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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 vaccine research.

"It does not stop here. Let researchers take results from this finding to better future vaccines," Bosire told SciDev.Net.

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