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Bushmeat seeds new virus
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TC
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Joined: 02 May 2005
Posts: 1814

PostPosted: Fri Jul 14, 2006 5:30 pm    Post subject: Re: Bushmeat seeds new virus Reply with quote

GMCarter wrote:
Quote:
On 14 Jul 2006 09:52:41 -0700, "TC" <tunderbar@hotmail.com> wrote:

snip
Oh.... and it has not met Koch's postulates. Isolation of the virus is
only one part of Koch's Postulates. And if it has been isolated it must
have happen not very long ago because the last time I looked it hadn't
been isolated. Do you have a cite for this?

Ah, you know what? Frankly, it doesn't HAVE to fulfill Koch's
postulates. Not all infectious diseases do.

But as it so happens, HIV does:
http://www.niaid.nih.gov/publications/hivaids/12.htm

And the ONLY people who think HIV hasn't been isolated are the whack
jobs of the so-called "Perth group", some armchair theorizing nut
jobs. See, the denialist community is split:
1) Thinks HIV doesn't exist. Perties.

2) Thinks it does, but doesn't cause AIDS. Duesberg.

Both groups consist of a tiny cadre of cranks and right wing nuts who
have sucked in a few gullible lefties to tote their propaganda.

There's LOTS of data on the isolation of HIV. If it hasn't been, then
there are no infectious diseases and you can join the rank of
crackpots that believe that nonsense.

George M. Carter

Some of those "cranks and right wing nuts" are pretty highly respected
in their fields.

TC
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TC
medicine forum Guru


Joined: 02 May 2005
Posts: 1814

PostPosted: Fri Jul 14, 2006 5:32 pm    Post subject: Re: Bushmeat seeds new virus Reply with quote

TC wrote:
Quote:
GMCarter wrote:
On 14 Jul 2006 09:52:41 -0700, "TC" <tunderbar@hotmail.com> wrote:

snip
Oh.... and it has not met Koch's postulates. Isolation of the virus is
only one part of Koch's Postulates. And if it has been isolated it must
have happen not very long ago because the last time I looked it hadn't
been isolated. Do you have a cite for this?

Ah, you know what? Frankly, it doesn't HAVE to fulfill Koch's
postulates. Not all infectious diseases do.

But as it so happens, HIV does:
http://www.niaid.nih.gov/publications/hivaids/12.htm

And the ONLY people who think HIV hasn't been isolated are the whack
jobs of the so-called "Perth group", some armchair theorizing nut
jobs. See, the denialist community is split:
1) Thinks HIV doesn't exist. Perties.

2) Thinks it does, but doesn't cause AIDS. Duesberg.

Both groups consist of a tiny cadre of cranks and right wing nuts who
have sucked in a few gullible lefties to tote their propaganda.

There's LOTS of data on the isolation of HIV. If it hasn't been, then
there are no infectious diseases and you can join the rank of
crackpots that believe that nonsense.

George M. Carter

Some of those "cranks and right wing nuts" are pretty highly respected
in their fields.

TC

Which is a hell of a lot more than can be said about the american that
made the HIV/AIDS discovery and announced it at a press conference and
faile to actually publish his findings in a peer reviewed journal and
needs body guards to travel in public.

TC
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GMCarter
medicine forum Guru Wannabe


Joined: 07 May 2005
Posts: 193

PostPosted: Fri Jul 14, 2006 5:40 pm    Post subject: Re: Bushmeat seeds new virus Reply with quote

On 14 Jul 2006 09:21:23 -0700, "TC" <tunderbar@hotmail.com> wrote:

Quote:

GMCarter wrote:
On 13 Jul 2006 07:38:54 -0700, "TC" <tunderbar@hotmail.com> wrote:


snip
Sadly, because those slimy profiteering shits kill people who can't
afford their overpriced drugs, diagnostics, etc., does NOT mean that
HIV does not cause AIDS.

It does not mean that HIV does cause AIDS either. One concept has
nothing to do with the other.

I agree--but many denialists try to claim that AZT causes AIDS or
other unsupportable nonsense.

AZT is a toxic cocktail that had little or no testing done to ensure
any kind of safety of effectiveness of the drugs in combination in the
real world. And AZT does damage that closely mimics the symptoms of
AIDS. If you immune system wasn't compromised by HIV it will be
compromised by AZT.

Wrong in every statement. AZT is NOT a cocktail. It is a single drug.
AZT does NOT do damage to the immune system that mimics AIDS; it does
NOT cause CD4 counts to drop!

It can cause a myopathy that bears a clinical similarity to an aspect
of AIDS wasting but it is not the same and is easily distinguished.

AZT does NOT cause AIDS. It IS toxic, there is no question. It can
cause anemia and neutropenia. Not in everyone.


Quote:
Did you know that the research that was first presented at a press
conference announcing the discovery that HIV causes AIDS has never been
actually published?

LOL--no, I do NOT know that. In fact, that happens to be not true. The
Gallo/HHS announcement was made PRIOR to the publication but the
material was "in press." It was indeed published. It was part of the
race to announce to be the "first" though history tells us that the
original discoverers were Francoise Barre-Sinoussi and, possibly, Jay
Levy. Gallo was a third in that.

It was published "in the press"??? What the frig does that mean?

There was a press conference and the press published it. That's what
press conferences are usually about. The press usually mangles it too.

But that doesn't mean HIV doesn't exist or cause AIDS.

Quote:
When I
say that the study was never published, I mean that it was never
published in a scientifc journal where it could be scrutinized,
duplicated, critiqued or otherwise examined by the scientists that work
in the field of virology. It has never been published to be peer
reviewed, and that my friend, peer review that is, is the very basic
cornerstone of the scientific method.

Then you really ARE a complete fucking crank because it HAS been
published in peer-reviewed journals. Wow. Can you really be that
fucking stupid?

For example:
http://www.aegis.org/topics/hiv_exist.html

Quote:


AIDS, my dear, is not marketing crap. It is a situation that pharma
has capitalized on horribly.

AIDS is not marketing crap, it is a real health problem. The idea that
HIV, a simple retro-virus, is the sole cause of AIDS is a bit of an
issue though.

Yes, but not the way you mean it. HIV causes AIDS. HOW it does so
remains an extremely important and not yet fully elucidated question.
But that being said, there is an ENORMOUS amount of information about
how HIV causes AIDS, its replication cycle etc.

But no vaccine. It's just a virus.

Now you say it exists. Well, that's a start.

Quote:
Like many viri before it. Except
this little retro-virus has eaten up literally billions of dollars in
research money. When it was first announced, it was predicted that we
would have a vaccine within 18 months, because that was the state of
the science at the time. Virology is a fairly advanced field. They have
a pretty good idea of what they are doing, but HIV just seems to have
them completely stumped. And there is no other comparable problem in
the field of virology. They have effective vaccines, albeit containing
nasty s**t like mercury and other poisons, but that is a processing and
manufacturing issue. Manufactured without the poisonous crap, vaccines
actually are effective and developing vaccines is a well understood
process. Why this little retro-virus would be so elusive to deal with
is a big question.

I couldn't agree more. The problem you have is that you do not
understand the process in play. And again, LOTS of diseases do not
have vaccines or they have a vaccine that is nominally effective,
relying on herd immunity to take up the slack.

Quote:

Fundamentally, it is simple. People with HIV see a chronic and
persistent decline in CD4 T cell counts toward zero, if untreated. As
the CD4 count plummets, the ability to fight off infections (mostly
those defended against via cell-mediated immunity) is impaired and
then AIDS develops.

Except that a significant number of people who are HIV positive never
see this happen. And many people with the same symptoms are not HIV
positive. And compound this with the fact that there are numerous other
factors that can lead to the same problems with acquired impaired
immunity, which have mostly been conveniently ignore or minimized. What
factors? Narcotics and other drug use. Excessive use of blood
transfusions. Illness. Malnourishment. Semen in the colon. And many
combinations of these factors.

NONE of those factors cause persistent, continual declines in CD4
count.

Semen in the colon doesn't cause AIDS. HIV-infected semen in the
vagina or anus will lead to AIDS. Malnutrition does not cause AIDS
though it can play hell with immune function; problem is, there are
not that many people with HIV who are starving. HIV DOES cause
depletion in peripheral micronutrient status.

Drugs don't cause AIDS. If they did, I'd know a LOT more people with
AIDS. Drugs can, of course, screw you up--recreational or otherwise.
They can kill you. They don't cause AIDS.

And actually, most of the factors that you mention HAVE been looked
at. You ever actually bothered to look at the research or do you just
enjoy being spoonfed? Somehow, I would think not.

Finally, EVERY infectious disease has a significant number of
individuals who are exposed but either remain uninfected or do not
develop clinical symptoms of disease. What makes HIV so horrific in my
mind is that so FEW people are "elite controllers" of virus,
maintaining persistently normal levels of CD4 cells.

Quote:

One of the most breathtakingly stupid "arguments" of denialists is
that HIV causes pneumonia or cancer. It doesn't--infection results in
the impaired immunity that then makes a potentially LETHAL situation
of death by Pneumocystis, CMV, etc.

Well, stupid people often come up with strange and silly points to back
their arguments. But you won't here that said by me or the dozens of
virologists that disagree with the HIV/AIDS connection.

Bullshit. I've heard it said by LOTS of denialists over the years.
Including some HIV+ ones who have since died of AIDS.

Quote:
What HIV DOES cause is neuropathy, dementia and wasting, the latter of
which can be lethal.

And the likelihood of invasive infections of all types.

Not exactly. The types of infections that opportunistically take hold
with a low CD4 count are generally those that are held in check by a
robust cell-mediated immune response.

Quote:
If HIV/AIDS were just marketing crap, I'd still have a hell of a lot
of friends alive.

Well I don't know about that. It is truly a tragic situation and I
sympathize. But I can't help but wonder what would have happened if
there had been research on other possible causes other than HIV, and if
treatments had taken that into account. What if HIV is only a marker or
is just a marker that shows up more in the high risk population? What
if HIV has nothing to do with AIDS? Then your friends treatments,
suffering, and their deaths may have been prevented with other less
tragic means.

Darling there HAS been research. LOOK before you make these bold
statements that only reveal the fact that you have NOT looked.

But virtually all the research assumes the HIV/AIDS causality, and
excludes any possibility of any other causality.

Because most people are not fooled by "tinfoil hat" thinking. But
that's like saying, "gee, TB doesn't exist and no one doing TB
research sets up experiments that show that!"

How for dumb.

Quote:
Since the press
conference that presented the HIV/AIDS causality, virtually all
research in other causalities have been shut down.

That's 20 years darling. I remember back in the early 90s reviewing
the literature of the 80s. They looked at LOTS of things. NOTHING
before or since has been compelling as the role of HIV in causing
AIDS. And there ARE data.

Quote:
They are researching
one paradigm, HIV and AIDS. And researching HIV has been very lucrative
for the researchers. It pays fo rthem to keep researching something
that will never make sense and will never be resolved by continuing to
research what they are researching. And as long as we buy into the
HIV/AIDS causality, no vaccine will ever be found and the
pharmaceutical companies will makes billions in drug sales to AIDS
victims. The people profitting from AIDS are very happy with a
causality paradigm that leads to nothing but more research and drug
sales.

Phew. Cognitive dissonance, sweetie. If people didn't believe HIV
caused AIDS, they probably wouldn't look for a vaccine for HIV, now
would they? What the hell are you smoking?

Most of my friends that are alive with HIV have survived because they
had access to antiretroviral therapy. I base my judgment both on the
voluminous clinical literature and an enormous amount of observation.

Quote:

Syphilis is NOT a co-factor. Parasitic infections are NOT a co-factor.
They are not necessary for HIV infection to result in AIDS. They ARE
however VERY significant co-infections that can accelerate disease
progression.

By contrast, you're right in the sense that understanding HOW HIV
causes AIDS has pointed us away from a variety of interventions. Yet
even there, data are developing, albeit painfully slowly. For example,
a multivitamin has been shown to reduce disease progression rate by
30%. Not a cure but a significant intervention in HIV disease
management (nothing is a cure at this point).

Good nutrition is the key to the health of the immune system. It cannot
function properly without the necessary nutrients. Did you notice that
in africa they are getting away from their traditional foods and eating
more and more westernized nutrient-depleted grains and sugars and other
assorted manufactured crap? And in the environment they are in with
more infectious diseases like malaria, their immune systems are being
pounded down daily. I am not surprised that they are experiencing more
and more immune system failures. And also remember that in africa they
do not need an HIV test to be considered AIDS.

