AIDS TREATMENT NEWS Issue #384, October 18, 2002
phone 800-TREAT-1-2, or 215-546-3776

CONTENTS

** Animal Retroviral Infections Suggest Third Kind of
Potential Treatment: HIV Harm Reduction
Besides antivirals and immune-based treatments, a third
approach is to reduce the harm caused indirectly by HIV,
which is probably more important than the direct killing of
infected cells. Some animals do not get sick when infected
with HIV-like viruses despite very high viral loads --
suggesting that they have successfully evolved to tolerate
the virus instead of eradicating or suppressing it.
Understanding how they do so might lead to a new kind of HIV
treatment.

**T-20 (FUZEON) Gets Priority Review
The FDA plans to decide on T-20 approval within six months.

** ICAAC Clinical Trials Review Available
You can read a quick summary of the HIV clinical trial
results presented at a scientific conference on anti-
infection drugs.

** Hepatitis C: FDA Public Meeting on Peginterferon Plus
Ribavirin, Nov. 14
An FDA advisory committee will hold a public meeting on a new
treatment for hepatitis C.

** Anti-HIV Factor Discovered
Scientists at the Aaron Diamond AIDS Research Center believe
they have discovered a major component of a long-sought
soluble anti-HIV factor produced by certain CD8 cells.

** Retroviruses Scholarship, Community Press, Other Deadlines
Soon
Scientific abstracts are due October 23, and important
community deadlines begin November 1 for international
travelers, November 8 for U.S. community press and
scholarship applicants.

** Treat-Your-Workers.org; International Coca-Cola Protest
October 17
ACT UP and others demand better medical coverage for African
workers with HIV.

** Chinese AIDS Activist Released
Dr. Wan Yan Hai was released September 20.

** Nonoxynol-9 Dangers: Health Experts Warn Against Rectal
Use
Dozens of experts and organizations call for stopping all
rectal use of N-9.


***** Animal Retroviral Infections Suggest Third Kind of
Potential Treatment: HIV Harm Reduction

Comment by John S. James

All the approved HIV treatments so far are antiretrovirals --
drugs that directly target some step in viral replication. In
the future we may have another kind of treatment, immune-
based therapy, which strengthen the immune system's ability
to control HIV, instead of attacking the virus directly.

A third approach, less talked about so far, might be called
HIV harm-reduction treatment -- preventing the virus from
causing harm despite a continuing high viral load. This could
work because HIV seems to cause most of its damage indirectly
-- by the toxic tat protein, for example, or by dysregulation
of immune responses leading them to kill normal cells --
rather than by killing infected cells, which the body could
normally replace. If so, then ways to block the indirect
damage might become a new kind of treatment. (We distinguish
HIV harm reduction from immune-based therapies because the
former would not necessarily target the immune system at all
-- and also because it would have to be tested differently,
since it might not decrease viral load, which immune-base
therapies might be expected to do.)

One observation supporting this way of thinking is described
in an abstract at the recent conference of the Institute of
Human Virology, September 9-13, 2002, in Baltimore.(1) Mark
Feinberg of Emory University noted that in monkeys and other
primates, all known retroviral infections in their natural
hosts did not cause AIDS-like disease. But the same viruses,
in primates that are not natural hosts, do cause persistent
infection, loss of CD4+ T-cells, and susceptibility to
opportunistic infections. And in these animals that do get
sick, low viral loads and strong cellular immune responses
predict slower disease progression -- as they do in humans
with AIDS.

