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From: B. Harris)
Subject: AIDS and Lentiviruses (was: The AIDS Heresies: Part 7)
Date: 28 Dec 1996
Newsgroups:,,, (chatski carl) in Message-ID:
<5a1bvf$> writes:

In article <59vuil$> you write:

>> ..... But AIDS doesn't just destroy the immune system. Rather, it
>> selectively destroys one part of it (cell mediated immunity), leaving
>> the other part (antibody production) intact. No drug has ever been
>> found to do anything like that. Not illegal drugs, not poppers, not
>> AZT. Retroviruses related to HIV, by contrast, can do this kind of
>> thing in animals.


>Thank you for this thought provoking post. It has been my observation
>that only retroviral infection of macrophage has this effect, that is why
>so many of the "Simian HIV Relatives" don't cause disease.

  Comment:  It's more complicated than that.  Infection of
macrophages or macrophage lines seems indirectly necessary for
long term immune deficiency to be produced (because it is
necessary for any long term infection at all), but it is not
sufficient.  After all, SIV chronically infects macrophages in
the monkeys it produces no clinical disease in, FIV chronically
infects African cats in the way, and HIV-1 chronically infects
the macrophages of the large fraction of chimps, and a lucky 8%
of humans, who may sustain HIV-1 infection chronically without
developing immune problems.  So, again, you need retroviral
macrophage infection for any kind of chronic infection at all,
whether symptomatic or not, but that by itself is not enough.
Retroviral *lymphocyte* infection ALSO seems necessary for immune
deficiency (see below), but again is not sufficient.  Some not
yet understood nasty interaction between virus and a host which
is not used to it, is necessary for development of a chronic
retroviral infection which ALSO produces the pathology of immune
deficiency (AIDS).  This type of thing may be seen in monkeys,
cats, and people.

   >>In the early days ( before 1985 ) HIV-1 was thought to be
most closely related to Visna, which has many aids like features
in sheep.  Have you thought about this and the great number of
simian viruses discovered only after 1985, and often only in
monkey colonies ( not in the wild ) ? <<

   You still haven't read my essay, yet, have you?

   Here's a bit of a primer on lentiviruses:

   Visna-medae (ovine lentivirus or OLV), is a retrovirus which
infects the macrophages, but not lymphocytes, of sheep.  It was
classed as lentivirus (slow virus) because the sheep develop lung
and brain disease (associated with macrocytes in those tissues)
years after initial infection.  This caused a lot of problems in
Iceland with sheep that had passed a strict quarantine, but only
became sick years later.  The OLV virus produces disease years
after experimental infection also, giving the lie to Peter "slow
viruses don't exist" Duesberg.  A similar virus (caprine
arthritis-encephalitis virus) causes slow disease in goats.  Both
these viruses look a bit like HIV, having an asymmetric core in a
membrane with spikes, but they are not identical to HIV, which
has a very distinctive core which looks a bit like a traffic
cone, with a dense base.  Their genomes are related to that of
HIV however, and like HIV they carry a magnesium dependent
reverse transcriptase which is characteristic of lentiviruses (it
isn't seen in other retroviruses such as HTLV-1, or Rous sarcoma-
- nor is it seen in normal human cells).

   A virus which looks something more like HIV, with a much more
elongated bar-like or sometimes even cone-shaped core, is the
equine infectious anemia virus, EIAV.  This horse virus also
infects macrophage lines only, but does so in lymph nodes and
marrow, causing an anemia and chronic lymphadenopathy.  The
chronic lymphadenopathy syndrome and conical core of EIAV, as
well as its sharing of antigens with HIV, are what convinced
Luc Montagnier in 1983 that his new virus isolated from humans
with AIDS-related-complex (then called LAV for lymphadenopathy
associated virus), was a lentivirus, like EIAV, and not a
lymphotropic retrovirus related to Gallo's HTLV-1.  Nevertheless,
for all its resemblance to HIV, the equine anemia virus, like
OLV, does not infect lymphocytes, and therefore does not produce
really severe lymphocyte depletion, or the immune deficiency
which accompanies nearly total loss of lymphocytes.  There is no
"horse-AIDS" or "sheep-AIDS," for this reason.

   To see what happens when a lentivirus infects both macrophages
and lymphocytes, you need to go to a virus even more closely
related to HIV, the bovine lentivirus now called BIV (bovine
immunodeficiency virus).  This virus not only causes
lymphadenopathy and immune problems, but also lymphoma.  It is
visually very similar to HIV.  And of course it has a magnesium
dependent reverse transcriptase.  Interestingly, BIV seems to
cause fewer problems in the African bovines where it is also
endemic, than it does in commercial cattle.  This is a common
theme with lentivirus (and indeed, all other viral) infections:
they cause disease in hosts they have moved to relatively
recently, but not in the hosts they have been with for a longer
time.  It takes time for a virus to adapt to a new host species,
and after this time has passed, the viral infection inevitably
has become less nasty for the host (since it is to the virus'
evolutionary advantage not to make the host any more ill than
necessary for maximum spread of the virus-- i.e., sniffles or
cough or biting behavior, maybe, but not prostration or death).