Oh, crap...you started out so well then wombled off into la-la land
again. Malnutrition is NOT AIDS...and the crap people eat in the US
that is resulting in rapidly escalating BMIs is VERY unhealthy. No
argument! But it is NOT AIDS.

Quote:

Yet politics prevents a vigorous embrace and utilization of this
because some fat miserable fucking stockholder doesn't make the
EXPECTED HUGE return on investment in pharma and fat fucking shits
like CEO Hank McKinnell won't make a murdering pofiteering killing on
selling multis that he can from selling Pfizer's drug.

As long as we believe that the cause is HIV, we will only research and
treat HIV. And the treatment is drugs. Pharma is making a killing, no
pun intended.

I agree--Pharma is making a killing. That doesn't mean the drugs don't
work, albeit with serious limitations.

Quote:
That you believe that HIV does not cause AIDS is the kind of rank
stupidity that renders all commentary on your otherwise sometimes
interesting posts of abstracts completely unreliable to me.

I think that the belief that a simple retro-virus could cause such a
plethora of various combinations of symptoms and system breakdowns is
kinda hard to believe.

Because you don't understand and just parrot some of the brain dead
crap denialists spout. Some of it was mildly entertaining or even
worth a look 17 years ago but at this point, it is just incredibly
stupid to parrot the same stupid and REFUTED whinings.

This is still a valid argument that has not been refuted. They've tried
to refute it but they haven't convinced some of the top virologits in
the world.

Aside from Duesberg, who else?

And if you want to start comparing lists of names of top research
scientists, I've got a bigger one than you!

And that's not even gay inches....

Quote:
And the fact that this simple retro-virus has
been able to completely baffle researchers and to evade being tamed by
vaccination is hard to believe. It is just a simple retro-virus like
thousands of other retro-viri.

Most retroviruses do NOT cause disease--and now name for me some
retroviruses for which a successful vaccine has been developed.

Exactly. Most do not cause disease. Retro-viri are not even full
fledged viri. Virulent viri are hard to kill, HIV can't even be grown
and isolated in the lab in optimal conditions, how is it going to be so
tough and persistent in less than optimal conditions in the human body?

What makes you repeat this idiotic and demonstrably refutable claim?
What data do you have?

HIV has been isolated. As has FIV, CAEV, EIAV, SIV--all of which cause
disease in their host animals.

Quote:
There's another story where the REAL disaster is missed by conspiracy
ditherings. The research community (and Pentagon) wasted HUGE amounts
of resources chasing after envelope vaccines that DO NOT WORK. And it
was quite apparent they did not work.

And what if the HIV/AIDS causality is bogus? What of the billions
wasted on useless research that could not possibly help anyone. And the
poison drug cocktails that were fed to patients to kill a non-existent
cause of the disease? And what of the ethics of those pushing the
HIV/AIDS causality while knowing that it is a bogus paradigm?

And what IF the moon is made of Green Cheese? And what IF you beat
your wife? And what IF there is a certain flatness to the world caused
by the sun swinging around it? I want PROOF I tells ya!

Show me the ONE PAPER that proves influenza causes ANY disease, huh?
SHOW ME!

Quote:

The disease has, for the most part, not gone much beyond the initial
risk groups in the Western world where a diagnosis requires a positive
HIV test. Many people with all the signs of AIDS are not HIV positive.

Provide evidence and clarification for this statement.

Check the stats.

Darling, you made the claim. I've been providing citations. I'd say
it's your turn to provide some back up for your commentary or STFU.

Quote:

Many HIV positive people have not developed any symptoms, even after
decades. A new term had to be created specifically for these people,
non-progressors.

You bet. Again--parroting ridiculous nonsense.

The term non-progressors did not exist until HIV researchers found HIV
positive people who failed to develop AIDS symptoms.

Well, of course not you fucking buffoon! LOL.

It also took a while before they realized that in the 80s not everyone
who was HIV+ was dying of AIDS. And then they began to look at them in
around the early 90s.

Quote:
First it was
thought that the virus took months to start doing the damage. Then when
HIV positive people failed to develop symptoms in the alloted time, the
time period was extended, and when the time lag became overly long and
the latent period had to be extended by years, the term was coined. It
is what scientists call a paradox, when one thing is expected and fails
to materialize as expected it becomes a paradox and yet another thing
for the to research, and of course, that means more research money for
them.

It's not in the slightest a paradox. Most people coming to see doctors
in the early 80s had AIDS: they had Pneumocystis or Kaposi's sarcoma.
And most died too quickly. By the mid-80s, a test was available. And
they realized that, like with EVERY infectious disease, there's a bell
curve. Some infected individuals develop AIDS VERY rapidly--with a few
months. That's the smaller proporiton. The majority, HIV disease is an
active, chronic infection that results in AIDS in about 8 years. That
hasn't changed.

Then there's a few--maybe 8-10%--who, though infected, do not develop
disease. These people are being investigated by folks like Jay Levy
and Bruce Walker to find out why--and if whatever about their bodies
(or the predominant circulating virus with which they are infected)
can lead us to better understanding of how to treat the disease.

It ain't over yet. By a long shot.

Indeed, 8000 men, women and children will die EVERY SINGLE DAY of
AIDS, mostly needlessly cause PHarma is so fucking greedy, they'd
rather let them die than lose a dime of profit.

Quote:

MOST infections have a pretty HUGE percentage of people who never
develop disease. Name me one that doesn't. TB. Ebola even!

That is some strange logic.

Explain why you think it is strange.

Quote:

What makes HIV so horrible is that so FEW people are long-term
non-progressors or "elite controllers" that sustain a low viral load
and no impact on CD4 counts.

In Africa, a positive HIV test is not even part of the official
definition. If you have a fever and have lost a significant amount of
weight, you are considered to have AIDS in Africa.

That is just WRONG. Yes, there are places in Africa where testing
(was) limited and clinical signs and symptoms were relied upon for a
diagnosis. However, these are fewer and fewer.

Money has been raised thru all kinds of intra-governmental granst and
aid that now they have money for testing. Pharma is now making a profit
there.

You bet. Profits are being made. It's disgusting and the very worst
distortion of the principles of capitalism.

That doesn't mean HIV doesn't cause AIDS.

snip...
Quote:
And darling, if you want to prove HIV causes AIDS--why gosh, take the
HIV challenge. Get a bit of infected blood--harmless right?

And inject it.

We'll see what happens.

I have no fears of HIV. And I would take you up on that. I kid you not.

Then you are an idiot. But if you're going to do it, I suggest you
make it a nice big public splash. What city do you live in?

You could get some terrific notoriety! The only thing is, if you're
wrong and develop AIDS, you'll piss of the denialists. But don't
worry, just like David Pasquarelli, they'll just blink and say "who"?

George M. Carter
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GMCarter
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Posts: 193

PostPosted: Fri Jul 14, 2006 5:44 pm    Post subject: Re: Bushmeat seeds new virus Reply with quote

On 14 Jul 2006 10:30:19 -0700, "TC" <tunderbar@hotmail.com> wrote:

Quote:


Some of those "cranks and right wing nuts" are pretty highly respected
in their fields.

LOL...by other cranks and nuts. BFD.
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GMCarter
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Joined: 07 May 2005
Posts: 193

PostPosted: Fri Jul 14, 2006 5:47 pm    Post subject: Re: Bushmeat seeds new virus Reply with quote

On 14 Jul 2006 10:32:30 -0700, "TC" <tunderbar@hotmail.com> wrote:

snip
Quote:
Which is a hell of a lot more than can be said about the american that
made the HIV/AIDS discovery and announced it at a press conference and
faile to actually publish his findings in a peer reviewed journal and
needs body guards to travel in public.

What the hell are you babbling about now? You're simply resorting to
making s**t up at this point. Who? What? When? Where??

George M. Carter

***
I take NEJM is not a peer-reviewed journal, eh?

Broder S, Gallo RC. A pathogenic retrovirus (HTLV-III) linked to AIDS.
N Engl J Med. 1984 Nov 15;311(20):1292-7.

PIP: Several converging lines of research have linked a human T-cell
lymphotropic retrovirus, human T-lymphotropic virus type III
(HTLV-III), to the pathogenesis of acquired immunodeficiency syndrome
(AIDS). This article traces the basic research that led to this
finding and outlines possible clinical implications of this new
information. Cultured cells derived from US patients with T-cell
growth factor receptive positive T-cell lymphoproliferative disease
were the source of the 1st isolates of human retroviruses in 1978-80.
It then became apparent that HTLV should be viewed as a family of
related T-cell lymphotropic retroviruses. The prototypical member of
the family is referred to as HTLV-I, while the 2nd member is
designated HTLV-II. HTLV-I has no common pattern of chromosomal
integration, yet can transform normal T cells in vitro, suggesting
that there is a trans mechanism for the leukomogenic effect of this
virus. All members of the HTLV family are exogenous viruses isolated
from mature T cells, infect mature T cells in vitro, have a reverse
transciptase with similar biochemical features, possess some
cross-reacting antigens, have major core proteins of similar size,
exhibit some homology in nucleotide sequence, have a pX sequence at
the 3' end of the genome, and induce formation of multinucleated giant
cells upon in vitro infection of some T cells. Knowledge of HTLV-III
is expected to affect many phases of basic research with clinical
implications. 1st, there are new possibilities for identifying early
cases of AIDS through antibody testing. 2nd, the discovery of an
immunosuppressive retrovirus in AIDS could serve as a stimulus to
re-examine endemic forms of cancer in Third World countries. 3rd, the
identification of HTLV-III makes it possible to study the effect of
more than 1 retrovirus in a given patient. 4th, current technology may
make it possible to begin formulating rational interventions directed
against a cause rather than the manifestations of AIDS.
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TC
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Joined: 02 May 2005
Posts: 1814

PostPosted: Fri Jul 14, 2006 8:50 pm    Post subject: Re: Bushmeat seeds new virus Reply with quote

GMCarter wrote:
Quote:
On 14 Jul 2006 10:32:30 -0700, "TC" <tunderbar@hotmail.com> wrote:

snip
Which is a hell of a lot more than can be said about the american that
made the HIV/AIDS discovery and announced it at a press conference and
faile to actually publish his findings in a peer reviewed journal and
needs body guards to travel in public.

What the hell are you babbling about now? You're simply resorting to
making s**t up at this point. Who? What? When? Where??

Dr. Robert Gallo announced that HIV causes aids at a press conference.
He still hasn't published the specific study that led to this finding.
The one below is not the seminal study that wasn't published. It is a
retrospective paper.

quote:

Several converging lines of research have linked a human T-cell
lymphotropic retrovirus, human T-lymphotropic virus type III
(HTLV-III), to the pathogenesis of acquired immunodeficiency syndrome
(AIDS). This article traces the basic research that led to this
finding and outlines possible clinical implications of this new
information.

unquote

It supposedly traces the basic research that led to the finding but his
own basic research that supposedly led to the finding announced at the
press conference was never and has never been published. And I see no
actual cites to any of the studies that he is supposedly reviewing in
this paper.

And he has seriously pissed off so many people with the way he did
science that he cannot freely move around in public without body
guards. A scientist cannot say: "This is the way it is and you all must
accept my word for it" and not publish the data for peer review.

The entire AIDS research machine had to spin around on a dime, stop
what they were doing, and accept his pronouncements without a published
paper. A lot of research that was not specifically pursuing the
HIV/AIDS connection was dumped and all funding went to only those
specifically studying HIV. All other lines of research, regardless of
validity was forcibly shut down.


Quote:

George M. Carter

***
I take NEJM is not a peer-reviewed journal, eh?

Broder S, Gallo RC. A pathogenic retrovirus (HTLV-III) linked to AIDS.
N Engl J Med. 1984 Nov 15;311(20):1292-7.

PIP: Several converging lines of research have linked a human T-cell
lymphotropic retrovirus, human T-lymphotropic virus type III
(HTLV-III), to the pathogenesis of acquired immunodeficiency syndrome
(AIDS). This article traces the basic research that led to this
finding and outlines possible clinical implications of this new
information. Cultured cells derived from US patients with T-cell
growth factor receptive positive T-cell lymphoproliferative disease
were the source of the 1st isolates of human retroviruses in 1978-80.
It then became apparent that HTLV should be viewed as a family of
related T-cell lymphotropic retroviruses. The prototypical member of
the family is referred to as HTLV-I, while the 2nd member is
designated HTLV-II. HTLV-I has no common pattern of chromosomal
integration, yet can transform normal T cells in vitro, suggesting
that there is a trans mechanism for the leukomogenic effect of this
virus. All members of the HTLV family are exogenous viruses isolated
from mature T cells, infect mature T cells in vitro, have a reverse
transciptase with similar biochemical features, possess some
cross-reacting antigens, have major core proteins of similar size,
exhibit some homology in nucleotide sequence, have a pX sequence at
the 3' end of the genome, and induce formation of multinucleated giant
cells upon in vitro infection of some T cells. Knowledge of HTLV-III
is expected to affect many phases of basic research with clinical
implications. 1st, there are new possibilities for identifying early
cases of AIDS through antibody testing. 2nd, the discovery of an
immunosuppressive retrovirus in AIDS could serve as a stimulus to
re-examine endemic forms of cancer in Third World countries. 3rd, the
identification of HTLV-III makes it possible to study the effect of
more than 1 retrovirus in a given patient. 4th, current technology may
make it possible to begin formulating rational interventions directed
against a cause rather than the manifestations of AIDS.