But at least some animals naturally infected with SIV (simian
immunodeficiency virus) successfully control the infection in
a very different way. In the sooty mangabey monkey, for
example, the immune system does not suppress viral load,
which stays high, yet the animal does not become ill. From
the abstract:

"... Surprisingly we have found that SIV-infected sooty
mangabey monkeys do not develop AIDS despite high level virus
replication, short longevity of infected cells and limited
anti-SIV specific cellular immune responses....
Interestingly, an attenuated host immune response to the
infection is manifest from early times during primary
infection, suggesting that sooty mangabey evolution has
selected for a limited, rather than an aggressive, host
response. In all, these data suggest that the direct
consequences of high level virus replication alone cannot
account for the progressive CD4+ T cell depletion leading to
AIDS, and that active antiviral cellular immune responses may
not always be beneficial. Indeed, SIV-infected sooty
mangabeys may be spared, by their failure to mount
significant antiviral immune responses, much of the indirect
bystander damage seen in pathogenic primate lentivirus
infections that both contributes to accelerated CD4 depletion
and compromises host immune regenerative capacity. In
contrast, following zoonotic transmission of SIV to non-
natural hosts, the generation of active but incompletely
effective immune responses may indirectly both increase the
magnitude of overall T cell destruction and reduce the host
immune regenerative capacity, thereby leading to the
development of progressive immune deficiency as T cells lost
to cumulative direct and indirect consequences of virus
infection are not replaced."(1)

How to Proceed

A treatment that prevents AIDS by reducing damage from HIV
might be hard to recognize. It might not decrease viral load
at all, or even increase it. The ultimate proof would be that
people would not get sick over a long period of time. But it
would probably be impossible to conduct clinical trials in
the straightforward way -- randomly assigning patients to
antiretrovirals with or without the new treatment -- because
the effectiveness of antiretrovirals has made it almost
impossible to run clinical-endpoint trials. Instead, new
drugs today are approved by their effect on viral load, an
endpoint that would not work in this case. (In fact, if an
existing drug for some other medical purpose happened to work
this way and prevent the development of AIDS without lowering
viral load, we would probably not know it, even if many
patients with HIV had used the drug coincidentally.)

How then might it be possible to get a handle on the
development of this kind of drug? Here are some possible
approaches:

* Many patients have "discordant" viral load and CD4 counts.
Instead of fitting the usual pattern of having higher CD4
counts if they have low viral load or vice versa, they either
have a high CD4 count despite a high viral load, or a low CD4
count even though their viral load is low.

These two kinds of discordant patients could be compared to
each other, to look for differences in how they respond to
HIV infection. What could be learned from patients who can
tolerate a high viral load and still maintain a high CD4
count -- especially those who remained healthy despite having
the high viral load for a long time? If the mechanisms could
be identified, perhaps some kind of pharmaceutical
intervention could help other patients do likewise.

If there are some patients who, like the sooty mangabeys, are
long-term non-progressors despite having a high viral load,
we probably would not have recognized them. Instead we would
have treated their viral load, and attributed non-progression
to the treatment. But these patients might be identified by
careful examination of their medical records.

* Basic research could look for the mechanisms involved,
either in sooty mangabeys, other animals, or in any humans
known to tolerate a high HIV viral loads and remain healthy.

Of course differences in the virus as well as the host could
be responsible for reduced disease progression despite high
viral load. But still the host somehow avoids disease even
though the virus reproduces well and does cause disease in
non-native hosts.

* For many years some physicians and researchers were
interested in immune suppressive drugs to treat HIV. Their
experience should be reviewed -- especially since sooty
mangabeys seem to have evolved an effective defense against
AIDS that includes a notably unaggressive immune response.
Existing drugs may be too non-selective or have too many side
effects for widespread use. More selective immune-suppressive
drugs could be developed.

* Once a candidate harm-reduction drug is identified, it
could be tested to see if it improves the health of patients
who cannot control the virus with any existing treatment.
Since their viral load cannot be controlled in any case, an
experimental treatment to reduce viral damage could ethically
be tested while the viral load stays high (necessary to see
if the new treatment worked). A placebo control would be used
since there is no approved HIV harm-reduction treatment. The
volunteers could either take antiretrovirals or not as they
chose. The study could look for T-cell count increases,
reduction of symptoms believed to be caused by the high viral
load, and/or other evidence of clinical improvement. Such
endpoints could show significant change quickly in a small
number of patients (unlike the "clinical endpoint" of disease
progression, which requires hundreds if not thousands of
volunteers because it counts low-probability, all-or-nothing
events instead of measuring continuous data on everybody).

