Innate Immunity to Enteric Hepatitis Viruses
- 1Center for Vaccines and Immunity, The Research Institute at Nationwide Children’s Hospital, The Ohio State University College of Medicine, Columbus, Ohio 43205
- 2Departments of Medicine and Microbiology & Immunology, Lineberger Comprehensive Cancer Center, The University of North Carolina, Chapel Hill, North Carolina 27599
- Correspondence: zongdi.feng{at}nationwidechildrens.org; smlemon{at}med.unc.edu
Abstract
Although hepatitis A virus (HAV) and hepatitis E virus (HEV) are both positive-strand RNA viruses that replicate in the cytoplasm of hepatocytes, there are important differences in the ways they induce and counteract host innate immune responses. HAV is remarkably stealthy because of its ability to evade and disrupt innate signaling pathways that lead to interferon production. In contrast, HEV does not block interferon production. Instead, it persists in the presence of an interferon response. These differences may provide insight into HEV persistence in immunocompromised patients, an emerging health problem in developed countries.