Where are these rational interventions being that they started
formulating in the 1980's?

TC
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TC
medicine forum Guru


Joined: 02 May 2005
Posts: 1814

PostPosted: Fri Jul 14, 2006 8:58 pm    Post subject: Re: Bushmeat seeds new virus Reply with quote

GMCarter wrote:
Quote:
On 14 Jul 2006 10:30:19 -0700, "TC" <tunderbar@hotmail.com> wrote:



Some of those "cranks and right wing nuts" are pretty highly respected
in their fields.

LOL...by other cranks and nuts. BFD.

Compared to Gallo, they are friggin' geniuses, even the crackpots.

I suggest that you actually check their scientific pedigrees before you
make such sweeping bigotted statements. You've just shown us your real
colors. You are closed-minded idiot hanging onto the words of corrupt
officials like Gallo. And you cast stones towards persons that can
intellectually run circles around Gallo.

Instead of attacking an entire cadre of highly respected virologists
based on Gallo's POV, how about actually looking at the issue in an
inquisitive, critical and informed manner. Just 'cause Gallo says so
does not make it so. He made a killing on the HIV tests that his lab
developed. That was the purpose of his announcement. Greed. And now it
doesn't matter to him if he was wrong or right, he is rich now.

TC
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PostPosted: Fri Jul 14, 2006 9:13 pm    Post subject: Re: Bushmeat seeds new virus Reply with quote

TC wrote:
Quote:
GMCarter wrote:
On 14 Jul 2006 10:30:19 -0700, "TC" <tunderbar@hotmail.com> wrote:



Some of those "cranks and right wing nuts" are pretty highly respected
in their fields.

LOL...by other cranks and nuts. BFD.

Compared to Gallo, they are friggin' geniuses, even the crackpots.

I suggest that you actually check their scientific pedigrees before you
make such sweeping bigotted statements. You've just shown us your real
colors. You are closed-minded idiot hanging onto the words of corrupt
officials like Gallo. And you cast stones towards persons that can
intellectually run circles around Gallo.

Instead of attacking an entire cadre of highly respected virologists
based on Gallo's POV, how about actually looking at the issue in an
inquisitive, critical and informed manner. Just 'cause Gallo says so
does not make it so. He made a killing on the HIV tests that his lab
developed. That was the purpose of his announcement. Greed. And now it
doesn't matter to him if he was wrong or right, he is rich now.

TC

http://www.avert.org/his81_86.htm

History of AIDS:

1984 History
At the CDC researchers had been continuing to investigate the cause of
AIDS through a study of the sexual contacts of homosexual men in Los
Angeles and New York. They identified a man as the link between a
number of different cases and they named him "patient O" for "Out of
California".65 The research appeared to confirm that AIDS was a
transmittable disease, and the co-operation of "patient O" contributed
to the study.66

However a problem arose when other people read the scientific paper.

"I called this guy Patient O... But my colleagues read it as Patient
Zero."

- Darrow for Newsweek -67

And so in March 1984 the myth of Patient Zero began.68 See 1987 for
more information about Patient Zero.

Just one month later, on April 22nd, Dr Mason of the CDC was reported
as saying:

"I believe we have the cause of AIDS."

He was referring to the French virus, LAV, and he was basing his
opinion on the findings made in the preceding weeks by the researchers
at the Pasteur Institute who had discovered the virus the previous
year.69


Margaret Heckler

Dr Robert Gallo
Just one day later, on April 23th, the United States Health and Human
Services Secretary Margaret Heckler announced that Dr. Robert Gallo of
the National Cancer Institute had isolated the virus which caused AIDS,
that it was named HTLV-III, and that there would soon be a commercially
available test able to detect the virus with "essentially 100 percent
certainty". It was a dramatic and optimistic announcement that also
included:

"We hope to have a vaccine [against AIDS] ready for testing in about
two years."

And it concluded with:

"yet another terrible disease is about to yield to patience,
persistence and outright genius".70, 71

The same day patent applications were filed covering Gallo's work, but
there was clearly a possibility that LAV and HTLV-III were the same
virus.72, 73 The scientific papers regarding Gallo's discovery of
HTLV-III were published on 4th May.74 By 17th May, private companies
were already applying to the Department of Health & Human Services for
licences to develop a commercial test, which would detect evidence of
the virus in blood, a test which it had already been said would be used
to screen the entire supply of donated blood in the USA.75, 76

**************

If HIV were the cause of AIDS, I think we would have a vaccine by now.

and

"yet another terrible disease....." would have yielded "to patience,
persistence and outright genius"

TC
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PostPosted: Fri Jul 14, 2006 10:14 pm    Post subject: Re: Bushmeat seeds new virus Reply with quote

On 14 Jul 2006 13:50:06 -0700, "TC" <tunderbar@hotmail.com> wrote:

Quote:

GMCarter wrote:
On 14 Jul 2006 10:32:30 -0700, "TC" <tunderbar@hotmail.com> wrote:

snip
Which is a hell of a lot more than can be said about the american that
made the HIV/AIDS discovery and announced it at a press conference and
faile to actually publish his findings in a peer reviewed journal and
needs body guards to travel in public.

What the hell are you babbling about now? You're simply resorting to
making s**t up at this point. Who? What? When? Where??

Dr. Robert Gallo announced that HIV causes aids at a press conference.

Yes. The paper referenced by Gallo was in press.

Quote:
He still hasn't published the specific study that led to this finding.

Yes, he has. You are misinformed or lying.

Quote:
The one below is not the seminal study that wasn't published. It is a
retrospective paper.

Here's another one. But it really doesn't matter: Gallo didn't
discover HIV.

Shaw GM, Broder S, Essex M, Gallo RC. Human T-cell leukemia virus: its
discovery and role in leukemogenesis and immunosuppression. Adv
Intern Med. 1984;30:1-27.

We have highlighted the events leading to the discovery of the first
human RNA tumor virus and then reviewed what is currently known about
its biology. From this, it is clear that we have only begun to
appreciate the biologic diversity, the geographic distribution, and
the disease spectrum of this family of human T-lymphotropic
retroviruses which we collectively term HTLV. At a basic level, HTLV
provides a unique opportunity to study in vitro and in vivo mechanisms
of cell transformation. Given its close association with adult T-cell
leukemia and its ability to efficiently immortalize primary cells in
vitro, we believe that HTLV will very likely harbor clues to the
biology of cell growth, differentiation, and transformation. At a more
clinical level, the close association between HTLV and a malignancy of
clonally expanded (HTLV-containing) mature T-cells argues strongly for
a causal relationship, although the mechanism for such is currently
unknown. It is likely that further study of the molecular and cellular
biology of this virus will bring together these basic and clinical
findings and elucidate, at least in part, one mechanism for human
leukemogenesis. From a more speculative viewpoint, the role of HTLV in
the pathogenesis of human disease appears even broader. As discussed
in this chapter, there are indications that all subtypes of HTLV may
produce immunosuppression both in vitro and in vivo, and there is now
exciting new data to suggest that a novel member of this family of
viruses, HTLV-III, is causally linked to the AIDS syndrome. Moreover,
the possibility has been raised that the immunosuppressive properties
of HTLV could predispose patients to non-T-cell malignancies as occurs
in patients with AIDS or chemically induced immunosuppression.
Finally, by employing the experimental strategies which were
successful in isolating HTLV-I, HTLV-II, and HTLV-III, it may be
possible in the future to identify still other human retroviruses.


snip
Quote:
It supposedly traces the basic research that led to the finding but his
own basic research that supposedly led to the finding announced at the
press conference was never and has never been published. And I see no
actual cites to any of the studies that he is supposedly reviewing in
this paper.


Quote:
And he has seriously pissed off so many people with the way he did
science that he cannot freely move around in public without body
guards. A scientist cannot say: "This is the way it is and you all must
accept my word for it" and not publish the data for peer review.

Provide evidence for this statement.

Quote:
The entire AIDS research machine had to spin around on a dime, stop
what they were doing, and accept his pronouncements without a published
paper. A lot of research that was not specifically pursuing the
HIV/AIDS connection was dumped and all funding went to only those
specifically studying HIV. All other lines of research, regardless of
validity was forcibly shut down.

Bullshit.

Research in the last 20+ years has looked at all sorts of situations,
conditions and populations.

NOTHING causes CD4 counts to decline like HIV.

Now you're simply making ridiculous declarative statements with
absolutely NO evidence to back them whatsoever.

Quote:
Where are these rational interventions being that they started
formulating in the 1980's?

There's 25 approved antiretroviral therapies for HIV. And there are
other strategies that can mitigate their side effects and as well
reduce HIV progression rate from the world of dietary supplements,
including a multivitamin, whey proteins, NAC and other interventions.

George M. Carter
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PostPosted: Fri Jul 14, 2006 10:16 pm    Post subject: Re: Bushmeat seeds new virus Reply with quote

On 14 Jul 2006 13:58:25 -0700, "TC" <tunderbar@hotmail.com> wrote:

Quote:

GMCarter wrote:
On 14 Jul 2006 10:30:19 -0700, "TC" <tunderbar@hotmail.com> wrote:



Some of those "cranks and right wing nuts" are pretty highly respected
in their fields.

LOL...by other cranks and nuts. BFD.

Compared to Gallo, they are friggin' geniuses, even the crackpots.

No, they're mostly not that bright or their intelligence has been
perverted. If Gallo were the ONLY researcher, I'd be worried too. But
he ain't by a long shot.

Quote:
I suggest that you actually check their scientific pedigrees before you
make such sweeping bigotted statements.

Dearest, why don't you provide them?

Hell, 13 years ago, Duesberg called me. I know most of these guys. And
indeed, some of the denialist lists include people who either don't
argue that HIV causes AIDS (Root-Bernstein, Joe Sonnabend) or who died
of AIDS (my friend Casper Schmidt).

Most of the rest of their lists are journalist and morons like Celia
Farber.

Quote:
You've just shown us your real
colors. You are closed-minded idiot hanging onto the words of corrupt
officials like Gallo. And you cast stones towards persons that can
intellectually run circles around Gallo.

Darling, I've been researching this for over 17 years.

Quote:
Instead of attacking an entire cadre of highly respected virologists

Oh, f*** off whack job. Name 'em or shut the f*** up.

George M. Carter
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PostPosted: Fri Jul 14, 2006 10:18 pm    Post subject: Re: Bushmeat seeds new virus Reply with quote

On 14 Jul 2006 14:13:22 -0700, "TC" <tunderbar@hotmail.com> wrote:

Quote:
If HIV were the cause of AIDS, I think we would have a vaccine by now.

WHat a fucking ignorant comment. Why? There's no vaccine for a lot of
infections. And again, as I stated earlier, there's a lot of political
NIGHTMARE with the vaccine search that assholes like you will forever
not get--the REAL problem is missed by you as you cling to this
fantasy that HIV is harmless.

George M. Carter

***
The Evidence That HIV Causes AIDS
BACKGROUND
The acquired immunodeficiency syndrome (AIDS) was first recognized in
1981 and has since become a major worldwide pandemic. AIDS is caused
by the human immunodeficiency virus (HIV). By leading to the
destruction and/or functional impairment of cells of the immune
system, notably CD4+ T cells, HIV progressively destroys the body's
ability to fight infections and certain cancers.

