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Hepatitis A And Hepatitis C Attack Same Protein To Block Immune Defenses, Scientists Find

Date:
April 19, 2007
Source:
University of Texas Medical Branch at Galveston
Summary:
Hepatitis A and hepatitis C, 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.

Cultured animal kidney cells infected with hepatitis A virus (HAV), showing HAV proteins in green, and the signaling molecule MAVS in red. MAVS is absent in the infected cells as it has been attacked and degraded by the 3ABC viral protease. The blue shows DNA within the nucleus of the cells.
Credit: Image courtesy of University of Texas Medical Branch at Galveston

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.

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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 inhibitor of virus replication. Recent research has shown that hepatitis C generates a protein called NS3/4A that chops up MAVS, interfering with immune signaling and possibly providing the cover the virus needs to survive so long in the liver. Now, Lemon and his group have demonstrated that hepatitis A does the same thing with a different protein, known as 3ABC.

"Hepatitis A never manages to establish a long-term infection like hepatitis C even though it also destroys MAVS," Lemon said. "This suggests that the degradation of this cell protein is not the main reason that hepatitis C becomes persistent. These results thus provide a new perspective on the chronicity of hepatitis C, which is a highly relevant virus clinically."

Hepatitis C has received far more research attention than hepatitis A in recent years, according to Lemon, largely because of hepatitis C's chronic nature and the lack of a vaccine against it. But while better sanitation has driven a decline in hepatitis A cases in the United States, Lemon said, "It's a significant risk for many people traveling overseas, because they fail to receive the vaccine." Hepatitis A has also been the cause of large food-borne outbreaks in the U.S. in recent years, including one in Pennsylvania that caused three deaths in otherwise healthy adults.

Other authors of the PNAS paper include lead author and former UTMB postdoctoral fellow Yan Yang, research associate Yuqiong Liang, graduate students Lin Qu and Zeming Chen, associate professor MinKyung Yi and assistant professor Kui Li. Funding for this research was provided by the National Institutes of Health, the American Liver Foundation, the James W. McLaughlin Endowment and the Effie and Wofford Cain Foundation.


Story Source:

The above story is based on materials provided by University of Texas Medical Branch at Galveston. Note: Materials may be edited for content and length.


Cite This Page:

University of Texas Medical Branch at Galveston. "Hepatitis A And Hepatitis C Attack Same Protein To Block Immune Defenses, Scientists Find." ScienceDaily. ScienceDaily, 19 April 2007. <www.sciencedaily.com/releases/2007/04/070418163709.htm>.
University of Texas Medical Branch at Galveston. (2007, April 19). Hepatitis A And Hepatitis C Attack Same Protein To Block Immune Defenses, Scientists Find. ScienceDaily. Retrieved November 28, 2014 from www.sciencedaily.com/releases/2007/04/070418163709.htm
University of Texas Medical Branch at Galveston. "Hepatitis A And Hepatitis C Attack Same Protein To Block Immune Defenses, Scientists Find." ScienceDaily. www.sciencedaily.com/releases/2007/04/070418163709.htm (accessed November 28, 2014).

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