1 year from AZT initiation,
respectively. The effect was greater among homosexual men than among i.v.
drug users. In conclusion, incident cohort studies may provide accurate
information on incubation time and co-factors for disease progression.
Observational studies may also provide useful information about the
effect of treatment at the community level, which may complement the
results of clinical trials.

Publication Types:
    Multicenter Study

PMID: 9586645 [PubMed - indexed for MEDLINE]

From: (Steve Harris
Subject: Re: The House That AIDS Built
Date: 31 Oct 2004 21:13:34 -0800
Message-ID: <>

World Peace NOW <> wrote in message

> The House That AIDS Built
> by
> Liam Scheff
> This article deals with pharmaceutical abuse in a children's home in
> NYC. This is a most controversial story ) however, it's entirely based
> in fact and good reporting. I hope you'll find it as compelling and
> shocking as I did investigating it.
> This piece was investigated and written in summer / winter 2003 and
> published in January 2004.
> Introduction:
> In New York's Washington Heights is a 4-story brick building called
> Incarnation Children's Center (ICC). This former convent houses a
> revolving stable of children who've been removed from their own homes by
> the Agency for Child Services. These children are black, Hispanic and
> poor. Many of their mothers had a history of drug abuse and have died.
> Once taken into ICC, the children become subjects of drug trials
> sponsored by NIAID (National Institute of Allergies and Infectious
> Disease, a division of the NIH), NICHD (the National Institute of Child
> Health and Human Development) in conjunction with some of the world's
> largest pharmaceutical companies ) GlaxoSmithKline, Pfizer, Genentech,
> Chiron/Biocine and others.
> The drugs being given to the children are toxic ) they're known to cause
> genetic mutation, organ failure, bone marrow death, bodily deformations,
> brain damage and fatal skin disorders. If the children refuse the drugs,
> they're held down and have them force fed. If the children continue to
> resist, they're taken to Columbia Presbyterian hospital where a surgeon
> puts a plastic tube through their abdominal wall into their stomachs.
>  From then on, the drugs are injected directly into their intestines.
> In 2003, two children, ages 6 and 12, had debilitating strokes due to
> drug toxicities. The 6-year-old went blind. They both died shortly
> after.  Another 14-year old died recently. An 8-year-old boy had two
> plastic surgeries to remove large, fatty, drug-induced lumps from his neck.
> This isn't science fiction. This is AIDS research. The children at ICC
> were born to mothers who tested HIV positive, or who themselves tested
> positive. However, neither parents nor children were told a crucial fact
> -- HIV tests are extremely inaccurate.(1,2)  The HIV test cross-reacts
> with nearly seventy commonly-occurring conditions, giving false positive
> results. These conditions include common colds, herpes, hepatitis,
> tuberculosis, drug abuse, inoculations and most troublingly, current and
> prior pregnancy.(3,4,5) This is a double inaccuracy, because the factors
> that cause false positives in pregnant mothers can be passed to their
> children ) who are given the same false diagnosis.
> Most of us have never heard this before. It's undoubtedly the biggest
> secret in medicine. However, it's well known among HIV researchers that
> HIV tests are extremely inaccurate ) but the researchers don't tell the
> doctors, and they certainly don't tell the children at ICC, who serve as
> test animals for the next generation of AIDS drugs. ICC is run by
> Columbia University's Presbyterian Hospital in affiliation with Catholic
> Home Charities through the Archdiocese of New York.


Sorry, but this is complete baloney. These days, no child would be
given HIV therapy without monitoring viral load to see if it was
working to slow replication of the virus. They measure virus RNA
levels for this and do it multiple times. It's impossible to have
false positives under such conditions.

