Hepatitis B virus e antigen and viral persistence☆
Kuen-NanTsai, Jing-Hsiung James Ou
Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine, 2011 Zonal Avenue, HMR-401, Los Angeles, CA, 90033, USA
Maternal HBeAg impacts Kupffer cells of the offspring to promote HBV persistence.
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HBeAg interacts with regulatory T cells to suppress natural killer cell activity.
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HBeAg suppresses death receptor-mediated apoptosis.
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HBeAg perturbs innate immune signaling of TLR 2, NF-κB and type I interferons.
Hepatitis B virus (HBV) e antigen (HBeAg) was discovered in the sera of HBV patients nearly 50 years ago. It is not essential for HBV to infect or replicate in hepatocytes. Earlier clinical studies suggested that this antigen might play an important role for HBV to establish persistence in babies after its mother-to-child transmission. Subsequent clinical studies also suggested that HBeAg might have immunomodulatory activities. In recent years, a large body of information on how HBeAg might modulate host immunity was published. In this review, we summarize recent research progresses on the immunomodulatory activities of HBeAg and discuss how these activities of HBeAg may promote HBV persistence.