ScienceDaily (June 20, 2011) 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.”
In addition to Lemon, the research team included Zongdi Feng, Ph.D., and Daisuke Yamane, D.V.M, Ph.D. from UNC-Chapel Hill; Robert Lanford, PhD, of the Texas Biomedical Research Institute and the Southwest National Primate Research Center; Deborah Chavez, MS, and Bernadette Guerra, BS, from the Texas Biomedical Research Institute; Kathleen Brasky, DVM, of the Southwest National Primate Center; Yan Zhou, PhD, and Christopher Walker, PhD, of the Center for Vaccines and Immunity at Nationwide Children’s Hospital in Columbus, OH; and Alan Perelson, PhD, from Los Alamos National Laboratory.
The research was funded by the National Institutes of Health.
The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of North Carolina School of Medicine.
- Robert E. Lanford, Zongdi Feng, Deborah Chavez, Bernadette Guerra, Kathleen M. Brasky, Yan Zhou, Daisuke Yamane, Alan S. Perelson, Christopher M. Walker, and Stanley M. Lemon. Acute hepatitis A virus infection is associated with a limited type I interferon response and persistence of intrahepatic viral RNA. PNAS, June 20, 2011 DOI: 10.1073/pnas.1101939108
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