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New avenue of HIV damage found

MINNEAPOLIS / ST. PAUL--Researchers at the University of Minnesota have discovered a new process by which HIV damages the immune system. They demonstrated that the portion of lymph nodes called the T cell zone is significantly damaged by chronic inflammation, which causes fibrosis. This is important because the T cell zone is where a significant portion of the human immune response occurs. The finding of accumulation of scar tissue in this portion of the lymph node may explain why aggressive anti-retroviral therapy (ART) does not improve the immune system in some people with HIV-1 infection. The study findings will be published in the Oct. 16, 2002, issue of the Journal of Clinical Investigation. The paper can be found at www.jci.org.

"HIV infection ultimately depletes the body of CD4 T cells, making it impossible to mount an immune response," said Timothy W. Schacker, M.D., associate professor of medicine and author of the study. "For the first time, we show that one mechanism of this depletion is damage to the structure that these cells need to maintain a normal-sized population and to mount an immune response to other infections. In essence, the T cell home is destroyed."

Researchers enrolled 11 individuals at various stages of HIV/AIDS infection. Their goal was to understand the specific changes that happen in the population of cells most directly affected by HIV--the CD4 T cells. These cells are responsible for coordinating the immune response and are the primary target for HIV infection and replication. Researchers biopsied and examined the lymph node tissue before and during treatment for HIV. They have developed sensitive methods to precisely measure both the size of the CD4 population in lymphatic tissue and the amount of scar tissue accumulated in the T cell zone.

Researchers noted two significant findings. First, the size of the CD4 T cell population measured in peripheral blood (commonly done to st
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Contact: Deane Morrison
morri029@umn.edu
612-624-2346
University of Minnesota
9-Oct-2002


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