|
First AIDS vaccine tested
in Africa
The first test of a human AIDS vaccine in
Africa has begun in Uganda, says the U.S. National
Institutes of Health, which is funding the study. It is
an important step toward developing a vaccine for
countries hardest hit by the epidemic. AIDS has
devastated Africa. In Uganda alone, it has killed nearly
a half-million people and left 1 million children
orphaned. The Uganda study tests a vaccine made by
Pasteur Merieux Connaught that uses a canarypox virus to
carry three HIV genes. The canarypox cannot cause human
disease, and the HIV genes by themselves aren't
infectious, the NIH said.
The National Institutes of Health says the
first test of a human AIDS vaccine in Africa has begun in
Uganda. Several AIDS vaccines have been tested in various
countries - particularly the United States, where the
most advanced study of another possible vaccine candidate
is under way. But this announcement by the NIH, which is
paying for the study in Uganda, was pegged as an
important step toward developing a vaccine for countries
hardest hit by the epidemic. The vaccine, known as ALVAC,
already has undergone safety testing in about 800 people
in the U.S. and France.
Thailand has given the go-ahead for the first
large-scale AIDS vaccine trial in a developing
country, the U.N.agency in charge of fighting AIDS
announced. Some 2,500 intravenous drug users in the Thai
capital of Bangkok will take part in the four-year trial
of the AIDS VAX vaccine, made by VaxGen Inc. of Brisbane,
Ca. "This trial signifies an important early step
toward the development of a safe and effective vaccine
against HIV, an essential strategy for bringing the
epidemic under control," said Peter Piot, executive
director of the UNAIDS program.
HIV -1 false positive
result with Western Blot testing
-how does one suspect?
The authors of this study aimed to assess the
frequency of false positive results of HIV-1 detection by
Western Blot in US Blood donors. They also aimed to
validate an algorithm for selecfing possible
false-positive cases for further evaluation. The authors
conducted a retrospective cohort study of HIV-1 enzyme
immunoassay (EIA) and results of Western Blot from a
donor cohort. Those donors with suspected false positive
results on Western Blot underwent HIV-1 RNA polymerase
chain reaction (PCR) testing and follow-up serology The
cohort included more than five million allogenic and
autologous blood donors.The rate of false positivity by
Western Bolt and the true HIV-status of the patient was
determined by the above discussed methods with them being
followed up more than five weeks after blood donation.
Out of the 421 donors who were positive for HIV-1 by the
Western Blot, 9.3% (39) met the criteria
of possible false positivity due to their lack of
positivity to p31. Of these 39, the PCR proved that 20 of
them were not infected. They were thus able to identity a
false-positive prevalence for Western Blot positivity for
HIV-1 among blood donors as 4.8% for all donors, the
value was 0.0004%.
The authors thus suggest that those HIV-1 positive
(Western Blot results) who lack the p31 band must be
counselled to undergo conclusive testing by RNA PCR and
HIV serologic analysis on follow-up samples. This is
stressed because of the social and psychologic
consequences that may arise.
CURRENT GUIDELINES
for use of drugs against HIV
HIV infection is associated with an
incredibly high rate of replication, even during the
asymptomatic phase of infection. Secondly, replication is
highly error prone. It has been estimated that every base
pair of t he genome mutates on a daily basis. Mutations
coding for resistance to antiretroviral drugs could
potentially arise during this process.
Given these facts, a drug regimen has to
be highly active - that is, potent enough to completely
suppress viral replica tion - in order to prevent
selection of resistant mutants. The overall potency of
the regimen is more important than the absolute number of
agents. With the currently available drugs, this usually
translates into a regimen containing at least 3
agents - generally, two nueleoside
analogue reverse transeriptase inhibitors and a
protease inhibitor with high potency .
Monotherapy or combination regimens that only partially
suppress viral replication actually contribute to
therapeutic failure by encouraging selection of resistant
variants.
Even a highly active regimen must be
initiated early in the course of the disease, rather than
after progression to the acquired immunodeficiency
syndrome (AIDS) or a decline in the patient's CD4 cell
count to less than 50O/uI. This is to prevent the
permanent loss of immunologic diversity. Data indicates
that the immune restoration that occurs in treated
patients with moderately advanced disease is incomplete.
Thus, opportunistic infections may occur in spite of
return of the CD4 cells to near-normal levels.
RATIONALE FOR COMBINATION THERAPY
None of the currently available
antiretroviral drugs can eradicate the infection.
However, when given in combination, they can suppress
viral replication, improve immunologic status, delay
infectious complications and prolong life.
Recent studies have shown that there are
reservoirs of HIV such as the resting memory CD4 cells,
cells in the brain, etc., which harbour the virus for
prolonged periods and make viral eradication difficult.
Individual drugs in combination can better penetrate
these sites. Moreover, the activity of nueleoside
analogues against HIV-1 varies depending on the
activation state of the infected cells.For example
zidovudine is more effective in replicating peripheral
blood mononuclear cells, whereas lamivudine, which is
usually used in combination, is more effective in resting
cells.
However the greatest deterrent in
following these regimens in poor countries because of
cost of therapy. If the cost of treating the various
opportunistic infections in these patients is added to
this, then it is evident that these triple drug regimens
can be used only in a select category of patients.
It is important to note that these
regimens do not assure complete suppression of viral
replication in lymphoid tissue or genital secretions.
Hence even patients with undetectable plasma virus should
be assumed to be capable of trasmitting HIV to sexual
partners.
The combination of Zidovudine, Lamivudine,
and Indinavir is synergic and has been shown to
significantly reduce plasma viral load for up to 1 year.
ORIGIN OF AIDS VIRUS
The AIDS virus came from chimps.Experts
have wondered about the origin of HIV ever since the
epidemic emerged almost two decades ago. The uncertainty
launched a variety of conspiracy theories, some
suggesting AIDS was a government plot created purposely
to kill. Now, research presented at an AIDS conference
provides what scientists say is convincing proof to the
contrary: The virus got its start in the forests of
Africa when humans caught it from chimpanzees. The chimp
version of the AIDS virus, called SIVcpz, could have been
passed to humans when someone was bitten by a chimp, or a
hunter was exposed to contaminated blood while field
dressing an animal.
Did the Polio vaccine
tests led to AIDS ??
Childbirth AIDS treatment
Researchers trying to reduce the rate of
AIDS among the world's poor have found that giving
mothers standard medicines for just a week, cuts the risk
of passing the virus on during childbirth by more than
one-third. Doctors have known for about five years that
the drug AZT during pregnancy blocks HIV-infected mothers
from giving the virus to their babies. However, such
information is of little use in places such as Africa and
India, where most mother-to-child transmission of AIDS
occurs. In wealthy countries, infected mothers typically
receive five months of AZT, a treatment that can cost
more than $1,000. Doctors reported that a far less
intensive kind of treatment works reasonably well, even
though not as effectively as the standard U.S. approach.
It has been found that
the combined use of Zidovudine and Elective Caesarian
section resulted in a 0% transmission rate in 31
consecutive children.
|
