Research Topic

Recent Advances in HBV and HCV Immunology

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More than 500 million people worldwide are persistently infected with the hepatitis B virus (HBV) and/or hepatitis C virus (HCV). Persistently infected individuals can develop chronic liver disease, cirrhosis and hepatocellular carcinoma. HBV and HCV share numerous pathogenic mechanisms and strategies of ...

More than 500 million people worldwide are persistently infected with the hepatitis B virus (HBV) and/or hepatitis C virus (HCV). Persistently infected individuals can develop chronic liver disease, cirrhosis and hepatocellular carcinoma. HBV and HCV share numerous pathogenic mechanisms and strategies of immune escape. Cytotoxic, helper, and regulatory T cells, dendritic cells (DCs), natural killer (NK), iNKT, and B cells play important roles in HBV and HCV clearance.

T cell responses are crucial to prevent and control viral infection; however, virus-specific T cell activities may be rapidly lost during persistent viral infections. This is largely caused by the fact that during viral persistence CD4 T cells do not produce the classical Th1 cytokines associated with control of acute viral infections. CD4 T cell help is critical for both CD8 T cell and B cell functions. The contributions of CD4+ and CD8+ T cells to the control of viral infection have been analyzed in a chimpanzee model of acute hepatitis B and study shows that CD8+T cells are the main effector cells responsible for virus elimination.

Topics of interest include, but are not limited to:

1. Mechanisms of protective immunity in acute infection
2. Immunological mechanisms of persistent infection
3. Contributions of specific immune cells and mediators to control of infection
4. Immunopathology of acute and/or persistent infection
5. Animal models
6. Immunity in HBV vs. HCV infection
7. Vaccine mechanisms and approaches
8. Roles of innate mechanisms in the generation of specific immunity

Contributions are welcome in the form of reviews, commentaries, hypothesis and theory, methods, and original data.


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