Researchers at the University of Pennsylvania School of Medicine discovered that an HIV-1 accessory protein called Vpr destroys the host cell’s ability to survive by binding to a host receptor. This, in turn, keeps an important enzyme from activating the cell’s immune system. These findings refine an earlier understanding of Vpr HIV pathogenesis and imply new approaches to treating AIDS, inflammatory diseases such as rheumatoid arthritis, and possibly sepsis. This research appears in the February print issue of Nature Cell Biology.
