( Despite the fact that they both infect ...)Researchers find hepatitis A and hepatitis C attack same protein to block immune defenses

Despite the fact that they both infect the liver, the hepatitis A and hepatitis C viruses actually have very little in common. The two are far apart genetically, are transmitted differently, and produce very different diseases. Hepatitis A spreads through the consumption of fecal particles from an infected person (in pollution-contaminated food or water, for example), but hepatitis C is generally transmitted only by direct contact with infected blood. Hepatitis A produces fever, nausea and abdominal pain that can last for weeks, but rarely lead to death; hepatitis C, by contrast, often spends decades quietly damaging the liver, until a victim’s only hope for survival is an organ transplant.

According to researchers at the University of Texas Medical Branch at Galveston (UTMB), though, these two otherwise unrelated liver viruses have one important thing in common: a trick for avoiding destruction by the immune system. Both dodge immune attacks by attacking the same protein ?an essential link in a chain of molecular signals that triggers antiviral responses.

"With 30,000-plus proteins in the cell, it’s really remarkable that these two very different viruses have chosen to strike at the same one," said Dr. Stanley Lemon, director of UTMB’s Institute for Human Infections and Immunity and National Institutes of Health-funded Hepatitis C Research Center. Lemon is senior author of a paper on the research appearing online this week in the Proceedings of the National Academy of Sciences. "This identifies the protein ?called MAVS, for mitochondrial antiviral signaling protein ?as extremely important for the survival of any virus in the liver."

MAVS proteins project from tiny structures called mitochondria, which are found in large numbers in each liver cell. When specialized receptor molecules detect viruses in the cell, they dock with the MAVS proteins, thereby triggering a sequence of signals ending with the production of interferon beta?a potent
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Source:University of Texas Medical Branch at Galveston

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