Washington, April 19 : Researchers at the University of Texas Medical Branch at Galvestone (UTMB) have found that hepatitis A and Hepatitis C attack the same protein to escape destruction by the body’s immune system.

Their study shows that both viruses dodge mitochondrial antiviral signaling(MAVS) protein to block immune defences, despite the fact that the two viruses are remarkably different from each other.

“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, Institute for Human Infections and Immunity, UTMB.

“This identifies the protein - called MAVS, for mitochondrial antiviral signaling protein - as extremely important for the survival
of any virus in the liver,” he added.

The study shows 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.

Lemon says that hepatitis A also does the same thing but 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. 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,” he said.

According to him, Hepatitis C has received far more research attention than hepatitis A in recent years because of the former’s chronic nature and the lack of a vaccine against it.

However, while better sanitation has driven a decline in hepatitis A cases in the US, Lemon said, “It’s a significant risk for many people traveling overseas, because they fail to receive the vaccine.” (ANI)