According to the patent for Dr. Jay Levy’s CAF, it has been
separated and characterized ! (Dr. Levy observed, almost a
decade ago, that CD8 cells from long-term non progressors
inhibit RT in vitro. He believes that ‘CAF’, and not the
chemokines  RANTES, MIP-1 alpha and MIP-1 beta, is
mainly responsible for this effect…

CD8.sup.+ cell antiviral factor (Assignee —
The Regents Of The University Of California)

 Source: MicroPatent

 MicroPatent: Abstract: A protein secreted by peripheral blood
mononuclear cells and specifically from CD8.sup.+
lyphocytes is purified and characterized here and designated CD8.sup.+

cell antiviral factor (CAF). The CAF is lipid free, has a molecular
weight of less than 30,000 and has been found to inhibit the
replication of retroviruses and in particular to inhibit the
replication of HIV-1, HIV-2, and SIV. CAF can be used to inhibit viral

RNA transcription which inhibits viral replication. Accordingly, CAF
can be used to treat patients infected with retroviruses. The CAF can
also generate antibodies which can be used to create assay reagents
for detecting CAF in a body fluid and on the surface of CD8.sup.+
cells to determine the condition of an HIV infected individual.

 Ex Claim Text: A substantially pure composition of CD8+ cell
antiviral factor defined by the following characteristics: (i) blocks
viral replication by inhibiting viral RNA transcription; (ii) does not

affect CD4.sup.+ cell activation or proliferation; and (iii) is not a
cytokine selected from the group consisting of  IL-1, IL-2, IL-3,
IL-4, IL-5, IL-6, IL-7, IL-8, IL-9, IL-10, IL-12, G-CSF, GM-CSF,
TNF.alpha., TNF.beta., IFN.alpha., IFN.beta., IFN.gamma., and
 TGF.beta..

 Assignee: The Regents Of The University Of California

 Patent Number: 5565549

 Issue Date: 1996 10 15

 Inventor(s): Levy, Jay A.Mackewicz, Carl E.
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Can someone please explain the biomechanics of the development of
resistance to anti-HIV drugs? Why does resistance occur when you stop
using them? After all, if a resistant strain develops, it ought to begin
to proliferate regardless of the presence or non-presence of a drug to
which it is resistant. One would think that resistance would occur due to
over-using the drugs, not stopping them.

Thanks, Mark

Can anyone tell me what is AIDS’s symptom?

  PAIN-L [an educational forum]
for all aspects of *CHRONIC PAIN*,
    including HEALTH & HEALING.
      Over 1050 SUBSCRIBERS.
             Join us
  [Health care providers and patients].              
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"SUBSCRIBE PAIN-L <Your full name>" to:
    <lists…@sjuvm.stjohns.edu>.

                -HR-

I’m interested in a product called Oxandrin that is used to treat weight
loss.  Specifically, I would like to know how it is working for you, how
much do you take daily, how long do you have to stay on therapy, and
what are the pros and cons of the product.  Any information is greatly
appreciated.

Hello,

this may sound like an unusual request to post but ..

Every month I begrudgingly venture to the beautician where I have a
half-leg wax. They say beauty is pain, but I never imagined it to be
this much!

I am becoming really turned off the procedure because of the pain, and
I was hoping someone here might be able to provide some help.

Is there a medicated lotion or herbal brew I could apply to my skin
that will dull the nerves while Im being waxed?

Please help me. Even if its only a one liner I would be eternaly
grateful, and in a lot less pain!

Thank you,

Jeanette.
t…@world.net

Anti-HIV viruses ?

Could the recent exciting news about a possible
Anti-cancer virus have relevance to a potential
treatment for HIV/AIDS ? Could this lead the way
to a method of attacking and killing proviral cells,
putting out the source of the fire ? Are there
other ways to target infected cells with good
specificity ? Could a virus which downregulates
a receptor be of benefit (HHV6A seems to upregulate
CD4, and there is sufficient evidence that HHV6A
plays a strong role in the pathogenesis of HIV, and
is largely responsible for the destruction of the
lymph node architecture)?…

