An international research team has identified immune-system genes that appear to play a key role in the body's defense against HIV, the virus that causes AIDS. The findings may lead to ways of circumventing the virus's ability to avoid vaccines by rapid mutation. The study in the Dec. 9 issue of Nature also describes how HIV infection is driving human evolution, since individuals with protective versions of the identified genes are more likely to survive and pass those genes along to children. Including researchers from the University of Oxford and the University of KwaZulu-Natal in South Africa, the investigation is a result of a program established by the Partners AIDS Research Center at Massachusetts General Hospital (MGH).

"This study identifies the genetic battleground where the struggle between HIV and the human immune response occurs," says Philip Goulder, MD, PhD, of the Partners AIDS Research Center at MGH, the study's principal investigator. "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." Goulder also has an appointment at the Peter Medawar Building for Pathogen Research at Oxford.

The human immune system learns to recognize and attack virus-infected cells through the activity of human leukocyte antigen (HLA) Class 1 molecules, which sit on the surface of cells. When new viruses are being produced within an infected cell, Class 1 molecules grab fragments of viral proteins from within the cell and display them at the cell surface, thereby alerting the body's "killer" T cells that something foreign is within the cell and it should be destroyed. Three genes called HLA-A, HLA-B, and HLA-C encode Class 1 molecules, and it is known that the HLA-B genes are extremely diverse, with more than 560 versions or "alleles" having been identified. The current study was designed to test the theory that the div
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Contact: Sue McGreevey
smcgreevey@partners.org
617-724-2764
Massachusetts General Hospital
8-Dec-2004

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