The
fight against HIV-AIDS turned an important corner with the recent announcement
of new data from News (Updated
August 15, 2010)
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Alan Bernstein and Peter
Piot
From Tuesday's Globe and
Mail Published on Tuesday, Aug. 10, 2010
The
fight against HIV-AIDS turned an important corner with the recent announcement
of new data from
Neither experimental
product is good enough to use today. The microbicide requires at least one more
large-scale clinical trial. The vaccine’s modest, short-term protection must
be improved on with better approaches. But both studies, along with other
research advances being reported with increasing frequency, provide clear
evidence we have entered a highly promising era in HIV-prevention research.
Microbicides, vaccines and other new approaches will one day join proven
HIV-prevention strategies, including condoms, male circumcision and clean
needles. How soon that day comes will depend on whether funders and the
scientific community can develop the more collaborative approaches to HIV
prevention research needed to address this fast-moving epidemic.
For years, global
attention has focused on enhancing access to AIDS treatment. Thanks to programs
such as the U.S. PEPFAR initiative, the Global Fund to Fight HIV, TB and
Malaria, United Nations programs and foundation efforts led by Bill Clinton and
a handful of others, the number of people receiving life-saving HIV treatment
has grown from 400,000 at the start of the decade to five million people. As a
result, AIDS-related mortality has dropped 18 per cent in sub-Saharan
Despite Herculean efforts
to expand access to treatment, however, only a third of those who need HIV drugs
receive them – a proportion sure to drop as millions more are infected each
year. While access to treatment deserves increased support, treatment alone will
not end this pandemic. Smarter, more nimble, better-funded research is needed to
build on recent successes and develop practical tools that can slow and one day
end this epidemic.
How do we do that? With
new approaches to bring funders and scientists from around the world working
together to advance HIV prevention and other major public-health goals. The
Global HIV Vaccine Enterprise is a unique approach that brings together major
funding and policy organizations committed to accelerating the development of an
HIV vaccine. HIV vaccine and microbicide research is supported by only a handful
of funders, with the
Canadian science has a
particular contribution to make. The recent announcement by Health Minister
Leona Aglukkaq of the renewed alliance between the government and the Gates
Foundation to support HIV vaccine research is welcome news. This will challenge
other G20 countries, which need to contribute more to this global effort.
As it becomes clearer that
vaccines, microbicides or other drug-based approaches may hold the key to HIV
prevention, the pharmaceutical industry can no longer watch from the sidelines.
HIV-prevention research requires systematic, strategic approaches that maximize
the scientific value of public-private partnerships, minimize risk for industry
and permit the sharing of research findings and data.
HIV-prevention trials
typically take three to seven years to plan, fund, conduct and analyze. With
nearly three million people newly infected each year, we need smarter approaches
to clinical trials that test more concepts in less time and for less money,
while preserving safety, community engagement and ethical guidelines. This
requires a new spirit of global collaboration among funders, researchers,
communities, local and national governments, and trial volunteers, as well as a
new generation of HIV researchers, encouraged to enter this field by the
conviction they can help end this epidemic.
HIV is too great a
challenge, and the results of these trials too promising, to continue with
hesitant approaches to prevention research. This epidemic is a holdover from the
20th century. It is time for 21st-century research approaches that will speed
the effort to end it.
Alan Bernstein is
executive director of the Global HIV Vaccine Enterprise and former president of
the Canadian Institutes of Health Research. Peter Piot is chair of the Global
HIV Vaccine Enterprise, director of the Institute of Global Health at Imperial
College, London, and former executive director of the Joint United Nations
Program on HIV-AIDS (UNAIDS).
Michael Carter
10 August 2010
Ongoing hepatitis C
replication inhibits improvements in the CD4 cell counts of HIV-positive
patients taking antiretroviral therapy, Canadian investigators report in the
July 31stedition of AIDS.
Researchers monitored
changes in the CD4 cell counts of HIV-positive patients who had antibodies to
hepatitis C virus. Falls in CD4 cell counts before HIV treatment was started,
and increases in such counts after the initiation of antiretroviral therapy were
compared between individuals who had spontaneously cleared hepatitis C, and
those who had chronic infection with the virus.
Ongoing hepatitis C
replication was associated with slightly higher CD4 cell count loss prior to
starting HIV treatment. There was also clear evidence that individuals with
chronic hepatitis C had blunted CD4 cell responses to antiretroviral therapy.
“Spontaneous clearance
of HCV [hepatitis C virus] is independently associated with a better rate of CD4
cell recovery once ART [antiretroviral therapy] is introduced”, comment the
investigators, who stress that their “findings were robust.”
Investigators from the
Canadian Coinfection Cohort Study performed their research because there is
uncertainty about the impact of hepatitis C co-infection on HIV disease
progression. Moreover, they were concerned that earlier research exploring this
question may have been limited because antibody status was used to define
hepatitis C infection. A significant proportion of patients infected with
hepatitis C spontaneously clear the infection, leading the researchers to
postulate that the results of some studies could have been confounded because
some individuals in the hepatitis C arm were in fact free from the infection.
Their study population
included 271 patients. All were infected with HIV, and all had antibodies to
hepatitis C.
However, they divided the
patients into two groups. The first involved 236 with chronic hepatitis C
infection (and therefore ongoing replication of the virus), the other, those who
had spontaneously cleared the infection.
