which keeps the immune system from recognizing the virus as foreign. HLA-C however is not thought to be turned off by HIV-1. The new results suggest that for some individuals at least HLA-C is involved in controlling HIV-1. Since HIV-1 appears unable to shut off HLA-C, unlike A and B, HLA-C may represent an Achilles heel of HIV, according to Goldstein, who said that a vaccine could be designed to elicit an HLA-C mediated response which HIV-1 might be unable to defuse.
This study was the first time a genome-wide approach has been used for an infectious disease. Past studies have looked at individual candidate genes. Since different people respond differently to infections, a better understanding of how immune system genes control responses to infections should help us to design better treatments and more effective vaccines, Goldstein said.
CHAVI was designed to do big science, and the results of this analysis represent just the first of what should be many advances. The technology used and collaborative efforts involved were truly remarkable: together as a group we were able to do something that none of us individually could accomplish. The results of this and future CHAVI studies should help individual laboratories across the world perform research to better understand the virus, lead researcher, Barton Haynes, M.D said.
When someone becomes infected with HIV, the amount of virus in the blood spikes as the virus multiplies. After this peak, the amount of virus in the blood, known as the viral load, gradually decreases and then levels off, a period during which patients do not exhibit symptoms of their disease. The viral load during this levelling out is an indication of how well the patients own immune system is battling the virus, and this is the point in the infections natural history that the researchers studied.
The CHAVI investigators wanted to study those patients who had many sequential blood samples tak
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