An HIV-infected person is diagnosed with AIDS when his or her immune
system is seriously compromised and manifestations of HIV infection
are severe. The U.S. Centers for Disease Control and Prevention (CDC)
currently defines AIDS in an adult or adolescent age 13 years or older
as the presence of one of 26 conditions indicative of severe
immunosuppression associated with HIV infection, such as Pneumocystis
carinii pneumonia (PCP), a condition extraordinarily rare in people
without HIV infection. Most other AIDS-defining conditions are also
"opportunistic infections" which rarely cause harm in healthy
individuals. A diagnosis of AIDS also is given to HIV-infected
individuals when their CD4+ T-cell count falls below 200 cells/cubic
millimeter (mm3) of blood. Healthy adults usually have CD4+ T-cell
counts of 600-1,500/mm3 of blood. In HIV-infected children younger
than 13 years, the CDC definition of AIDS is similar to that in
adolescents and adults, except for the addition of certain infections
commonly seen in pediatric patients with HIV. (CDC. MMWR
1992;41(RR-17):1; CDC. MMWR 1994;43(RR-12):1).

In many developing countries, where diagnostic facilities may be
minimal, healthcare workers use a World Health Organization (WHO) AIDS
case definiton based on the presence of clinical signs associated with
immune deficiency and the exclusion of other known causes of
immunosuppression, such as cancer or malnutrition. An expanded WHO
AIDS case definition, with a broader spectrum of clinical
manifestations of HIV infection, is employed in settings where HIV
antibody tests are available (WHO. Wkly Epidemiol Rec. 1994;69:273).

As of the end of 2000, an estimated 36.1 million people worldwide -
34.7 million adults and 1.4 million children younger than 15 years -
were living with HIV/AIDS. Through 2000, cumulative
HIV/AIDS-associated deaths worldwide numbered approximately 21.8
million - 17.5 million adults and 4.3 million children younger than 15
years. In the United States, an estimated 800,000 to 900,000 people
are living with HIV infection. As of December 31, 1999, 733,374 cases
of AIDS and 430,441 AIDS-related deaths had been reported to the CDC.
AIDS is the fifth leading cause of death among all adults aged 25 to
44 in the United States. Among African-Americans in the 25 to 44 age
group, AIDS is the leading cause of death for men and the second
leading cause of death for women (UNAIDS. AIDS epidemic update:
December 2000; CDC. HIV/AIDS Surveillance Report 1999;11[2]:1; CDC.
MMWR 1999;48[RR13]:1).

This document summarizes the abundant evidence that HIV causes AIDS.
Questions and answers at the end of this document address the specific
claims of those who assert that HIV is not the cause of AIDS.
EVIDENCE THAT HIV CAUSES AIDS
HIV fulfills Koch's postulates as the cause of AIDS.

Among many criteria used over the years to prove the link between
putative pathogenic (disease-causing) agents and disease, perhaps the
most-cited are Koch's postulates, developed in the late 19th century.
Koch's postulates have been variously interpreted by many scientists,
and modifications have been suggested to accommodate new technologies,
particularly with regard to viruses (Harden. Pubbl Stn Zool Napoli
[II] 1992;14:249; O'Brien, Goedert. Curr Opin Immunol 1996;8:613).
However, the basic tenets remain the same, and for more than a century
Koch's postulates, as listed below, have served as the litmus test for
determining the cause of any epidemic disease:

1. Epidemiological association: the suspected cause must be
strongly associated with the disease.
2. Isolation: the suspected pathogen can be isolated - and
propagated - outside the host.
3. Transmission pathogenesis: transfer of the suspected pathogen to
an uninfected host, man or animal, produces the disease in that host.

With regard to postulate #1, numerous studies from around the world
show that virtually all AIDS patients are HIV-seropositive; that is
they carry antibodies that indicate HIV infection. With regard to
postulate #2, modern culture techniques have allowed the isolation of
HIV in virtually all AIDS patients, as well as in almost all
HIV-seropositive individuals with both early- and late-stage disease.
In addition, the polymerase chain (PCR) and other sophisticated
molecular techniques have enabled researchers to document the presence
of HIV genes in virtually all patients with AIDS, as well as in
individuals in earlier stages of HIV disease.

Postulate #3 has been fulfilled in tragic incidents involving three
laboratory workers with no other risk factors who have developed AIDS
or severe immunosuppression after accidental exposure to concentrated,
cloned HIV in the laboratory. In all three cases, HIV was isolated
from the infected individual, sequenced and shown to be the infecting
strain of virus. In another tragic incident, transmission of HIV from
a Florida dentist to six patients has been documented by genetic
analyses of virus isolated from both the dentist and the patients. The
dentist and three of the patients developed AIDS and died, and at
least one of the other patients has developed AIDS. Five of the
patients had no HIV risk factors other than multiple visits to the
dentist for invasive procedures (O'Brien, Goedert. Curr Opin Immunol
1996;8:613; O'Brien, 1997; Ciesielski et al. Ann Intern Med
1994;121:886).

In addition, through December 1999, the CDC had received reports of 56
health care workers in the United States with documented,
occupationally acquired HIV infection, of whom 25 have developed AIDS
in the absence of other risk factors. The development of AIDS
following known HIV seroconversion also has been repeatedly observed
in pediatric and adult blood transfusion cases, in mother-to-child
transmission, and in studies of hemophilia, injection-drug use and
sexual transmission in which seroconversion can be documented using
serial blood samples (CDC. HIV AIDS Surveillance Report 1999;11[2]:1;
AIDS Knowledge Base, 1999). For example, in a 10-year study in the
Netherlands, researchers followed 11 children who had become infected
with HIV as neonates by small aliquots of plasma from a single
HIV-infected donor. During the 10-year period, eight of the children
died of AIDS. Of the remaining three children, all showed a
progressive decline in cellular immunity, and two of the three had
symptoms probably related to HIV infection (van den Berg et al. Acta
Paediatr 1994;83:17).

Koch's postulates also have been fulfilled in animal models of human
AIDS. Chimpanzees experimentally infected with HIV have developed
severe immunosuppression and AIDS. In severe combined immunodeficiency
(SCID) mice given a human immune system, HIV produces similar patterns
of cell killing and pathogenesis as seen in people. HIV-2, a less
virulent variant of HIV which causes AIDS in people, also causes an
AIDS-like syndrome in baboons. More than a dozen strains of simian
immunodeficiency virus (SIV), a close cousin of HIV, cause AIDS in
Asian macaques. In addition, chimeric viruses known as SHIVs, which
contain an SIV backbone with various HIV genes in place of the
corresponding SIV genes, cause AIDS in macaques. Further strengthening
the association of these viruses with AIDS, researchers have shown
that SIV/SHIVs isolated from animals with AIDS cause AIDS when
transmitted to uninfected animals (O'Neil et al. J Infect Dis
2000;182:1051; Aldrovandi et al. Nature 1993;363:732; Liska et al.
AIDS Res Hum Retroviruses 1999;15:445; Locher et al. Arch Pathol Lab
Med 1998;22:523; Hirsch et al. Virus Res 1994;32:183; Joag et al. J
Virol 1996;70:3189).

AIDS and HIV infection are invariably linked in time, place and
population group.

Historically, the occurence of AIDS in human populations around the
world has closely followed the appearance of HIV. In the United
States, the first cases of AIDS were reported in 1981 among homosexual
men in New York and California, and retrospective examination of
frozen blood samples from a U.S. cohort of gay men showed the presence
of HIV antibodies as early as 1978, but not before then. Subsequently,
in every region, country and city where AIDS has appeared, evidence of
HIV infection has preceded AIDS by just a few years (CDC. MMWR
1981;30:250; CDC. MMWR 1981;30:305; Jaffe et al. Ann Intern Med
1985;103:210; U.S. Census Bureau; UNAIDS).

Many studies agree that only a single factor, HIV, predicts whether a
person will develop AIDS.

Other viral infections, bacterial infections, sexual behavior patterns
and drug abuse patterns do not predict who develops AIDS. Individuals
from diverse backgrounds, including heterosexual men and women,
homosexual men and women, hemophiliacs, sexual partners of
hemophiliacs and transfusion recipients, injection-drug users and
infants have all developed AIDS, with the only common denominator
being their infection with HIV (NIAID, 1995).

In cohort studies, severe immunosuppression and AIDS-defining
illnesses occur almost exclusively in individuals who are
HIV-infected.

For example, analysis of data from more than 8,000 participants in the
Multicenter AIDS Cohort Study (MACS) and the Women's Interagency HIV
Study (WIHS) demonstrated that participants who were HIV-seropositive
were 1,100 times more likely to develop an AIDS-associated illness
than those who were HIV-seronegative. These overwhelming odds provide
a clarity of association that is unusual in medical research.

In a Canadian cohort, investigators followed 715 homosexual men for a
median of 8.6 years. Every case of AIDS in this cohort occurred in
individuals who were HIV-seropositive. No AIDS-defining illnesses
occurred in men who remained negative for HIV antibodies, despite the
fact that these individuals had appreciable patterns of illicit drug
use and receptive anal intercourse (Schechter et al. Lancet
1993;341:658).

Before the appearance of HIV, AIDS-related diseases such as PCP, KS
and MAC were rare in developed countries; today, they are common in
HIV-infected individuals.

Prior to the appearance of HIV, AIDS-related conditions such as
Pneumocystis carinii pneumonia (PCP), Kaposi's sarcoma (KS) and
disseminated infection with the Mycobacterium avium complex (MAC) were
extraordinarily rare in the United States. In a 1967 survey, only 107
cases of PCP in the United States had been described in the medical
literature, virtually all among individuals with underlying
immunosuppressive conditions. Before the AIDS epidemic, the annual
incidence of Kaposi's sarcoma in the United States was only 0.2 to 0.6
cases per million population, and only 32 individuals with
disseminated MAC disease had been described in the medical literature
(Safai. Ann NY Acad Sci 1984;437:373; Le Clair. Am Rev Respir Dis
1969;99:542; Masur. JAMA 1982;248:3013).

By the end of 1999, CDC had received reports of 166,368 HIV-infected
patients in the United States with definitive diagnoses of PCP, 46,684
with definitive diagnoses of KS, and 41,873 with definitive diagnoses
of disseminated MAC (personal communication).

In developing countries, patterns of both rare and endemic diseases
have changed dramatically as HIV has spread, with a far greater toll
now being exacted among the young and middle-aged, including
well-educated members of the middle class.

In developing countries, the emergence of the HIV epidemic has
dramatically changed patterns of disease in affected communities. As
in developed countries, previously rare, "opportunistic" diseases such
as PCP and certain forms of meningitis have become more commonplace.
In addition, as HIV seroprevalence rates have risen, there have been
significant increases in the burden of endemic conditions such as
tuberculosis (TB), particularly among young people. For example, as
HIV seroprevalence increased sharply in Blantyre, Malawi from 1986 to
1995, tuberculosis admissions at the city's main hospital rose more
than 400 percent, with the largest increase in cases among children
and young adults. In the rural Hlabisa District of South Africa,
admissions to tuberculosis wards increased 360 percent from 1992 to
1998, concomitant with a steep rise in HIV seroprevalence. High rates
of mortality due to endemic conditions such as TB, diarrheal diseases
and wasting syndromes, formerly confined to the elderly and
malnourished, are now common among HIV-infected young and middle-aged
people in many developing countries (UNAIDS, 2000; Harries et al. Int
J Tuberc Lung Dis 1997;1:346; Floyd et al. JAMA 1999;282:1087).

In studies conducted in both developing and developed countries, death
rates are markedly higher among HIV-seropositive individuals than
among HIV-seronegative individuals.

For example, Nunn and colleagues (BMJ 1997;315:767) assessed the
impact of HIV infection over five years in a rural population in the
Masaka District of Uganda. Among 8,833 individuals of all ages who had
an unambiguous result on testing for HIV-antibodies (either 2 or 3
different test kits were used for blood samples from each individual),
HIV-seropositive people were 16 times more likely to die over five
years than HIV-seronegative people (see table). Among individuals ages
25 to 34, HIV-seropositive people were 27 times more likely to die
than HIV-seronegative people.

In another study in Uganda, 19,983 adults in the rural Rakai District
were followed for 10 to 30 months (Sewankambo et al. AIDS
2000;14:2391). In this cohort, HIV-seropositive people were 20 times
more likely to die than HIV-seronegative people during 31,432
person-years of observation.

