Acute Hepatitis A evades immune system more effectively than chronic cousin

Ongoing research into the problem of how Hepatitis C becomes a chronic disease has uncovered a deeper mystery about its sister strain, Hepatitis A. Hepatitis C is a continuing public health problem, which is difficult to measure because symptoms occur months to years after infection. The World Health Organization estimates as many as 2 to 4 million people in the United States may have chronic Hepatitis C, and most do not know they are infected. More than a third of those who are long-term carriers may develop chronic liver disease or liver cancer.

"Hepatitis viruses have co-evolved with humans over a very long period of time and they are good at evading the immune system, but nobody understands how Hepatitis C becomes a chronic infection," says Stanley M. Lemon, MD, professor of microbiology and immunology and a member of UNC Lineberger Comprehensive Cancer Center and the Center for Translational Immunology.

Lemon and his colleagues thought that Hepatitis C might become chronic by disrupting the host's interferon response – part of the innate immune system that protects the body against any kind of 'foreign' invader.

However, their study, published on-line in the Early Edition of the journal Proceedings of the National Academy of Sciences U.S.A., came up with some surprising findings.

In comparing data from experiments with Hepatitis A and Hepatitis C, the team found that Hepatitis A virus, which causes only acute, self-limited disease, is more efficient at inhibiting the host's interferon response, and that the virus can actually linger in the body for almost a year.

"These results undermine the theory that evasion of the interferon response is a key mechanism in the development of chronic Hepatitis C – the outcome of infection with these viruses is very different, highlighting how little we understand the unique environment within the liver for virus-host interactions," Lemon notes.

"It is actually the acute infection, Hepatitis A, that is stealthier at evading the interferon response."

Source: University of North Carolina School of Medicine