A treatment that prevented viral damage without reducing
viral load would not have the public-health advantage of
antiretroviral treatment in making patients less likely to
transmit the virus to others. But in practice, this kind of
treatment would probably be combined with antiretrovirals for
maximum benefit, so the risk of transmission would still be
reduced.

A possible advantage of HIV harm reduction is that HIV
develops resistance to all known antiretrovirals -- and to
the body's immune responses as well. But a harm-reduction
treatment would create different evolutionary incentives, as
HIV variants would not need to evade either the therapy or
the body's defenses in order to survive. They could do best
by not provoking the immune system. And in the sooty mangabey
example the viral load does not increase without limit until
it kills the animal; there is still a setpoint, still a
limit, and the animal remains healthy. So a harm-reduction
treatment may also allow relatively harmless viruses (which
would have an advantage here) to help crowd out more
dangerous ones.

Perhaps such reasons explain why animals apparently evolved a
strategy of maintaining health by preventing harm, even from
continuous high levels of viruses still able to cause disease
in other species. Human long-term non-progressors (at least
those who have been identified) use a different strategy, of
aggressive immune defense that keeps viral replication low
enough to greatly delay escape from immune control. It seems
likely that the former approach is the better one for
controlling a virus that can mutate so rapidly. Possibly some
patients are already benefiting from it, but under current
medical and research practices we do not see them. For where
viral load testing is available, treatment is available too,
and almost no one gets viral load tests repeatedly unless
they plan to treat a high viral load. Usually antiretroviral
treatment would reduce the viral load and be credited for
non-progression. And experimental HIV therapies that fail to
lower viral load are not studied today.

As a result, a new kind of potential treatment for AIDS may
have been overlooked.

References

1. Feinberg M. Ignorance is bliss: how the natural hosts for
SIV infection remain healthy despite long-term, high-level
virus replication. JOURNAL OF VIROLOGY. 2002; volume 5,
number 1, abstract #8.


***** T-20 (FUZEON) Gets Priority Review

On October 11 Roche and Trimeris, Inc. announced that the FDA
had granted priority review to FUZEON (TM) (generic name
enfuvirtide, formerly known as T-20). This means that the FDA
plans to review the application for approval in six months,
and announce the results by March 16, 2003 (six months after
the application for approval was submitted).

Enfuvirtide works differently from any currently approved HIV
drugs: it blocks a step in the process by which HIV fuses
with a cell membrane and enters the cell. Since it has an
entirely different mechanism of action, virus that has become
resistant to approved drugs will not automatically be
resistant to this one. However, resistance to enfuvirtide
does develop, as with other antiretrovirals. This drug also
must only be used in combination treatments, never alone.

Enfuvirtide must be injected twice a day, can be difficult to
use, and is difficult to manufacture so it will probably be
expensive. For these reasons it will likely be used mainly by
patients who do not have other good options.


***** ICAAC Clinical Trials Review Available

ICAAC, the Inter-Science Conference on Antimicrobial Agents
and Chemotherapy, was held this year in San Diego, September
27 - 30. This annual conference focuses mainly on the
development of new antibiotics and antivirals. On October 11
HIVandHepatitis.com published a review of the HIV clinical
trial presentations at ICAAC, by Charles Hicks, M.D.; it is
available at:
http://www.hivandhepatitis.com/2002conf/iccac2002/pages/35.html

Some of the topics:

* Atazanavir, an experimental protease inhibitor being
developed by Bristol-Myers Squibb, was compared in a large
international trial with efavirenz (brand name Sustiva -- or
Stocrin in some countries);

* 3TC (Epivir) was successfully dosed for once-daily use;

* Coviracil, an experimental nucleoside reverse-transcriptase
inhibitor, was compared with d4T; and

* For certain advanced patients, a combination of amprenavir
(Agenerase) and lopinavir plus ritonavir (Kaletra), with some
extra ritonavir (Norvir) added to overcome an interaction
that would reduce the levels the other two drugs, appeared to
work well.

