Washington, March 3 (IANS): In a path-breaking finding, researchers have discovered how the immune system makes a powerful antibody that blocks HIV infection of cells by targeting the V1V2 site on the virus.
It is believed that if a vaccine could elicit potent antibodies to a specific conserved site in the V1V2 region, then the vaccine could protect people from HIV infection. The V1V2 is a region on the virus envelope which increases the susceptability to neutralistion by antibodies.
"The new findings point the way toward a potentially more effective vaccine that would generate V1V2-directed HIV neutralising antibodies," said scientists from the National Institute of Allergy and Infectious Diseases, part of the US National Institutes of Health.
Scientists from Columbia University, the Centre for AIDS Programme of Research in South Africa, and the National Institute for Communicable Diseases, Johannesburg, were part of the research.
The team began its work by identifying an HIV-infected volunteer, who naturally developed V1V2-directed HIV neutralising antibodies after several months of infection.
Using techniques similar to those employed in an earlier study of HIV-antibody co-evolution, the researchers analysed blood samples donated by the volunteer between 15 weeks and four years after getting infected.
This enabled the scientists to determine the genetic make-up of the original form of the antibody.
They also identified and defined the structures of a number of the intermediate forms taken as the antibody mutated toward its fullest breadth and potency.
The study revealed that after relatively few mutations, even the early intermediates of V1V2-directed HIV neutralising antibodies can neutralise a significant proportion of known HIV strains.
According to the scientists, this improves the chances that a V1V2-directed HIV vaccine developed based on the new findings would be effective.
They have now started working on a set of vaccine components designed to elicit V1V2 neutralising antibodies and guide their maturation, said NIH in a press release.