Changes in the CD4 cell
counts of these two groups were then compared before and after the initiation of
antiretroviral therapy.
A total of 95 patients, 25
of whom had spontaneously cleared hepatitis C, were naïve to HIV treatment on
recruitment to the study.
CD4 cell counts fell by a
non-significant average of 44 cells/mm<sup>3</sup> per year amongst
the patients who had cleared hepatitis C, and by an average of 84 cells/mm3each
year in those with ongoing replication of the virus. However, after adjustment
for follow-up time the association between chronic hepatitis C infection and
greater loss of CD4 cells was not significant.
Information on CD4 cell
count increases after the initiation of antiretroviral therapy was available for
226 individuals. Once again, 25 patients had spontaneously cleared their
hepatitis C infection. The median duration of follow-up was 18 months for those
with chronic hepatitis C and 15 months for those who had cleared the infection.
Average annual CD4 cell
count increases were seven-fold higher for patients who had cleared hepatitis C
infection than for those with ongoing hepatitis C replication (4 vs. 24
cells/mm3 p < 0.001).
The association between
spontaneous clearance of hepatitis C virus and more robust increases in CD4 cell
count during HIV therapy remained significant after the investigators adjusted
their results to take into account potentially confounding factors.
Moreover, the researchers
also founded that the blunted CD4 cell response seen in the patients with
chronic hepatitis C did not improve over time.
Limiting analysis to
patients who started HIV treatment for the first time after entry to the study
cohort did not affect the results.
However, when the
researchers restricted their analysis to patients who maintained an undetectable
HIV viral load throughout follow-up, the impact of chronic hepatitis C virus
infection on CD4 cell count recovery was attenuated. CD4 cell counts still
increased more slowly in those with ongoing replication of hepatitis C, but the
interaction between chronic infection and CD4 cell gain ceased to be
statistically significant.
“We found that CD4 cell
progression is negatively affected by the presence of ongoing HCV replication in
coinfected individuals taking ART”, write the investigators. They add,
“elucidating the mechanisms by which this difference occurs and investigating
the impact of HCV treatment on CD4 cell progression should be prioritised.”
The study’s authors
conclude, “when successful, HCV treatment might have an important role not
only in improving HCV related outcomes, but for HIV-related prognosis as
well”.
Reference
Potter M et al. Impact of
hepatitis C viral replication on CD4 T-lymphocyte progression in HIV – HCV
coinfection before and after antiretroviral therapy. AIDS 24: 1857-65, 2010.
By Simeon Bennett - Aug
11, 2010
Crucell will participate
in a trial of the vaccine in adults who don’t have HIV to assess its safety
and ability to prompt an immune response, the
The vaccine combines shots
made by Crucell and the New York-based International AIDS Vaccine Initiative in
a so-called prime-boost approach that’s designed to both kill infected cells
and prevent HIV from entering those that are uninfected. The theory was tested
with another vaccine in
“Our program to develop
this combination vaccine represents one of the most advanced AIDS vaccine
programs in the world,” Jaap Goudsmit, Crucell’s chief scientific officer,
said in the statement.
Researchers from
It would take five to six
years before the first successful microbicide gel to prevent HIV infection in
women could be put out for public consumption, the International Partnership for
Microbicides' National Women's Day breakfast heard in Durban on on Thursday.
Professor Gita Ramjee, of the HIV Research Unit in the SA Medical Research
Council, said: "We know that 39 percent efficacy in HIV prevention is not
enough. We are looking at five to six years before the gel can possibly be used
by women." - Mercury Reporter
WEDNESDAY, Aug. 11 (HealthDay
News) -- A natural mechanism that may help prevent the development of AIDS in
sooty mangabey monkeys has been discovered by scientists.
Sooty mangabey monkeys are
a natural host for the simian immunodeficiency virus (SIV), but they don't
develop AIDS even if they have a very high viral load. SIV -- a virus that
infects monkeys -- is related to the human immunodeficiency virus (HIV) in
people.
These monkeys may be able
to avoid developing AIDS because they are better at regenerating T cells -- a
type of white blood cell that allows the immune system to fight off microbial
invaders.
Specifically, SIV-infected
sooty mangabeys maintain effective levels of CD4+ T cells through rapid
regeneration of their pool of naive CD4+ T cells (mature cells not yet exposed
to toxins or other substances that stimulate the production of antibodies).
The finding may help
explain why SIV and HIV lead to AIDS in other types of monkeys and nonhuman
primates and in humans, according to the researchers at the
For this study, the
researchers compared sooty mangabeys and rhesus macaques infected with SIV.
"The results showed
that while both species showed a similar extent of CD4+ T cell replenishment,
the rhesus macaques regenerated their naive CD4+ T cells more slowly," team
leader Mirko Paiardini said in an Emory news release. He also noted that in
another primate species, macaques, giving the monkeys new CD4+ T cells heightens
the animal's vulnerability to SIV. However, in the sooty mangabey this doesn't
happen - in fact, the replenished cells appear to make the monkey "more
resistant to SIV infection," Paiardini said.
Paiardini believes the new
findings "have increased our understanding of the immune system and are
critical to our continuing research to determine why some species are more
susceptible than others to infectious diseases."