 A study published Friday in the journal Science,
describes what is probably the first ever "smart-virus"
which could be used as an anti-virus drug.
 The virus is a mutated form of one which naturally
gives people a cold, and in lab mice, the engineered
form destroyed about 60% of human tumors !
  Frank McCormick, a researcher for Onyx Pharmaceuticals
in Richmond, California says that "the mutated virus
takes over and turns the (cancer) cell into a factory
to make more virus. After a day or two, the cell is
killed and it releases a whole bunch of new virus,
which then infect neighboring cancer cells."
  The virus apparently only affects the cancer cells – the
target of the smart virus is the most common cancer gene,
the P53 mutation which causes cells grow out of control.
It is hoped that since the P53 is found in so many types
of cancer, there could be benefits in fighting cancers such
as lung, prostate and bladder cancers.
 Dr. Bert Vogelstein of the Johns Hopkins University
was the first to determine that an altered or missing
P53 gene can lead to cancer said the study is promising
since it "exploits an alteration that is present in
many different cancers." One of the unknowns in this
type of research is whether the patients immune system
will respond to the smart virus before it eliminates
the cancer.

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Hi, I’m looking for some information about aids or HIV.
I need info about the structure of the virus, researches/treatment on the
virus.
who’s the most/least to get it in the age groups
ethnic background etc.
It’s for a research paper and it’s due by the end of the semester.
If you have any knowledge of such information on websites to visit or books
to buy,
please contact me at spwo…@ucs.com and let me know

thanks

Steven Harris (sbhar…@ix.netcom.com) wrote to/about Calif…@netcom.com:

:   While he’s at it, I’d like there to be an explanation of why studies
: of short term illegal drug use aren’t supposed to be predictive of (or
: correlate in the slightest with) lifetime illegal drug use.

Don’t play games with me by throwing strawman arguments into the
discussion as has been done already with me this past weekend. I’m sure
there is at least some correlation between recent use and lifetime use.
The point is not that recent use is a poor measure, but that attempts to
measure lifetime use (to the extent such attempts are valid and reliable)
are *better* measures relative to providing support for the lifetime drug
use hypothesis. If on the other hand one wants to fail to support the
lifetime drug use-"AIDS" hypothesis he should design the study not to look
too far beyond recent use.

However, even the above paragraph does not address some important
principles of study design. I find it amusing to have to spoon-feed these
to you, a person who never hesitates to whip out his abstracts and should
already be familiar with the following points. But who knows, maybe you
might learn something from me. Okay, here goes:

Here are two ways to attempt to quantify drug use:

MODEL 1:
Did you consume drug X at any time in the last 7 days? Yes/no?
Did you consume drug X at any time in the last 6 months but not the last
7 days? Yes/no?
Did you consume drug X at any time in the last 2 years but not in the
last 6 months? Yes/no?

MODEL 2:
How often, if at all, did you consume drug X in the last 7 days, and what
was the estimated typical dose?
How often, if at all, did you consume drug X in the last 6 months, and what
was the estimated typical dose?
How often, if at all, did you consume drug X in the last 2 years, and what
was the estimated typical dose?
How often, if at all, did you consume drug X between 2 years and 4 years
ago, and what was the estimated typical dose?
How often, if at all, did you consume drug X between 4 years and 6 years
ago, and what was the estimated typical dose?
How often, if at all, did you consume drug X between 6 years and 8 years
ago, and what was the estimated typical dose?
How often, if at all, did you consume drug X between 8 years and 10 years
ago, and what was the estimated typical dose?
How often, if at all, did you consume drug X between 10 years and 15 years
ago, and what was the estimated typical dose?
              —   —   —

Is the above perfect, no, not at all, it’s meant to be illustrative only
and we can both improve on it. But if one is going to try to support the
theory that cumulative doseages of intake (lifetime use) of recreational
and/or medical drugs correlate with the probability of a later "AIDS"
diagnosis then one MUST use the survey design principles of model 2. If on
the other hand we want to convince everyone to believe there is no support
for said hypothesis we will use model 1. The MACS, a study which analyzed
the drug consumption of a couple thousand gay men and supposedly found no
correlation with AIDS, used model 1, of course, and model 1 is not a valid
model for measuring *extent* of drug use. It throws heavy drug consumers
in with occasional users for each time period, and therefore has mediocre
(invalid) results. This is a major weakness with the MACS and other studies.

A second weakness is that AZT and other medical drugs were not measured.
Consequently it is a poor study for use in analyzing the effects of
*medical* drugs, drugs which have been consumed in great quantities and
are a major component of Peter Duesberg’s drug use-AIDS hypothesis.)

Calif…@netcom.com

Has anyone been to NIH to be involved in a pediatric study?  My sister will be
making her first visit there next week, to see if she will be in a study
involving IL-2.  If anyone else has been in any studies at the NIH, please
email me with your opinions of the experience…and any other information you
think would be useful to us before we leave (10/23).