HIV-combating genes
Scientists have suceeded in identifying key genes that help the body to fend off deadly viruses.
HIV infection might soon be curtailed as scientists have reportedly suceeded in identifying key genes that help the body to fend off deadly viruses.

The study, a joint project by the Universities of Oxford, KwaZulu-Natal and Harvard and published in Nature, provides a greater understanding of how some people can survive symptom free for years, while others rapidly develop AIDS.
The researchers collected data from HIV-positive women attending antenatal clinics in Durban, South Africa and found that type B molecules do the best job of identifying HIV infected cells for termination, and consequently the speed of progression in the infection seemed to be strongly linked to which version of the B molecule gene each woman carried.
Not only were HIV-positive women with a protective form of the gene more likely to survive, they were also less likely to pass the virus to their children.
"We have known for some time that HLA-B molecules are evolving more rapidly than other types, but it has been unclear why this is happening.These data suggest an explanation for the more rapid evolution of HLA-B in response to other infectious diseases, not only HIV," ead researcher Dr Philip Goulder, said.
The researchers hope that the findings may also aid the development of a vaccine to prevent HIV infection as they would help in understanding precisely how the immune system can succeed or fail against HIV.
"This is an exciting time for infectious disease research because we are witnessing the evolutionary fight between the human immune system and the HIV virus happening right now, rather than over a period of thousands of years. This study identifies the genetic battleground where the struggle between HIV and the human immune response occurs.The findings will help in understanding precisely how the immune system can succeed or fail against HIV, a prerequisite for a rational approach towards design of an HIV vaccine," he added.
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