Medical News

HIV Produces Proteins Linked to Progression of AIDS-Related Dementia, Study Says

April 21, 2004

This article is part of The Body PRO's archive. Because it contains information that may no longer be accurate, this article should only be considered a historical document.

Proteins produced by HIV can activate two biochemical pathways and accelerate the natural death of neurons, possibly leading to AIDS-related dementia, according to a study published Monday in the online edition of the Proceedings of the National Academy of Sciences, the Seattle Post-Intelligencer reports. Unlike other brain disease-causing agents, such as meningitis or herpes, HIV causes little brain inflammation or increase in white blood cells; however, brain cells die and the brain weakens, according to the Post-Intelligencer (Bowman, Seattle Post-Intelligencer, 4/20). Dr. Roger Pomerantz and colleagues at Thomas Jefferson University in Philadelphia set up experiments to determine whether the virus itself or a substance produced by infected cells caused brain cell death. The researchers first looked at the difference between how CD4+ T cells infected with HIV and CD4+ cells not infected with HIV affected brain cells. "When we looked at T cells, the only thing that killed neurons was the virus. Once the virus is removed nothing from the T cells would kill neurons," Pomerantz said (BBC News, 4/20). The researchers then tested whether macrophages, another type of cell in the immune system, also killed neurons. The researchers found that both HIV-infected and uninfected macrophages cause neuron death but to a significantly lesser degree than that of the HIV-infected CD4+ cells (Pomerantz et al., Proceedings of the National Academy of Sciences, 4/19). "We feel that it's mainly the virus and viral proteins causing neuronal cell death, and now may know the precise pathways involved," Pomerantz said, adding, "Now we not only have the ability to block (the dementia process) by blocking the virus, but we also have a way of designing drugs to specifically protect neurons even if virus is there" (Seattle Post-Intelligencer, 4/20).

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