Similar findings have emerged from other studies (Boerma et al. AIDS
1998;12(suppl 1):S3); for example,

* in Tanzania, HIV-seropositive people were 12.9 time more likely
to die over two years than HIV-seronegative people (Borgdorff et al.
Genitourin Med 1995;71:212)
* in Malawi, mortality over three years among children who
survived the first year of life was 9.5 times higher among
HIV-seropositive children than among HIV-seronegative children (Taha
et al. Pediatr Infect Dis J 1999;18:689)
* in Rwanda, mortality was 21 times higher for HIV-seropositive
children than for HIV-seronegative children after five years (Spira et
al. Pediatrics 1999;14:e56). Among the mothers of these children,
mortality was 9 times higher among HIV-seropositive women than among
HIV-seronegative women in four years of follow-up (Leroy et al. J
Acquir Immune Defic Syndr Hum Retrovirol 1995;9:415).
* in Cote d'Ivoire, HIV-seropositive individuals with pulmonary
tuberculosis (TB) were 17 times more likely to die within six months
than HIV-seronegative individuals with pulmonary TB (Ackah et al.
Lancet 1995; 345:607).
* in the former Zaire (now the Democratic Republic of Congo),
HIV-infected infants were 11 times more likely to die from diarrhea
than uninfected infants (Thea et al. NEJM 1993;329:1696).
* in South Africa, the death rate for children hospitalized with
severe lower respiratory tract infections was 6.5 times higher for
HIV-infected infants than for uninfected children (Madhi et al. Clin
Infect Dis 2000;31:170).

Kilmarx and colleagues (Lancet 2000; 356:770) recently reported data
on HIV infection and mortality in a cohort of female commercial sex
workers in Chiang Rai, Thailand. Among 500 women enrolled in the study
between 1991 and 1994, the mortality rate through October 1998 among
women who were HIV-infected at enrollment (59 deaths among 160
HIV-infected women) was 52.7 times higher than among women who
remained uninfected with HIV (2 deaths among 306 uninfected women).
The mortality rate among women who became infected during the study (7
deaths among 34 seroconverting women) was 22.5 higher than among
persistently uninfected women. Among the HIV-infected women, only 3 of
whom received antiretroviral medications, all reported causes of death
were associated with immunosuppression, whereas the reported causes of
death of the two uninfected women were postpartum amniotic embolism
and gunshot wound.

Excess mortality among HIV-seropositive people also has been
repeatedly observed in studies in developed countries, perhaps most
dramatically among hemophiliacs. For example, Darby et al. (Nature
1995;377:79) studied 6,278 hemophiliacs living in the United Kingdom
during the period 1977-91. Among 2,448 individuals with severe
hemophilia, the annual death rate was stable at 8 per 1,000 during
1977-84. While death rates remained stable at 8 per 1,000 from
1985-1992 among HIV-seronegative persons with severe hemophilia,
deaths rose steeply among those who had become HIV-seropositive
following HIV-tainted transfusions during 1979-1986, reaching 81 per
1,000 in 1991-92. Among 3,830 individuals with mild or moderate
hemophilia, the pattern was similar, with an initial death rate of 4
per 1,000 in 1977-84 that remained stable among HIV-seronegative
individuals but rose to 85 per 1,000 in 1991-92 among seropositive
individuals.

Similar data have emerged from the Multicenter Hemophilia Cohort
Study. Among 1,028 hemophiliacs followed for a median of 10.3 years,
HIV-infected individuals (n=321) were 11 times more likely to die than
HIV-negative subjects (n=707), with the dose of Factor VIII having no
effect on survival in either group (Goedert. Lancet 1995;346:1425).

In the Multicenter AIDS Cohort Study (MACS), a 16-year study of 5,622
homosexual and bisexual men, 1,668 of 2,761 HIV-seropositive men have
died (60 percent), 1,547 after a diagnosis of AIDS. In contrast, among
2,861 HIV-seronegative participants, only 66 men (2.3 percent) have
died (A. Munoz, MACS, personal communication).

HIV can be detected in virtually everyone with AIDS.

Recently developed sensitive testing methods, including the polymerase
chain reaction (PCR) and improved culture techniques, have enabled
researchers to find HIV in patients with AIDS with few exceptions. HIV
has been repeatedly isolated from the blood, semen and vaginal
secretions of patients with AIDS, findings consistent with the
epidemiologic data demonstrating AIDS transmission via sexual activity
and contact with infected blood (Hammer et al. J Clin Microbiol
1993;31:2557; Jackson et al. J Clin Microbiol 1990;28:16).

Numerous studies of HIV-infected people have shown that high levels of
infectious HIV, viral antigens, and HIV nucleic acids (DNA and RNA) in
the body predict immune system deterioration and an increased risk for
developing AIDS. Conversely, patients with low levels of virus have a
much lower risk of developing AIDS.

For example, in an anlysis of 1,604 HIV-infected men in the
Multicenter AIDS Cohort Study (MACS), the risk of a patient developing
AIDS with six years was strongly associated with levels of HIV RNA in
the plasma as measured by a sensitive test known as the branched-DNA
signal-amplification assay (bDNA):

Plasma RNA concentration
(copies/mL of blood)

Proportion of patients
developing AIDS within six years
<500
501 - 3,000
3,001 - 10,000
10,001 - 30,000
Quote:
30,000

5.4%
16.6%
31.7%
55.2%
80.0%

(Source: Mellors et al. Ann Intern Med 1997;126:946)

Similar associations between increasing HIV RNA levels and a greater
risk of disease progression have been observed in HIV-infected
children in both developed and developing countries (Palumbo et al.
JAMA 1998;279:756; Taha et al. AIDS 2000;14:453).

In the very small proportion of untreated HIV-infected individuals
whose disease progresses very slowly, the amount of HIV in the blood
and lymph nodes is significantly lower than in HIV-infected people
whose disease progression is more typical (Pantaleo et al. NEJM
1995;332:209; Cao et al. NEJM 1995;332:201; Barker et al. Blood
1998;92:3105).

The availability of potent combinations of drugs that specifically
block HIV replication has dramatically improved the prognosis for
HIV-infected individuals. Such an effect would not be seen if HIV did
not have a central role in causing AIDS.

Clinical trials have shown that potent three-drug combinations of
anti-HIV drugs, known as highly active antiretroviral therapy (HAART),
can significantly reduce the incidence of AIDS and death among
HIV-infected individuals as compared to previously available HIV
treatment regimens (Hammer et al. NEJM 1997;337:725; Cameron et al.
Lancet 1998;351:543).

Use of these potent anti-HIV combination therapies has contributed to
dramatic reductions in the incidence of AIDS and AIDS-related deaths
in populations where these drugs are widely available, among both
adults and children (Figure 1; CDC. HIV AIDS Surveillance Report
1999;11[2]:1; Palella et al. NEJM 1998;338:853; Mocroft et al. Lancet
1998;352:1725; Mocroft et al. Lancet 2000;356:291; Vittinghoff et al.
J Infect Dis 1999;179:717; Detels et al. JAMA 1998;280:1497; de
Martino et al. JAMA 2000;284:190; CASCADE Collaboration. Lancet
2000;355:1158; Hogg et al. CMAJ 1999;160:659; Schwarcz et al. Am J
Epidemiol 2000;152:178; Kaplan et al. Clin Infect Dis 2000;30:S5;
McNaghten et al. AIDS 1999;13:1687;).

For example, in a prospective study of more than 7,300 HIV-infected
patients in 52 European outpatient clinics, the incidence of new
AIDS-defining illnesses declined from 30.7 per 100 patient-years of
observation in 1994 (before the availability of HAART) to 2.5 per 100
patient years in 1998, when the majority of patients received HAART
(Mocroft et al. Lancet 2000;356:291).

Among HIV-infected patients who receive anti-HIV therapy, those whose
viral loads are driven to low levels are much less likely to develop
AIDS or die than patients who do not respond to therapy. Such an
effect would not be seen if HIV did not have a central role in causing
AIDS.

Clinical trials in both HIV-infected children and adults have
demonstrated a link between a good virologic response to therapy (i.e.
much less virus in the body) and a reduced risk of developing AIDS or
dying (Montaner et al. AIDS 1998;12:F23; Palumbo et al. JAMA
1998;279:756; O'Brien et al. NEJM 1996;334:426; Katzenstein et al.
NEJM 1996;335:1091; Marschner et al. J Infect Dis 1998;177:40; Hammer
et al. NEJM 1997;337:725; Cameron et al. Lancet 1998;351:543).

This effect has also been seen in routine clinical practice. For
example, in an analysis of 2,674 HIV-infected patients who started
highly active antiretroviral therapy (HAART) in 1995-1998, 6.6 percent
of patients who achieved and maintained undetectable viral loads (<400
copies/mL of blood) developed AIDS or died within 30 months, compared
with 20.1 percent of patients who never achieved undetectable
concentrations (Ledergerber et al. Lancet 1999;353:863).

Nearly everyone with AIDS has antibodies to HIV.

A survey of 230,179 AIDS patients in the United States revealed only
299 HIV-seronegative individuals. An evaluation of 172 of these 299
patients found 131 actually to be seropositive; an additional 34 died
before their serostatus could be confirmed (Smith et al. N Engl J Med
1993;328:373).

Numerous serosurveys show that AIDS is common in populations where
many individuals have HIV antibodies. Conversely, in populations with
low seroprevalence of HIV antibodies, AIDS is extremely rare.

For example, in the southern African country of Zimbabwe (population
11.4 million), more than 25 percent of adults ages 15 to 49 are
estimated to be HIV antibody-positive, based on numerous studies. As
of November 1999, more than 74,000 cases of AIDS in Zimbabwe had been
reported to the World Health Organization (WHO). In contrast,
Madagascar, an island country off the southeast coast of Africa
(population 15.1 million) with a very low HIV seroprevalence rate,
reported only 37 cases of AIDS to WHO through November 1999. Yet,
other sexually transmitted diseases, notably syphilis, are common in
Madagascar, suggesting that conditions are ripe for the spread of HIV
and AIDS if the virus becomes entrenched in that country (U.S. Census
Bureau; UNAIDS, 2000; WHO. Wkly Epidemiol Rec 1999;74:1; Behets et al.
Lancet 1996;347:831).

The specific immunologic profile that typifies AIDS - a persistently
low CD4+ T-cell count - is extraordinarily rare in the absence of HIV
infection or other known cause of immunosuppression.

For example, in the NIAID-supported Multicenter AIDS Cohort Study
(MACS), 22,643 CD4+ T-cell determinations in 2,713 HIV-seronegative
homosexual and bisexual men revealed only one individual with a CD4+
T-cell count persistently lower than 300 cells/mm3 of blood, and this
individual was receiving immunosuppressive therapy. Similar results
have been reported from other studies (Vermund et al. NEJM
1993;328:442; NIAID, 1995).

Newborn infants have no behavioral risk factors for AIDS, yet many
children born to HIV-infected mothers have developed AIDS and died.

Only newborns who become HIV-infected before or during birth, during
breastfeeding, or (rarely) following exposure to HIV-tainted blood or
blood products after birth, go on to develop the profound
immunosuppression that leads to AIDS. Babies who are not HIV-infected
do not develop AIDS. In the United States, 8,718 cases of AIDS among
children younger than age 13 had been reported to the CDC as of
December 31, 1999. Cumulative U.S. AIDS deaths among individuals
younger than age 15 numbered 5,044 through December 31, 1999.
Globally, UNAIDS estimates that 480,000 child deaths due to AIDS
occurred in 1999 alone (CDC. HIV/AIDS Surveillance Report
1999;11[2]:1; UNAIDS. AIDS epidemic update: June 2000).

Because many HIV-infected mothers abuse recreational drugs, some have
argued that maternal drug use itself causes pediatric AIDS. However,
studies have consistently shown that babies who are not HIV-infected
do not develop AIDS, regardless of their mothers' drug use (European
Collaborative Study. Lancet 1991;337:253; European Collaborative
Study. Pediatr Infect Dis J 1997;16:1151; Abrams et al. Pediatrics
1995;96:451).

For example, a majority of the HIV-infected, pregnant women enrolled
in the European Collaborative Study are current or former injection
drug users. In this ongoing study, mothers and their babies are
followed from birth in 10 centers in Europe. In a paper in Lancet,
study investigators reported that none of 343 HIV-seronegative
children born to HIV-seropositive mothers had developed AIDS or
persistent immune deficiency. In contrast, among 64 seropositive
children, 30 percent presented with AIDS within 6 months of age or
with oral candidiasis followed rapidly by the onset of AIDS. By their
first birthday, 17 percent died of HIV-related diseases (European
Collaborative Study. Lancet 1991;337:253).

In a study in New York, investigators followed 84 HIV-infected and 248
HIV-uninfected infants, all born to HIV-seropositive mothers. The
mothers of the two groups of infants were equally likely to be
injection drug users (47 percent vs. 50 percent), and had similar
rates of alcohol, tobacco, cocaine, heroin and methadone use. Of the
84 HIV-infected children, 22 died during a median follow-up period of
27.6 months, including 20 infants who died before their second
birthday. Twenty-one of these deaths were classified as AIDS-related.
Among the 248 uninfected children, only one death (due to child abuse)
was reported during a median follow-up period of 26.1 months (Abrams
et al. Pediatrics 1995;96:451).