All of these trials showed promising results that may
improve HIV treatment in the future.


***** Hepatitis C: FDA Public Meeting on Peginterferon Plus
Ribavirin, Nov. 14

On November 14 the Antiviral Drugs Advisory Committee will
review the application by Hoffmann-La Roche for approval of
peginterferon alfa-2a combined with ribavirin. The meeting
will include time for public comment, and comments can also
be submitted in writing. If you want to address the committee
you need to notify the staff before November 6 and submit a
brief written statement about your presentation. Written
statements to the Committee should be submitted by November
6.

The meeting will be held November 14, 2002, from 8:30 a.m. to
4 p.m. at the Holiday Inn, Versailles Ballroom, 8120
Wisconsin Avenue, Bethesda, MD. This location is near
Washington D.C. and easily reachable by the Red Line subway.

More information is available from the FDA Advisory Committee
Information Line, 1-800-741-8138 or 301-443-0572. You will be
asked to enter a code; the code for the Antiviral Advisory
Committee is 12531.

Comment

We have heard that peginterferon will be approved as a single
drug soon, maybe this week. The Advisory Committee will
consider the combination with ribavirin. Our understanding is
that Roche plans to sell its peginterferon alone as well.

FDA advisory committee meetings are often the best place to
learn in-depth information about a new drug before it is
approved. They are not called for every new drug application,
only for those that present new, difficult, or particularly
important issues. Usually a transcript and a summary appear
later on the FDA Web site.

The FDA is not required to follow the recommendations of its
advisory committees, but it almost always does.


***** Anti-HIV Factor Discovered

by John S. James

On September 26 scientists at the Aaron Diamond AIDS Research
Center (ADARC) announced that they had identified a
significant contributor to a long-sought antiviral factor,
secreted by certain CD8 T-cells, that inhibits HIV
replication.(1) This work does not change treatment now, but
could lead to the development of a new class of HIV drugs. It
was widely reported in the press.

The research team at ADARC, headed by Linqi Zhang, believes
that this factor includes three previously known chemicals
called alpha defensins. Through various tests, they found
that these chemicals were produced by stimulated CD8 cells of
three of the long-term non-progressors they are studying
(they picked their three best non-progressors among their
patients, in order to have the best chance of identifying how
their cells are able to keep HIV in check). After the
chemicals were identified -- with the help of a protein-chip
technology that allows rapid, sensitive testing -- it was
found in laboratory tests that antibodies to those chemicals
could largely eliminate the anti-HIV activity of those cells
-- helping to confirm that an anti-HIV factor is really these
three defensins.

Only one to two percent of HIV patients are long-term non-
progressors. Since 1986 it has been known that their cells
can produce some substance or substances that inhibit HIV.(2)
In 1995 it was shown that some of the activity was due to
three other chemicals called beta chemokines. But the beta
chemokines only block some HIV viruses, those that use the
CCR5 receptor on the CD4 cell to enter the cell -- not
viruses that use the CXCR4 receptor, which often evolve later
in HIV infection.

The defensins are believed to block all HIV, and to act
through a completely different mechanism -- possible
involving viral transcription, instead of viral entry into
the cell. These chemicals have been found not only in long-
term non-progressors but in at least some healthy uninfected
persons as well, and in several primate species. However they
are seldom found in HIV patients who are not non-progressors.

The defensins would be very difficult to use as drugs, if
they could be used at all. But when their action is better
understood, it may be possible to devise other treatments
that have the same effect. Another approach would be to
maintain and enhance the body's ability to produce defensins.
Either kind of treatment might convert patients into long-
term non-progressors who would not become ill despite HIV
infection.

References

(1) Zhang L, Yu W, He T and others. Contribution of human
alpha-defensin-1, -2, and -3 to the anti-HIV activity of CD8
antiviral factor. SCIENCE EXPRESSs. September 26, 2002.

