Scientists identify a chink in HIV's armour - The HIV virus
Kimani Chege
16 February 2007
Source: Science & Development Net
A weak spot in HIV that leaves it vulnerable to antibody attack has been identified and mapped, paving the way for a potential vaccine.
Researchers at the US National Institute of Allergy and Infectious Diseases (NIAID) found that, despite HIV's known ability to mutate, some surfaces of the virus must remain unchanged for it to bind to the host cell. Their findings are published in Nature today (15 February).
The researchers generated an image of a key point on the virus's surface and how it behaves when exposed to a HIV-neutralising antibody, b12.
The scientists say that this area on the surface of HIV is stable — meaning it does not mutate as quickly as other areas of the virus — and thus more vulnerable to attacks from antibodies. Peter Kwong, lead researcher on the project, highlighted the significance of finding a suitable target. "Not only does the HIV virus mutate rapidly, and so constantly defeat immune systems, the virus is also coated with sugary molecules which prevents antibodies from slipping in and blocking the proteins the virus uses to latch on a host cell," he said.
The target is made up of a glycoprotein called gp120, which binds to the receptors of the host cell when HIV attacks.
Gary Nabel, director of NIAID Vaccine Research Centre and a co-author of the paper, said the results present an opportunity for targeting where to deploy vaccines.
"The structure of gp120 and its susceptibility to attacks [by the antibody] shows us a critical area of vulnerability in the virus that we may be able to target with vaccines," he said.
NIAID director Elias Zerhouni said, "Creating an HIV vaccine is one of the greatest scientific challenges of our time. The researchers have been able to identify a gap in HIV's amour and have thereby opened an avenue to meeting that challenge".
Kefa Bosire, a researcher at the Kenya Aids Vaccine Initiative, stressed that this is just the beginning of HIV va ccineresearch."It does not stop here. Let researchers take results from this finding to better future vaccines,"
Phi Huynh Do <huynhdophi@...> thông tin: [AIDSPREVENTIONPROJECT]
NIDA Drug Use and HIV/AIDS Funding Opportunity Announcement
dear members
FYI
Non-Injection Drug Abuse and HIV/AIDS (R03)
WHAT: Purpose. The purpose of this Funding Opportunity Announcement (FOA) with set-aside funds from the National Institute on Drug Abuse is to encourage drug abuse research that elucidates the contribution of non-injection drug abuse to the acquisition and/or transmission and/or disease progression of HIV/AIDS. Specifically, it seeks to:
1) investigate how, where, why, and among whom HIV/AIDS is spreading through non-injection drug use associated high-risk sexual behavior; 2) develop effective prevention and treatment interventions for non-injection drug users at risk for or infected with HIV; and
3) improve accessibility and utilization of evidence-based, integrated care for non-injection drug abuse, risky sexual behavior, and HIV/AIDS and other infectious diseases. -Mechanism of Support. This FOA will utilize the NIH Small Research Grant (R03) award mechanism: and runs in parallel with an FOA of identical scientific scope, PAS-07-115, that solicits applications under the R01 mechanism and PAS-07-262, that solicits applications under the R21 mechanism. -The R03 grant mechanism supports different types of projects including pilot and feasibility studies; secondary analysis of existing data; small, self-contained research projects; development of research methodology; and development of new research technology.
FULL ANNOUNCEMENT: http://grants.nih.gov/grants/guide/pa-files/PAS-07-261.html best
HDP
Phi
Huynhdo <huynhdophi@...>
thông tin: [AIDSPREVENTIONPROJECT]
Herpes drug helps control HIV
11:54 22 February 2007
NewScientist.com news service
Roxanne Khamsi
London School of Hygiene and Tropical Medicine
New England Journal of Medicine
A drug designed to combat genital herpes can also reduce levels of HIV
in the blood by 70% a small trial in Africa has revealed. The herpes medication,
valacyclovir, also appears to reduce levels of HIV in the genital tract.
The researchers behind the study suggest that valacyclovir, and other
herpes drugs, might dramatically reduce the spread of HIV.
Philippe Mayaud of the London School of Hygiene and Tropical Medicine,
UK, and colleagues recruited 140 women infected with both HIV and herpes
in the West African nation of Burkina Faso.
All of the women had high levels of CD4 immune cells, meaning they were
still relatively healthy and ineligible to receive antiretroviral HIV
drugs under World Health Organization guidelines. In addition, none of
the women had visible symptoms of herpes so they would not normally be
given herpes medication such as valacyclovir.
Sustained effect.
The researchers gave half of the women valacyclovir and the other half
women placebo pills. At the end of three months, copies of HIV in those
who received valacyclovir had dropped from 25,000 copies per millilitre
of blood to 8000 per millilitre at a 70% reduction.
This is the same effect one would expect if the women had been given an
anti-HIV drug such as Zidovudine (AZT), according to Mayaud. Levels of
HIV found in the blood of women who received the placebo, by comparison,
had increased slightly on average.
Because all of the women were healthy to start with, there was no difference
in symptoms during the 3-month period. But Mayaud says that such a dramatic
drop in virus particles could potentially delay the onset of AIDS.
"It's important to know if the effect is sustained over a long period,"
he adds, stressing the need for long-term studies of valacyclovir's effect
on HIV infection.
Researchers believe that valacyclovir indirectly reduces HIV infection
by decreasing copies of the herpes virus. They note that untreated herpes
can cause lesions in the genital region, which subsequently attract a
type of immune cell that harbours HIV.
Halting spread
Mayaud points out that the women who received valacyclovir also had half
as many copies of HIV in their genital tracts compared to those who received
the placebo. This also suggests that valacyclovir has the potential to
reduce the spread of HIV, he says.
In Africa, between five and nine out of 10 HIV-infected patients are also
infected with herpes
In Europe, the figure is between three and seven out of 10.
Lawrence Corey at the University of Washington in Seattle, Washington,
US, says this is good reason to explore herpes drugs as a treatment for
HIV. "Because so many people in the world are co-infected we should
spend more time on that," he told New Scientist.
Mayaud adds that some herpes drugs, such as acyclovir, cost just $40 per
year while the triple-drug regimens normally used to lower HIV levels
in patients cost anywhere from $150 to $300 per year.
However, it remains unclear whether valacyclovir would offer an additional
benefit if taken with a triple-drug HIV treatment.
Journal reference: New England Journal of Medicine (vol 356, p 790).
Phi HuynhDo, M.D., MPH
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