   Even more closely related to HIV than BIV, is FIV, the feline
immunodeficiency virus.  This virus may once have been BIV, but
was transferred to large African cats, which carry it, in some
bloody battle between a leopard and a horned beast of pray.  The
FIV virus has now adapted to large African cats, which spread it
in their saliva by biting behavior, and via nursing.  It doesn't
make lions or leopards sick, but when it infects house-cats it
causes slow lymphadenopathy, wasting, lymphoma, and lymphocyte
depletion with opportunistic fungal infections of the sort that
cats would be exposed to (candida, toxoplasmosis, etc).  Call it
cat-AIDS.  FIV infects lymphocytes, but not selectively (it
infects CD8s as well as CD4s).  It is visually identical to HIV,
and includes not only the cone-shaped core, but also features
such as the distinctive clear lateral bodies, which are lateral
to the core.  No scientist has ever reported any virus with these
visual features which did not turn out to be a lentivirus which
likes lymph nodes.  The "HIV" virus which some skeptics do not
believe in, of course looks like this.

   Even closer to HIV (genetically and antigenically), and still
identical in appearance, are the SIV viruses (simian immunodefic-
iency viruses).  These viruses are native to African monkeys,
which they infect chronically but apparently do not cause disease
in.  These viruses, however, do cause AIDS when given to Asian
species of primates, such as the stump tailed macaque, and the
rhesus macaque.  SIV viruses infect macrophages and CD4 cells
selectively, just as the HIV strains do.  The syndrome they cause
in Asian monkeys includes lymphadenopathy, wasting, lymphoma,
lymphocyte depletion, and many opportunistic infections such as
Pneumocystis pneumonia, CMV retinitis, chronic cryptosporidia
diarrhea, and invasive candidiasis.  They also cause encephalitis
and brain dysfunction (Duesberg has said they do not cause
dementia, but what else would you call it? -- monkeys don't do
the range of intellectual tasks whose loss we call dementia in
humans).  Monkeys, unlike cats and people who eat more meat,
don't get toxoplasmosis with SIV.  And they don't get Kaposi's
sarcoma, which is associated with HIV plus another human virus,
HHV-8 (which doesn't infect monkeys).   The reason monkey AIDS
appears in caged monkeys is that it appears only when Asian
monkeys pick up an African monkey virus they don't ordinarily
come in contact with.  That happens only in captivity.  Notably,
it may be that SIV in monkeys is FIV which has been transferred
to an escaped monkey by the bite of a leopard (monkey escapes
from such attacks have been documented many times by biologists).

   The two known lentiviruses found in humans are HIV-1 and
HIV-2, both again identical to SIV in appearance, and similar in
genetics.  Especially similar to SIV (90% identical genome) is
HIV-2, the lentivirus isolated from humans with AIDS in West
Africa.  Because SIV strains differ as much from each other as
they do from HIV-2, it would be correct to say that HIV-2 is
essentially the same virus as SIV (if it had been found in a some
monkey species, it would have been named as one more SIV, without
even a comment).  HIV-2, exactly like the various strains of SIV,
causes AIDS in Asian monkeys, but not in African monkeys (ie, it
satisfies the Koch postulates).  It is undoubtedly a recent
evolutionary transfer from African monkeys to humans.

   HIV-1, which is 40 to 50% identical to HIV-2 and SIV, causes
most AIDS in Africa, and essentially all AIDS in the West.  HIV-1
differs from HIV-2 and SIV about as much as oral herpes (herpes
1) differs from genital herpes (herpes 2).  Although it has not
been proven, it seems likely to some scientists that HIV-1 had
its origin in chimpanzees (which perhaps were infected long ago
separately by FIV, which evolved in then in parallel to its
evolution in African monkeys).  This because HIV-1 is endemic in
parts of equatorial Africa where wild chimps abound (and are
still captured and traded), and also because HIV-1 is somewhat
more similar to the chimpanzee SIV (called SIVcpz-- cpz for
chimpanzee) than it is to other SIVs. Finally, HIV-1 infects
chimps, establishing a macrophage infection, but usually without
disease.  This is the behavior of a lentivirus which is "used" to
that host (i.e., HIV-1 infects chimps in the same way FIV infects
lions, and SIV infects African monkeys).  By contrast with HIV-2,
HIV-1 cannot establish macrophage infection or chronic infection
in monkeys, though it does infect their lymphocytic tissue
acutely. (I don't know whether or not the chimp/ape virus SIVcpz
can, but this would be a fascinating experiment.)

   I hope the above will be useful to those hearing about "animal
AIDS" and lentiviruses.  It should be noted that the immune
deficiency syndromes caused by some of these viruses in
appropriate animals, resemble human AIDS far more than the
effects of any drug has ever been found to, in any experimental
circumstances-- either in animal or humans.  Moreover these
viruses are genetically related to HIV, and visually identical to
it.  The conclusion to be made from these facts is inescapable.
HIV-1 is only one member of a family of closely related viruses
which are capable of causing long delayed chronic infections of
the immune system, with eventual destruction of same.  The AIDS
plague in humans is not an isolated phenomenon in humans, but a
part of a general phenomenon of nature involving many species.

                                Steve Harris, M.D.

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