The HIV-infected twin develops AIDS while the uninfected twin does
not.

Because twins share an in utero environment and genetic relationships,
similarities and differences between them can provide important
insight into infectious diseases, including AIDS (Goedert. Acta
Paediatr Supp 1997;421:56). Researchers have documented cases of
HIV-infected mothers who have given birth to twins, one of whom is
HIV-infected and the other not. The HIV-infected children developed
AIDS, while the other children remained clinically and immunologically
normal (Park et al. J Clin Microbiol 1987;25:1119; Menez-Bautista et
al. Am J Dis Child 1986;140:678; Thomas et al. Pediatrics 1990;86:774;
Young et al. Pediatr Infect Dis J 1990;9:454; Barlow and Mok. Arch Dis
Child 1993;68:507; Guerrero Vazquez et al. An Esp Pediatr
1993;39:445).

Studies of transfusion-acquired AIDS cases have repeatedly led to the
discovery of HIV in the patient as well as in the blood donor.

Numerous studies have shown an almost perfect correlation between the
occurrence of AIDS in a blood recipient and donor, and evidence of
homologous HIV strains in both the recipient and the donor (NIAID,
1995).

HIV is similar in genetic structure and morphology to other
lentiviruses that often cause immunodeficiency in their animal hosts
in addition to slow, progressive wasting disorders, neurodegeneration
and death.

Like HIV in humans, animal viruses such as feline immunodeficiency
virus (FIV) in cats, visna virus in sheep and simian immunodeficiency
virus (SIV) in monkeys primarily infect cells of the immune system
such as T cells and macrophages. For example, visna virus infects
macrophages and causes a slowly progressive neurologic disease (Haase.
Nature 1986;322:130).

HIV causes the death and dysfunction of CD4+ T lymphocytes in vitro
and in vivo.

CD4+ T cell dysfunction and depletion are hallmarks of HIV disease.
The recognition that HIV infects and destroys CD4+ T cells in vitro
strongly suggests a direct link between HIV infection, CD4+ T cell
depletion, and development of AIDS. A variety of mechanisms, both
directly and indirectly related to HIV infection of CD4+ T cells, are
likely responsible for the defects in CD4+ T cell function observed in
HIV-infected people. Not only can HIV enter and kill CD4+ T cells
directly, but several HIV gene products may interfere with the
function of uninfected cells (NIAID, 1995; Pantaleo et al. NEJM
1993;328:327).
ANSWERING THE SKEPTICS:
RESPONSES TO ARGUMENTS THAT HIV DOES NOT CAUSE AIDS
MYTH: HIV antibody testing is unreliable.

FACT: Diagnosis of infection using antibody testing is one of the
best-established concepts in medicine. HIV antibody tests exceed the
performance of most other infectious disease tests in both sensitivity
(the ability of the screening test to give a positive finding when the
person tested truly has the disease ) and specificity (the ability of
the test to give a negative finding when the subjects tested are free
of the disease under study). Current HIV antibody tests have
sensitivity and specificity in excess of 98% and are therefore
extremely reliable WHO, 1998; Sloand et al. JAMA 1991;266:2861).

Progress in testing methodology has also enabled detection of viral
genetic material, antigens and the virus itself in body fluids and
cells. While not widely used for routine testing due to high cost and
requirements in laboratory equipment, these direct testing techniques
have confirmed the validity of the antibody tests (Jackson et al. J
Clin Microbiol 1990;28:16; Busch et al. NEJM 1991;325:1; Silvester et
al. J Acquir Immune Defic Syndr Hum Retrovirol 1995;8:411; Urassa et
al. J Clin Virol 1999;14:25; Nkengasong et al. AIDS 1999;13:109;
Samdal et al. Clin Diagn Virol 1996;7:55.

MYTH: There is no AIDS in Africa. AIDS is nothing more than a new name
for old diseases.

FACT: The diseases that have come to be associated with AIDS in Africa
- such as wasting syndrome, diarrheal diseases and TB - have long been
severe burdens there. However, high rates of mortality from these
diseases, formerly confined to the elderly and malnourished, are now
common among HIV-infected young and middle-aged people, including
well-educated members of the middle class (UNAIDS, 2000).

For example, in a study in Cote d'Ivoire, HIV-seropositive individuals
with pulmonary tuberculosis (TB) were 17 times more likely to die
within six months than HIV-seronegative individuals with pulmonary TB
(Ackah et al. Lancet 1995; 345:607). In Malawi, mortality over three
years among children who had received recommended childhood
immunizations and who survived the first year of life was 9.5 times
higher among HIV-seropositive children than among HIV-seronegative
children. The leading causes of death were wasting and respiratory
conditions (Taha et al. Pediatr Infect Dis J 1999;18:689). Elsewhere
in Africa, findings are similar.

MYTH: HIV cannot be the cause of AIDS because researchers are unable
to explain precisely how HIV destroys the immune system.

FACT: A great deal is known about the pathogenesis of HIV disease,
even though important details remain to be elucidated. However, a
complete understanding of the pathogenesis of a disease is not a
prerequisite to knowing its cause. Most infectious agents have been
associated with the disease they cause long before their pathogenic
mechanisms have been discovered. Because research in pathogenesis is
difficult when precise animal models are unavailable, the
disease-causing mechanisms in many diseases, including tuberculosis
and hepatitis B, are poorly understood. The critics' reasoning would
lead to the conclusion that M. tuberculosis is not the cause of
tuberculosis or that hepatitis B virus is not a cause of liver disease
(Evans. Yale J Biol Med 1982;55:193).

MYTH: AZT and other antiretroviral drugs, not HIV, cause AIDS.

FACT: The vast majority of people with AIDS never received
antiretroviral drugs, including those in developed countries prior to
the licensure of AZT in 1987, and people in developing countries today
where very few individuals have access to these medications (UNAIDS,
2000).

As with medications for any serious diseases, antiretroviral drugs can
have toxic side effects. However, there is no evidence that
antiretroviral drugs cause the severe immunosuppression that typifies
AIDS, and abundant evidence that antiretroviral therapy, when used
according to established guidelines, can improve the length and
quality of life of HIV-infected individuals.

In the 1980s, clinical trials enrolling patients with AIDS found that
AZT given as single-drug therapy conferred a modest (and short-lived)
survival advantage compared to placebo. Among HIV-infected patients
who had not yet developed AIDS, placebo-controlled trials found that
AZT given as single-drug therapy delayed, for a year or two, the onset
of AIDS-related illnesses. Significantly, long-term follow-up of these
trials did not show a prolonged benefit of AZT, but also never
indicated that the drug increased disease progression or mortality.
The lack of excess AIDS cases and death in the AZT arms of these
placebo-controlled trials effectively counters the argument that AZT
causes AIDS (NIAID, 1995).

Subsequent clinical trials found that patients receiving two-drug
combinations had up to 50 percent increases in time to progression to
AIDS and in survival when compared to people receiving single-drug
therapy. In more recent years, three-drug combination therapies have
produced another 50 percent to 80 percent improvements in progression
to AIDS and in survival when compared to two-drug regimens in clinical
trials. Use of potent anti-HIV combination therapies has contributed
to dramatic reductions in the incidence of AIDS and AIDS-related
deaths in populations where these drugs are widely available, an
effect which clearly would not be seen if antiretroviral drugs caused
AIDS (Figure 1; CDC. HIV AIDS Surveillance Report 1999;11[2]:1;
Palella et al. NEJM 1998;338:853; Mocroft et al. Lancet 1998;352:1725;
Mocroft et al. Lancet 2000;356:291; Vittinghoff et al. J Infect Dis
1999;179:717; Detels et al. JAMA 1998;280:1497; de Martino et al. JAMA
2000;284:190; CASCADE Collaboration. Lancet 2000;355:1158; Hogg et al.
CMAJ 1999;160:659; Schwarcz et al. Am J Epidemiol 2000;152:178; Kaplan
et al. Clin Infect Dis 2000;30:S5; McNaghten et al. AIDS
1999;13:1687).

MYTH: Behavioral factors such as recreational drug use and multiple
sexual partners account for AIDS.

FACT: The proposed behavioral causes of AIDS, such as multiple sexual
partners and long-term recreational drug use, have existed for many
years. The epidemic of AIDS, characterized by the occurrence of
formerly rare opportunistic infections such as Pneumocystis carinii
pneumonia (PCP) did not occur in the United States until a previously
unknown human retrovirus - HIV - spread through certain communities
(NIAID, 1995a; NIAID, 1995b).

Compelling evidence against the hypothesis that behavioral factors
cause AIDS comes from recent studies that have followed cohorts of
homosexual men for long periods of time and found that only
HIV-seropositive men develop AIDS.

For example, in a prospectively studied cohort in Vancouver, 715
homosexual men were followed for a median of 8.6 years. Among 365
HIV-positive individuals, 136 developed AIDS. No AIDS-defining
illnesses occurred among 350 seronegative men despite the fact that
these men reported appreciable use of inhalable nitrites ("poppers")
and other recreational drugs, and frequent receptive anal intercourse
(Schechter et al. Lancet 1993;341:658).

Other studies show that among homosexual men and injection-drug users,
the specific immune deficit that leads to AIDS - a progressive and
sustained loss of CD4+ T cells - is extremely rare in the absence of
other immunosuppressive conditions. For example, in the Multicenter
AIDS Cohort Study, more than 22,000 T-cell determinations in 2,713
HIV-seronegative homosexual men revealed only one individual with a
CD4+ T-cell count persistently lower than 300 cells/mm3 of blood, and
this individual was receiving immunosuppressive therapy (Vermund et
al. NEJM 1993;328:442).

In a survey of 229 HIV-seronegative injection-drug users in New York
City, mean CD4+ T-cell counts of the group were consistently more than
1000 cells/mm3 of blood. Only two individuals had two CD4+ T-cell
measurements of less than 300/mm3 of blood, one of whom died with
cardiac disease and non-Hodgkin's lymphoma listed as the cause of
death (Des Jarlais et al. J Acquir Immune Defic Syndr 1993;6:820).

MYTH: AIDS among transfusion recipients is due to underlying diseases
that necessitated the transfusion, rather than to HIV.

FACT: This notion is contradicted by a report by the Transfusion
Safety Study Group (TSSG), which compared HIV-negative and
HIV-positive blood recipients who had been given transfusions for
similar diseases. Approximately 3 years after the transfusion, the
mean CD4+ T-cell count in 64 HIV-negative recipients was 850/mm3 of
blood, while 111 HIV-seropositive individuals had average CD4+ T-cell
counts of 375/mm3 of blood. By 1993, there were 37 cases of AIDS in
the HIV-infected group, but not a single AIDS-defining illness in the
HIV-seronegative transfusion recipients (Donegan et al. Ann Intern Med
1990;113:733; Cohen. Science 1994;266:1645).

MYTH: High usage of clotting factor concentrate, not HIV, leads to
CD4+ T-cell depletion and AIDS in hemophiliacs.

FACT: This view is contradicted by many studies. For example, among
HIV-seronegative patients with hemophilia A enrolled in the
Transfusion Safety Study, no significant differences in CD4+ T-cell
counts were noted between 79 patients with no or minimal factor
treatment and 52 with the largest amount of lifetime treatments.
Patients in both groups had CD4+ T cell-counts within the normal range
(Hasset et al. Blood 1993;82:1351). In another report from the
Transfusion Safety Study, no instances of AIDS-defining illnesses were
seen among 402 HIV-seronegative hemophiliacs who had received factor
therapy (Aledort et al. NEJM 1993;328:1128).

In a cohort in the United Kingdom, researchers matched 17
HIV-seropositive hemophiliacs with 17 HIV-seronegative hemophiliacs
with regard to clotting factor concentrate usage over a ten-year
period. During this time, 16 AIDS-defining clinical events occurred in
9 patients, all of whom were HIV-seropositive. No AIDS-defining
illnesses occurred among the HIV-negative patients. In each pair, the
mean CD4+ T cell count during follow-up was, on average, 500 cells/mm3
lower in the HIV-seropositive patient (Sabin et al. BMJ 1996;312:207).

Among HIV-infected hemophiliacs, Transfusion Safety Study
investigators found that neither the purity nor the amount of Factor
VIII therapy had a deleterious effect on CD4+ T cell counts (Gjerset
et al., Blood 1994;84:1666). Similarly, the Multicenter Hemophilia
Cohort Study found no association between the cumulative dose of
plasma concentrate and incidence of AIDS among HIV-infected
hemophiliacs (Goedert et al. NEJM 1989;321:1141.).

