Researchers discover how herpes tricks the imm...( St. Louis August 20 2002 -- Herpes vi...)

St. Louis, August 20, 2002 -- Herpes viruses enter the body and hide away in cells, often re-emerging later to cause illnesses such as shingles, genital herpes and cancer. How these viruses evade the immune system remains poorly understood, but researchers at Washington University School of Medicine in St. Louis discovered that a mouse herpes virus uses molecules that mimic a cell's own proteins to help thwart an immune attack.

The findings also suggest that a branch of the immune system known as the complement system may play a more important role in controlling herpes virus infections than previously thought. The study is published in the August issue of the journal Immunity.

"These findings reveal another molecular mechanism by which viruses evade the immune system," says study leader Herbert W. Virgin, M.D., Ph.D., professor of pathology and immunology and of molecular microbiology. "By targeting this viral protein or by manipulating the complement system, perhaps someday we can develop better treatments for herpes virus infections."

The complement system consists of about 20 different proteins that are transported in the bloodstream. When activated by certain disease-causing organisms, the proteins unite and collect on viruses or on the membranes of virus-infected cells and kill them by punching holes in the membranes. To help prevent the inadvertent and dangerous triggering of this complement reaction, healthy cells produce molecules known as regulators of complement activation (RCA).

Virgin's team found that one type of herpes virus makes its own version of RCA to trick the immune system and evade destruction by complement, but that the RCA mimic proteins help the virus only during acute infection.

The researchers used a mouse virus called gamma-herpes virus 68 (gHV68), which is similar to Epstein Barr virus and the herpes virus that causes Kaposi's sarcoma, a cancer that occurs in some people with immune deficiency.
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Contact: Darrell E. Ward
wardd@msnotes.wustl.edu
314-286-0122
Washington University School of Medicine
20-Aug-2002

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