There are no citations given for the wild statements in the article,
but doubtless they're the same old tired stuff which misinterpreted
part of the old antibody tests for HIV which were the standard in the
late 80's (look at the dates on the citations if you dare post them),
but are certainly never used alone in the 21st century. Any child part
of a research drug protocol would have their viral load levels
measured many times, and probably in many ways. And probably even have
viral drug-resistance genes mapped. Something hard to do if there's no

Which is not to say that it's possible that some doctors not looking
at the big picture are not capable of using drugs to make a child who
really has HIV, perhaps even rapidly replicating HIV, a lot sicker
with the drugs than the child would have been if left alone with
untreated HIV. That's a matter of clinical judgment, and it can be
lacking. But it's a totally separate question from this really stupid
suggestion that the kids never had the virus in the first place.


From: Steve Harris <>
Subject: Re: Drugmakers not following up speedy approval-US study
Date: 6 Jun 2005 10:53:23 -0700
Message-ID: <>

>>I am familiar with his work and have corresponded with him. I think
these four nutrients are indeed critically important aspects to the
development of HIV disease. However, I do not believe prior deficiency
will necessarily thwart progression any more than repletion will
completely prevent disease progression. <<


Out of curiousity, what are they?  We've known of a Se connection with
HIV for years, and I"ve been advising people with HIV to supplement
with selenium for  a decade. Recently it's been suggested that
manganese (Mn) might be important also, as most retroviruses are Mn
dependent, but the lentiviruses like HIV use Mg for their reverse
transcriptase, and perhaps Mn fouls them up.  That would be interesting
as well.

Now, I can't guess the two others.


From: Steve Harris <>
Subject: Re: Drugmakers not following up speedy approval-US study
Date: 8 Jun 2005 13:12:34 -0700
Message-ID: <>

>>However, even THAT review fails to recognize Skurnick's work on
reduced magnesium and the MASSIVE loss of sulfur (mostly via cysteine)
that Droge's group has identified. <<


Yeah, I know Droge as being Dr. Glutathione. But just about any bad
chronic condition seriously screws up glutathione. It's sort of a
biochemical marker for looking skinny and crappy. So much so that we
seriously thought of testing glutathione ester (which is absorbed) as
an anti-aging drug.  Cysteine has been tested, of course, and although
initially looking good, probably is no better than the dietary
restriction it causes.

These amino acids all cause problems when given individually. If
there's anything in this, you'd want to feed proteins with specially
high sulfur and tryptophan contents, like whey.  And I see that there
have been some such studies in HIV.


From: Steve Harris <>
Subject: Re: Dairy & Allegies
Date: 19 Jun 2005 15:33:05 -0700
Message-ID: <>

>>The AIDS curve is slowly decreasing statistically <<

What the devil do you mean by that?  Worldwide HIV infection and AIDS
deaths both increase exponentially year by year. With no end to the
increase in sight until most of the people in Africa and East Asia who
practice unsafe sex, are dead. Even then, without a vaccine, this
plague will continue to burn among newborns and the young, killing a
fresh % every generation.


Subject: Re: Dairy & Allegies
From: (David Wright)
Message-ID: <ELpte.477$>
Date: Mon, 20 Jun 2005 02:22:28 GMT

In article <>,
Steve Harris <> wrote:
>>>The AIDS curve is slowly decreasing statistically <<
>What the devil do you mean by that?  Worldwide HIV infection and AIDS
>deaths both increase exponentially year by year. With no end to the
>increase in sight until most of the people in Africa and East Asia who
>practice unsafe sex, are dead. Even then, without a vaccine, this
>plague will continue to burn among newborns and the young, killing a
>fresh % every generation.

And the situation is even worse than the official reports say it is.

I had a fascinating conversation a couple of weeks ago with a woman
who goes to Kenya every few months to work with various NGOs there;
her main goal is to make the groups she works with self-sustaining.