(2) Walker CM, Moody DJ, Stites DP, and Levy JA. CD8+
lymphocytes can control HIV infection in vitro by suppressing
virus replication. SCIENCE. December 19, 1986; volume 234,
number 4783, pages 1563-1566.


***** Retroviruses Scholarship, Community Press, Other
Deadlines Soon

by John S. James

The annual Retroviruses conference, one of the world's most
important scientific meetings on HIV, will not take place
until February 2003, but scholarship and other deadlines are
approaching. For community members without an accepted
scientific abstract, the scholarship or community press
applications are the only way to get into this meeting.
Therefore some will need to apply for the scholarship whether
or not they need the money.

This year the 10th Conference on Retroviruses and
Opportunistic Infections will be held in Boston for the first
time, at the Hynes Convention Center, February 10-14, 2003.

Deadlines by Date

* For scientists, abstracts are due October 23 at 5:30
Eastern time (except late breakers).

* Also for scientists, the Fellow Travel Grant applications
are due October 23.

* For international scholarships, the application deadline is
November 1.

* For U.S. community scholarships, the deadline is November
8.

* For community press, the deadline is also November 8.

* Preferred registration and housing for invited speakers and
authors of accepted abstracts (two per abstract) is open
November 18 - 29.

* Registration for other researchers and clinicians (without
an accepted abstract) is open December 2 - January 10.
Caution -- sometimes this conference fills almost
immediately; in case that happens these applications must be
sent as soon as this period begins. This year the conference
will accept 3,800 registrations.

* The late breaker abstract deadline is January 6 at 5:30
Eastern time.

Be sure to check the conference Web site,
http://www.retroconference.org, to confirm these dates and to
get the forms and other information needed to apply.


***** Treat-Your-Workers.org; International Coca-Cola Protest
October 17

by John S. James

"AIDS is the crisis of our generation, and we will be defined
by our response to it. Years from now, we will have to answer
to our own children: did we stand by as millions died, or did
we take action? We have a chance to make a real difference in
shaping the outcome of this pandemic. We hope you will join
us in this endeavor." From Student Global AIDS Campaign,
cover letter transmitting THE COCA-COLA CAMPAIGN: A MANUAL
FOR STUDENT ORGANIZERS.

Since a July 2002 announcement in Barcelona during the
international AIDS conference there, activists in Africa, the
U.S., and Europe have called for a global day of protest
against Coca-Cola on October 17, asking for better health
coverage for African workers and their families. Behind this
protest are several developments.

Coca-Cola already provided health coverage including
antiretrovirals to its corporate employees in Africa -- about
1200 workers, mostly white collar. But that is only about 2%
of the 60,000 workers producing and distributing Coca-Cola
products in Africa. Most of the work is outsourced to
bottlers and other independent contractors, who typically
compete against each other with low prices and margins --
creating a race to the bottom in worker health care, unless
the larger corporation sets standards for contractors or
otherwise intervenes. African and other activists saw that if
multinational corporations could wash their hands of
responsibility simply by outsourcing their work, access to
treatment in developing countries would be gravely set back.
While treatment can reduce employee turnover and associated
costs, sometimes it is cheaper to abandon and replace low-
wage, low-skill workers who get sick, than to provide medical
care.

On September 26 the Coca-Cola Africa Foundation announced a
major treatment initiative in which the Foundation and three
partners (GlaxoSmithKline, PharmAccess International, and
Population Services International) will work with Coca-Cola's
40 bottlers in Africa to help them expand their health
coverage to include HIV infection and antiretroviral drug
treatment. This program is estimated to cost the Coca-Cola
Africa Foundation $4 million to $5 million per year.
According to Coca-Cola Africa, a total of 44% of bottler
employees "had agreed to this program or were on exiting
programs that covered prevention and awareness and
treatment," as of October 14.

While acknowledging that this program is potentially an
important step forward, activists said there were several
deficiencies, including that:

* This program covers workers and their spouses -- but not
their children or other dependents;

* The cost sharing required of the bottlers, and co-payments
required from the workers, are likely to prevent many from
participating; and

* There is no proof of commitment to rapid rollout of the
treatment program, and no plan to expand it beyond Africa.

