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Two-Pronged Attack On Immune System Cells Engineered By HIV Gene vpr: Effects Markedly Reversed By Antisteroid Compound RU-486

In the early years of research on HIV-1, six of the nine genes that constitute the retrovirus's genome were referred to as accessory genes because they were thought unnecessary for infection and replication. Scientists have since learned that these genes play important, if not yet fully defined roles in HIV's remarkable ability to elude the immune system and, in fact, directly infect the very cells tasked with defending the body against infection.

The protein product of one of these accessory genes -- vpr -- is found in significant quantities in the extracellular free virus, suggesting that it may be crucial in the early stages of infection by the virus.

Now, researchers at the University of Pennsylvania Medical Center report that Vpr, the protein product of vpr, blocks the production of cytokines in the cells first infected by HIV, called macrophages, thus blunting immune activation of these cells. Cytokines are chemicals used by the immune system to initiate and control much of the its response to infection.

Additionally, the investigators found that Vpr is able to prevent apoptosis -- or programmed cell death -- in the infected cells, thus preserving them for use as viral production factories. And, in a further blow to the body's ability to defend against the infection, Vpr actively induces apoptosis in neighboring immune system cells that have not yet been infected, known as CD4 T cells. It also interferes with the ability of those cells to proliferate. The new findings appear in the October issue of Nature Medicine.

"In the test tube, Vpr suppresses production of the cytokines needed to fight any infection, bacterial or viral," says David B. Weiner, PhD, senior author and an associate professor of pathology and laboratory medicine. "It also prevents apoptosis in the cells it infects, so those cells can stay alive to make more virus. And then it kills the uninfected cells that would otherwise be involved in providing
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Contact: Franklin Hoke or Karen Kreeger
media@mail.med.upenn.edu
215-662-2560
University of Pennsylvania School of Medicine
1-Oct-1997


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