MYTH: The distribution of AIDS cases casts doubt on HIV as the cause.
Viruses are not gender-specific, yet only a small proportion of AIDS
cases are among women.

FACT: The distribution of AIDS cases, whether in the United States or
elsewhere in the world, invariably mirrors the prevalence of HIV in a
population. In the United States, HIV first appeared in populations of
homosexual men and injection-drug users, a majority of whom are male.
Because HIV is spread primarily through sex or by the exchange of
HIV-contaminated needles during injection-drug use, it is not
surprising that a majority of U.S. AIDS cases have occurred in men
(U.S. Census Bureau, 1999; UNAIDS, 2000).

Increasingly, however, women in the United States are becoming
HIV-infected, usually through the exchange of HIV-contaminated needles
or sex with an HIV-infected male. The CDC estimates that 30 percent of
new HIV infections in the United States in 1998 were in women. As the
number of HIV-infected women has risen, so too has the number of
female AIDS patients in the United States. Approximately 23 percent of
U.S. adult/adolescent AIDS cases reported to the CDC in 1998 were
among women. In 1998, AIDS was the fifth leading cause of death among
women aged 25 to 44 in the United States, and the third leading cause
of death among African-American women in that age group.

In Africa, HIV was first recognized in sexually active heterosexuals,
and AIDS cases in Africa have occurred at least as frequently in women
as in men. Overall, the worldwide distribution of HIV infection and
AIDS between men and women is approximately 1 to 1 (U.S. Census
Bureau, 1999; UNAIDS, 2000).

MYTH: HIV cannot be the cause of AIDS because the body develops a
vigorous antibody response to the virus.

FACT: This reasoning ignores numerous examples of viruses other than
HIV that can be pathogenic after evidence of immunity appears. Measles
virus may persist for years in brain cells, eventually causing a
chronic neurologic disease despite the presence of antibodies. Viruses
such as cytomegalovirus, herpes simplex and varicella zoster may be
activated after years of latency even in the presence of abundant
antibodies. In animals, viral relatives of HIV with long and variable
latency periods, such as visna virus in sheep, cause central nervous
system damage even after the production of antibodies (NIAID, 1995).

Also, HIV is well recognized as being able to mutate to avoid the
ongoing immune response of the host (Levy. Microbiol Rev 1993;57:183).

MYTH: Only a small number of CD4+ T cells are infected by HIV, not
enough to damage the immune system.

FACT: New techniques such as the polymerase chain reaction (PCR) have
enabled scientists to demonstrate that a much larger proportion of
CD4+ T cells are infected than previously realized, particularly in
lymphoid tissues. Macrophages and other cell types are also infected
with HIV and serve as reservoirs for the virus. Although the fraction
of CD4+ T cells that is infected with HIV at any given time is never
extremely high (only a small subset of activated cells serve as ideal
targets of infection), several groups have shown that rapid cycles of
death of infected cells and infection of new target cells occur
throughout the course of disease (Richman J Clin Invest 2000;105:565).

MYTH: HIV is not the cause of AIDS because many individuals with HIV
have not developed AIDS.

FACT: HIV disease has a prolonged and variable course. The median
period of time between infection with HIV and the onset of clinically
apparent disease is approximately 10 years in industrialized
countries, according to prospective studies of homosexual men in which
dates of seroconversion are known. Similar estimates of asymptomatic
periods have been made for HIV-infected blood-transfusion recipients,
injection-drug users and adult hemophiliacs (Alcabes et al. Epidemiol
Rev 1993;15:303).

As with many diseases, a number of factors can influence the course of
HIV disease. Factors such as age or genetic differences between
individuals, the level of virulence of the individual strain of virus,
as well as exogenous influences such as co-infection with other
microbes may determine the rate and severity of HIV disease
expression. Similarly, some people infected with hepatitis B, for
example, show no symptoms or only jaundice and clear their infection,
while others suffer disease ranging from chronic liver inflammation to
cirrhosis and hepatocellular carcinoma. Co-factors probably also
determine why some smokers develop lung cancer while others do not
(Evans. Yale J Biol Med 1982;55:193; Levy. Microbiol Rev 1993;57:183;
Fauci. Nature 1996;384:529).

MYTH: Some people have many symptoms associated with AIDS but do not
have HIV infection.

FACT: Most AIDS symptoms result from the development of opportunistic
infections and cancers associated with severe immunosuppression
secondary to HIV.

However, immunosuppression has many other potential causes.
Individuals who take glucocorticoids and/or immunosuppressive drugs to
prevent transplant rejection or for autoimmune diseases can have
increased susceptibility to unusual infections, as do individuals with
certain genetic conditions, severe malnutrition and certain kinds of
cancers. There is no evidence suggesting that the numbers of such
cases have risen, while abundant epidemiologic evidence shows a
staggering rise in cases of immunosuppression among individuals who
share one characteristic: HIV infection (NIAID, 1995; UNAIDS, 2000).

MYTH: The spectrum of AIDS-related infections seen in different
populations proves that AIDS is actually many diseases not caused by
HIV.

FACT: The diseases associated with AIDS, such as PCP and Mycobacterium
avium complex (MAC), are not caused by HIV but rather result from the
immunosuppression caused by HIV disease. As the immune system of an
HIV-infected individual weakens, he or she becomes susceptible to the
particular viral, fungal and bacterial infections common in the
community. For example, HIV-infected people in certain midwestern and
mid-Atlantic regions are much more likely than people in New York City
to develop histoplasmosis, which is caused by a fungus. A person in
Africa is exposed to different pathogens than is an individual in an
American city. Children may be exposed to different infectious agents
than adults (USPHS/IDSA, 2001).
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http://content.nejm.org/cgi/content/full/349/24/2283
PERSPECTIVE

The Discovery of HIV as the Cause of AIDS
Robert C. Gallo, M.D., and Luc Montagnier, M.D.
Progress in scientific research rarely follows a
straight path. Generally, it entails many unexpected
meanderings, with a mix of good and bad ideas,
good and bad luck. The discovery of the human immunodeficiency
virus (HIV) as the cause of AIDS
did not avoid this pattern.

The story began in an unfavorable environment:
during the late 1970s, many people thought that epidemic
diseases caused by microbes, including viruses,
no longer posed a threat in industrialized
countries. Other prevailing beliefs were that viruses
did not cause any human cancers and that there was
no such thing as a retrovirus that infected humans.
Some of these beliefs were justified, since attempts
to find tumor viruses and, in particular, retroviruses
in cancers or other diseases in humans had a troubled
history, and many of the groups that had the
greatest expertise in the study of retroviruses had
turned their efforts toward research on oncogenes.
Luckily and rather amazingly, however, the conceptual
and technical tools arrived in our hands just before
the first patients with AIDS were identified in
1981. In addition, there remained a few heretical or
“old-fashioned” groups — among which were our
two laboratories — that persisted in searching for
retroviruses in human cancers, particularly breast
cancers and leukemias. This search finally paid off
with the discovery of human T-cell leukemia virus
types 1 and 2 (HTLV-1 and HTLV-2), the first of
which was shown to cause an unusual T-cell leukemia.
This discovery was made possible by 15 years
of basic research on leukemogenic retroviruses in
animals, including the design and development
of highly sensitive biochemical assays that were
based on reverse transcriptase — the enzyme that
is present in all retroviruses, which was discovered
in 1970 by Temin and Baltimore.

An additional important contributor was the development
of methods for growing T lymphocytes
in culture for a period sufficient to allow the expression
of putative latent retroviruses. This effort was
helped greatly by the isolation of specific factors —
in particular, the T-cell growth factor (now called interleukin-
2) in Bethesda, Maryland. The role of interferon
in repressing the production of retroviruses
in mouse cells was demonstrated in Paris, and this
discovery led to the use of anti-interferon serum in
the search for human retroviruses. Thus, at the beginning
of the 1980s, we had the essential tools required
to search for a retrovirus in this new and
menacing disease called AIDS. But why search for a
virus, and specifically a retrovirus, in AIDS? The answer
was far from obvious in 1982.

At that time, AIDS had already appeared as a
long-lasting disease, with an extremely long lag time
between exposure to the agent (through blood or
sexual activity) and the profound state of immune
suppression characterized by the occurrence of opportunistic
infections or cancers. Many factors —
fungi, chemicals, and even an autoimmunity to leukocytes
— were invoked at that time as possible
causes. However, for us, there were clues. First, the
various manifestations of AIDS were unified by a
biologic marker: a decrease in the levels of a specific
subgroup of T cells that harbored the CD4 surface
antigen. CD4 and other CDs had been identified
only a few years earlier with the use of specific monoclonal
antibodies, thanks to the work of Milstein
and Kohler. The findings regarding the T-cell subgroup
suggested an agent that specifically targeted
CD4+ T cells, and HTLV was one such agent.
Moreover, there were animal models in which
lymphotropic retroviruses caused not only leukemias
or lymphomas, but also an AIDS-like wasting
syndrome. Furthermore, HTLV was transmitted
through blood and sexual activity, as well as from
mother to infant, which was consistent with some
of what we learned early on about the epidemiology
of AIDS. Finally, the Centers for Disease Control and
Prevention (CDC) reported cases of AIDS in patients
with hemophilia who had received only filtered clotting
factors, which seemed to eliminate the possibility
that the agent was a microorganism larger than
a virus.

This set of arguments convinced us, as well as
Max Essex in Boston, each independently to start a
search for an HTLV-like virus in patients with AIDS.
We began conducting this research at the National
Institutes of Health in Bethesda and at the Pasteur
Institute in Paris. The theory that a retrovirus caused
AIDS was correct, but the hypothesis that it was a
close relative of HTLV proved to be wrong. In Bethesda,
an earlier survey involving the use of molecular
and immunologic probes seemed to favor a
variant similar to HTLV-1. In fact, some patients
with AIDS were doubly infected with HTLV-1 and
the new agent, which complicated the interpretation
of the nature of the virus causing AIDS.

In early 1983, a clear-cut isolate was obtained in
Paris, with the help of interleukin-2 and anti-interferon
serum, from cultured T lymphocytes derived
from a lymph-node–biopsy specimen from a patient
with lymphadenopathy, a syndrome that was considered
to be a precursor of AIDS. This virus proved
to be different from HTLV in terms of antigenicity
and morphology, but it could be propagated only in
fresh cultures of T lymphocytes and not in permanent
T-cell lines, which impeded its full characterization.
The idea that the causative agent of AIDS
should be sought in swollen lymph nodes was partly
right, since we now know that lymph nodes are
the main site where the virus hides during the presymptomatic
phase. At this early stage, it seemed
more likely that the isolate was causative than that
it was opportunistic, since the immunosuppression
was very mild. In some ways, however, it was also a
misleading idea that delayed the full characterization
of the virus and its mass production for seroepidemiologic
studies, because only some viral isolates
from patients with fully developed AIDS grow quickly
in permanent cell lines, as we would soon learn.

This technical breakthrough was first achieved
in late 1983 in Bethesda. Among a few strains in the
Bethesda laboratory that grew in continuous cell
lines, one came, unbeknownst to both of us, from
the third isolate from a patient with Kaposi’s sarcoma
in Paris. The origin of the HIV strain with a very
high capacity for growth that could readily overcome
other HIV strains in culture — and which
contaminated cell cultures in several laboratories,
beginning with both of ours — was unraveled only
in 1991, thanks to the use of the polymerase-chainreaction
technique.

The year 1984 was a time of both intense excitement
and harsh discussions between members of
our two groups. Identifying the cause of AIDS presented
a unique challenge, because unlike other viral
diseases responsible for past epidemics (or, more
recently, the severe acute respiratory syndrome),
AIDS was characterized by clinical signs that developed
years after the infection had occurred, and by
then, patients usually had numerous other infections.
Thus, an exceptional linkage of agent to disease
had to be established. This linkage was made
(particularly in Bethesda) through the repeated isolation
of HIV from patients with AIDS and, more
important, through the development of a readily
reproducible blood test. The growth of the putative
virus in T-cell lines was an enormous step, facilitating
the development of a blood test for HIV, which
became available in blood-transfusion centers in
1985 and produced convincing evidence of the association
between HIV infection and AIDS. The
blood test also helped in the cloning and molecular
characterization of the genetic material of the virus
at the end of 1984, which clearly proved that the
new virus belonged to the subfamily of lentiretroviruses;
this finding, in turn, opened the way for the
design of specific drugs and vaccines.