For More Information

The best Web site on this campaign is
http://www.treat-your-workers.org, by Health GAP. It includes
background, contacts, and activist toolkits including a 30-
page manual on how to organize, from the Student Global AIDS
Campaign -- a handbook we hope is adapted to other campaigns
to change the appalling lack of political will on the global
HIV catastrophe.

The Web site of the Coca-Cola Africa Foundation is:
http://www.aidsprogramsinafrica.coca-cola.com.


***** Chinese AIDS Activist Released

Dr. Wan Yan Hai, the AIDS activist detained by Chinese
security on August 24, (see AIDS TREATMENT NEWS #383,
September 6, 2002) was unexpectedly released in Beijing on
September 20. His release came after United Nations and the
U.S. State Department officials negotiated behind the scenes,
and ACT UP led an international activist mobilization to free
him. The groups Human Rights in China, The Committee to
Protect Journalists, Human Rights Watch, the Canadian
HIV/AIDS Legal Network, and Amnesty International also worked
for Dr. Wan's release.

On September 13, Human Rights Watch and the Canadian HIV/AIDS
Legal Network gave Dr. Wan its first Award for HIV and Action
on Human Rights, which was accepted by his wife, Su
Zhaosheng. Other factors may also have played a role: major
news outlets such as THE NEW YORK TIMES covered the case
early and extensively, and scholars and diplomats worldwide
sent letters to Chinese government officials.

Wan was detained for posting information about China's AIDS
epidemic on his organization's web site
(http://www.aizhi.org), one of the best independent sources
of AIDS information available in China. The United Nations
estimates that China may have 10 million HIV-positive
citizens by 2010 if aggressive measures are not taken.


***** Nonoxynol-9 Dangers: Health Experts Warn Against Rectal
Use

by John S. James

On September 27 over 80 health experts and organizations
released a letter warning against all rectal use of
nonoxynol-9 (N-9) -- a spermicide mistakenly used to kill
HIV, when actually it makes transmission worse. The letter
came after a quiet campaign that persuaded most but not all
manufacturers to remove the substance from their products.
Experts agree that rectal use is dangerous and never
appropriate -- and that N-9 should not be included in any
condoms or lubricant.

On October 10 the Bay Area Reporter, a San Francisco gay
newspaper, reported that all lubricant manufacturers had now
promised to stop making lubricant with N-9. This followed an
earlier series of articles in the B.A.R. that prompted some
local retailers to remove N-9 products from their shelves.

From the September 27 consensus letter:

"Call to Discontinue Nonoxynol-9 for Rectal Use

"We, the undersigned, in light of recent statements by the
World Health Organization and the Centers for Disease
Control, urge all people to cease the rectal use of products
containing Nonoxynol-9 (N-9). We are concerned that many
people mistakenly believe that N-9 provides extra protection
against HIV and STDs when used rectally when in fact there is
reason to think that rectal use of N-9 may increase risk of
infection.

"The Centers for Disease Control states: 'N-9 can damage the
cells lining the rectum, thus providing a portal of entry for
HIV and other sexually transmissible agents. Therefore, N-9
should not be used as a microbicide or lubricant during anal
sex.'

"The World Health Organization states: 'N-9 should not be
used rectally.' (Further) 'There is no published scientific
evidence that N-9-lubricated condoms provide any additional
protection against pregnancy or STIs compared with condoms
lubricated with other products.

"'Since adverse effects due to the addition of N-9 to condoms
cannot be excluded, such condoms should no longer be
promoted.'"

For More Information

* On September 25 The Wall Street Journal published "Some
Makers, Venders Drop N-9 Spermicide on HIV Risk.

* The World Health Organization consensus report is at:
http://www.who.int/reproductive-health/rtis/nonoxynol9.html

* And on September 28, 2002, The Lancet formally published
results of a major study in Africa that showed that N-9 could
increase HIV transmission -- available at
http://www.thelancet.com (free registration required).


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