In any case, she told me that the whole idea of adopting infants from
Africa (at least that part of Africa) has never been an issue, because
children were considered part of the entire village, and as long as
there was one chief or one grandmother left in the village, that's
where the children would stay.  But now we have the unprecedented
situation of *all* the adults in a village dying.  In addition, she
told me the actual AIDS infection rate far exceeds the claimed rate;
this is not publicized because they don't want to scare off the
tourists.  On the other hand, it also leads to a fatalistic attitude
where almost every adult assumes he or she is infected -- and then
sometimes they find out that they aren't, which can actually come as a

  -- David Wright :: alphabeta at
     These are my opinions only, but they're almost always correct.
     "Are you going to come quietly, or do I have to use earplugs?"
                                        -- The Goon Show

From: Steve Harris <>
Subject: Re: sometimes we have to tell the dying "no"
Date: 22 Jul 2005 11:50:52 -0700
Message-ID: <>

Happy Dog wrote:
> "outrider" <> wrote in message news:

> > Statins make multiple millions upon millions for shareholders every
> > year. Drugs shilled for a disease that doesn't exist. To do no-one
> > knows what. Profit. They make a lot of profit; while creating injured
> > living unproductive limping lives, sliding into dying from the drug and
> > the drug induced diseases. This is an example of profits being pieces
> > of information about what things are working efficiently.
> If you can prove that statins are sold under the auspices of a conspiracy,
> then you have something.  But, you won't.  Fortunately, you can officially
> avail yourself of plenty of money liberated from taxpayers and feel proud to
> have defended legalized larceny.  You have no friends here.  I'd recommend a
> sock-puppet to pump you up.
> moo


Christ. This reminds me of the AIDS deniers, who vasilated between the
idea that HIV doesn't exist, or else that it does, but is harmless and
AIDS, as an infectious disease doesn't "exist" (rather, it's just a
giant phara conspiracy fronted by shills). This went on for quite
awhile and provided quite a lot of sparks back during the days when the
anti-HIV drugs weren't much good.

About 1995 the protease inhibitors arrived and high active
antiretroviral cocktails began to be possible. The HIV-infected HIV
skeptics who had low lymphocyte counts were then faced with a grim
choice: take the drugs and admit they were wrong, or else die. Some of
them chose to die. The rest of them now take the drugs and have shut
up. The only people we really have left in the debate are the people
who never had HIV to begin with, or else are among the small and lucky
group who actually can live wtih HIV without much viral reproduction or
immunosuppression, even without the drugs (10 to 15%).

These last group of people cause hell of course, because some of them
are narcisists. THey figure if the HIV doesn't harm THEM, why then, it
can't be harming *anybody.* Because their own experience trumps that of
the WHOLE world. Hey, I don't wear MY seatbelt and *I've* never been
hurt! And therefore the entire world MUST BE engaged in a VAST
conspiracy to make everybody with their diagnosis do something none of
them would really benefit from doing. It's sort of like those 85
year-old 3-pack-a-day smokers you find now and again, puffing away and
cackling about the stupid health nuts.

People who happen to win at slots sometimes think the light of God
shines directly upon them. It's infantile, but some people never quite
grow up.


From: "Steve Harris" <>
Subject: Re: "Studies say sex not main AIDS cause"
Date: Wed, 5 Mar 2003 15:33:16 -0800
Message-ID: <b461jl$klk$>

"DGiunti" <> wrote in message
>   What planet are these people reporting from?  The heterosexual segment
> of the HIV epidemic has never ever decreased in America.  It's almost to
> the point where they make up the majority!

That all depends on whether or not you want to count women
being infected by bisexual men as part of the "heterosexual

The "hetero" AIDS epidemic in the developed world has always
had two very distinct parts:

Male-->female (common and not news)
Female-->male (still a very small fraction of total cases in
the West)

This is a very different situation from Africa and Asia. The
reasons for the difference are STILL not clear. They're
working on it. Without a really good female->male
transmission route, however, AIDS will never make it as a
pandemic in the West.  Sorry if that's not a politically
correct viewpoint, but there it is.

> Even with all the precautions take, and the
> denialism that articles like this continually feed, the epidemic is still
> growing among young heterosexuals!

Yes. More and more woman are being infected by bisexual men.

> If you get in and read some of the predicates for this paper, namely the
> transmission rates from the infected to the uninfected, (ranging from 1
> in 100 to 1 in 1000) you begin to see that these folks *want* to live in
> fantasyland! Their figures are orders of magnitude on the optimistic
> side!

Not for HIV+female-->male transmission in the US, they

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