Other indirect evidence that HIV was the cause
of AIDS came from the demonstration, in 1984, of
its high degree of tropism for the subgroup of CD4+
T cells, its consistent isolation from patients of different
origins who had AIDS, and the isolation of
similar viruses that cause AIDS in nonhuman primates
(specifically, macaques). Thus, the causative
relation between HIV and AIDS was accepted by the
scientific and medical community in 1984 and was
further verified through the later isolation of HIV
type 2 in West African patients with AIDS. The relation
was also supported by the clinical efficacy of
drugs that specifically inhibit HIV enzymes and the
demonstration that mutations in one of the coreceptors
for HIV (CCR5) make some persons highly
resistant to HIV infection and AIDS.

Many lessons can be drawn from this early intense
period, and most suggest that science requires
greater modesty. Our experience with AIDS underscores
the importance of basic research, which gave
us the technical and conceptual tools to find the
cause less than three years after the disease was first
described. The work of numerous researchers is required
for such efforts, and we have described the
contributions of many scientists in other publications.
1,2
It has also become clear that finding the
cause of an infectious disease is the alpha but not
the omega of its eradication. The identification of
HIV has allowed us to eliminate transmission of the
disease through the transfusion of blood and blood
products, create rational policies for prevention, and
design efficient antiretroviral therapies. These therapies
are not a cure, however, and the epidemic is
still growing in many countries for lack of accessible
treatments and preventive vaccines. Moreover, we
must recognize that we are still far from having exhausted
the list of potential new pathogens. Finally,
one lesson that should be clear is that effective collaboration
among groups of scientists and clinicians
is essential — and that it is possible to achieve such
collaboration without excluding a certain dose of the
competitive spirit as a stimulant.

From the Institute of Human Virology, University of Maryland
Biotechnology
Institute and University of Maryland, Baltimore
(R.C.G.); and the World Foundation AIDS Research and Prevention,
Paris (L.M.).
1. Gallo RC. Virus hunting. New York: Basic Books, 1991.
2. Montagnier L. Virus. New York: Norton, 2000.
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From
http://www.aegis.com/law/journals/1988/ALAW0019.html
The Discovery of HIV

One June 5, 1981, the Centers for Disease Control (CDC) in Atlanta
published a report received from Dr. Michael Gottlieb several weeks
earlier bout five men he had recently treated in Los Angeles.10
Commenting on the report, the editors of the CDC's Morbidity and
Mortality Weekly Report noted:

"Pneumocystis pneumonia in the United States is almost exclusively
limited to severely immuno- suppressed patients. The occurrence of
pneumo- cystosis in these 5 previously health individuals without a
clinically apparent underlying immuno- deficiency is unusual."11

One month later, following reports from physicians in New York of an
unexpected outbreak of Kaposi's sarcoma, rare malignancy, the CDC
requested that "Physicians . . . be alert for Kaposi's sarcoma, PC
pneumonia, and other opportunistic infections associated with
immunosuppression . . . ."12 Official responses to the AIDS epidemic
had begun.

Neither Gottlieb nor the New York physicians could establish any basis
for their patients' immune deficiencies. They hd not been taking
immune suppression drugs nor did they suffer from genetic defects that
can cause such problems. The deficiencies, which left these
individuals fatally without immunity to opportunistic infections and
cancers so rare that they caused their physicians to report their
occurrence to the federal center for tracking the nation's health,
seemed to have been acquired. The question epidemiologists at the CDC
had to answer was, "from what?"

In the months that followed, reports flowed in regarding similar cases
of unexplained immune deficiencies resulting in Kaposi's sarcoma (KS)
and exotic opportunistic infections such as pneumocystis (PCP),
cytomegalovirus, toxoplasmosis and candidiasis. On September 24, 1982,
the CDC published its first "Update on Acquired Immune Deficiency
Syndrome (AIDS)."13 Following a statistical report, the editors
concluded:

"CDC defines a case of AIDS as a disease, at least moderately
predictive of a defect in cell- mediated immunity, occurring in a
person with no known cause for diminished resistance to that disease.
Such diseases include KS, PCP. However, this case definition may not
include the full spectrum of AIDS manifestations, which may range from
absence of symptoms . . . to non-specific symptoms . . . to specific
diseases that are insufficiently predictive of cellular
immunodeficiency to be included in incidence monitoring . . . Absence
of a reliable, inexpensive, widely available test for AIDS, however,
may make the working case definition the best currently available for
incidence monitoring."14

Like police following up an all-points bulletin, CDC epidemiologists
investigated each reported case of AIDS, searching for clues and
patterns. By November 5, 1982, they announced:

"The etiology of the underlying immune deficiencies seen in AIDS cases
is unknown. One hypothesis consistent with current observations is
that a transmissible agent may be involved. If so, transmission of the
agent would appear most commonly to require intimate, direct contact
involving mucosal surfaces, such as sexual contact . . . or through
parenteral spread such as occurs among intravenous drug abusers and
possibly hemophilia patients . . . Airborne spread and interpersonal
spread through casual contact do not seem likely [for] . . . these
patterns [of transmission] resemble the . . . modes of spread of
hepatitis B (a blood-borne virus)."15

Finally, on December 10, 1982, CDC researchers established a link that
established conclusively the emerging blood-borne transmission
pattern:

". . . a 20-month old infant . . . developed unexplained cellular
immunodeficiency and opportunistic infection. This occurred after
multiple transfusions, including a transfusion . . . from the blood of
a male subsequently found to have the acquired immune deficiency
syndrome (AIDS)."16

Six months later, in June 1983, a French research team at the Pasteur
Institute in Paris led by Dr. Luc Montagnier announced the isolation
of a new retrovirus from the lymph nodes of a man with AIDS.17 On
April 23, 1984, Dr. Robert Gallo of the National Institutes of Health
and Secretary Margaret Heckler of the Department of Health and Human
Services announced that the Americans, too, had isolated the new
retrovirus.18 Its name was eventually agreed upon as HIV, the human
immunodeficiency virus.

HIV infects the T-4 helper cell, master coordinator of the immune
system, the body's internal defense against infection. It insinuates
itself into the cell's genetic structure, where it may lie dormant for
years. Eventually, however, it alters the cell's replicative process,
causing the cell to produce new HIV virus at one thousand times the
rate of normal cell replication.

This replicative function destroys the T-cell, freeing thousands of
new HIV to infect thousands of new T-cells. Dropping T-cell levels
signal a faltering immune system, leaving infected individuals prone
to a variety of ailments.

HIV also infects the macrophage cells of the central nervous system.
Jay Levy of the University of California, San Francisco, described the
breadth of neurological problems HIV can cause as "equivalent to the
table of contents in a neurology textbook."19 These can range from
short term/long term memory loss to psychomotor dysfunction to
dementia through to virtually any other cognitive impairment.

snip...

FOOTNOTES

*Deputy City Attorney David Schulman heads the AIDS Discrimination
Unit in the office of Los Angeles City Attorney James K. Hahn.

1. P. Monette, BORROWED TIME: AN AIDS MEMOIR, 83(1988).

2. S. Sontag, ILLNESS AS METAPHOR, 57(1979).

3. Ross, "Ethics and the Language of AIDS," AIDS ETHICS AND PUBLIC
POLICY (C. Pierce and D. Vandeveer, eds. 1988); Ross, "An Ethics of
Compassion: A Language of Division, Working Out the AIDS Metaphor,"
AIDS PRINCIPLES, PRACTICES & POLITICS(I. Corless and M.
Pitman-Lindeman, eds. 1988).

4. A. Camus, THE PLAGUE 236(Vintage Books ed. 1972).

5. See generally: W. McNeill, PLAGUES AND PEOPLE (1976).

6. Brandt, "AIDS: From Social History to Public Policy," 14 LAW MED. &
HEALTH CARE 231, 233 (1986).

7. Korematsu v. U.S., 319 U.S. 432, 87 L.Ed 1497, 63 S.Ct. 1124
(1943).

8. Camus, supra n.4 at 117-18.

9 Id.

10. Pneumocystis Pneumonia--Los Angeles, 30 MORBIDITY AND MORTALITY
WEEKLY REPORT (hereinafter cited as MMWR) 250(1981).

11. Id.

12. Kaposi's Sarcoma and Pneumocystis Pneumonia Among Homosexual Men
-- New York City and California. 30 MMWR at 305.

13. Update on Acquired Immunodeficiency Syndrome (AIDS) - United
States, 31 MMWR 507(1982).

14. Id.

15. Acquired Immunodeficiency Syndrome (AIDS) Precautions for Clinical
and Laboratory Staffs, 31 MMWR at 577.

16. Possible Transfusion Associated Acquired Immunodeficiency Syndrome
(AIDS)--California, 31 MMWR at 652.

17. Shilts, AND THE BAND PLAYED ON: POLITICS, PEOPLE AND THE AIDS
EPIDEMIC, 319(1987).

18. Id. at 450-51.

19. L.A. Times, Dec. 12, 1986, Section E at 1 (NEXIS).

20. L.A. MUN. CODE Section(s) 45.80 et. seq. (1985)

21. American Medical News, June 17, 1988, at 1, col. 4.

22. Id. at 32, col. 1.

23. REPORT OF THE PRESIDENTIAL COMMISSION ON THE HUMAN
IMMUNODEFICIENCY VIRUS EPIDEMIC (1988)(hereinafter cited as REPORT OF
THE PRES. COMM) 124.

24. N.Y. Times, Aug. 18, 1985, Section 4, at 18.

25. West Hollywood, San Francisco, Berkeley, and Oakland.

26. Including Santa Monica, San Diego, and Laguna Beach.

27. Department of Fair Employment and Housing v. Raytheon Company
(real party in interest, estate of John Chadbourne) FEHC Dec. No.
87-12(1987), aff'd. Raytheon Company v. Fair Employment and Housing
Commission, Santa Barbara Superior Court Case No. 167995 (Apr. 22,
1988).

28. School Board of Nassau County v. Arline, 107 S.Ct. 1913
(1987)(holding that persons with contagious diseases are protected by
the physical handicap civil rights provisions of the Federal
Rehabilitation Act of 1973); Chalk v. U.S. District Court, 840 F.2d
701 (9th Cir. 1988)(holding that Arline, id., protects people with
AIDS); Doe v. Centinela Hospital, No. CV 87-2514 PAR (PX)(June 30,
1988)(holding that HIV-infected, asymptomatic individuals are
protected by the Federal Rehabilitation Act as individuals perceived
as handicapped when discriminated against because of irrational fears
of contagion). Thomas v. Atascadero Unified School District, 662 F.
Supp. 376 (C.D. Cal. 1987).

29. See generally, Dolgin, AIDS: Social Meanings and Legal
Ramifications, 14 Hofstra L. Rev. 193, 204-07 (1985) and Gostin and
Curran, "Legal Control Measures for AIDS: Reporting Requirements,
Surveillance, Quarantine, and Regulation of Public Meeting Places," 77
PUB HEALTH & THE LAW 214 (1987).

30. Jew Ho v. Williamson, 103 F. 10 (C.C.N.D. Cal. 1900).

31. Id. at 24 (quoting Yick Wo v. Hopkins, 118 U.S. 356, 373-74
(1886).

32. E.g. Dolgin, supra, n. 29.

33. Gostin and Curran, supra n. 29.

34. City of Cleburne Texas v. Cleburne Living Center, 105 S.Ct. 3249
(1985).

35. Gostin and Curran, supra n. 29 at 217 (footnote omitted).

36. 105 S.Ct. at 3258-59.

37. L.A. MUN. CODE Section 45.90(B)(2).

38. L.A. MUN. CODE Section 45.89.

39. Supra n. 27.

40. Id.

41. Chalk, supra n. 28.

42. Panel Discussion on AIDS and Civil Rights, Whittier College of Law
Symposium (March 4, 1988).

43. See, e.g. Los Angeles City Attorney Report No. R-85-0711 at 1.2
(Aug. 13, 1985).

44. L.A. MUN. CODE Section 45.90(B)(2).

45. REPORT OF THE PRES. COMM. Recommendations 9-1 - 9-8 at 121-24.

46. Id. Recommendations 9-9 at 124.

47. Id. Recommendations 9-10, 9-11 at 124, Recommendations 9-12 - 9-15
at 124-25 (regarding community responses); Recommendations 9-16 - 9-23
at 125-26 (regarding schools); Recommendations 9-24 - 9-27 at 126
(regarding health care settings).

48. Id. Recommendations 9-28 - 9-35 at 127-28.

49. Haseltine, Volberging, and Blattner, Editorial, ACQ. IMM. DEF.
SYNDR. 1 (1988).

50. Camus, supra n.4 at 154.

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