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Li, K., Foy, E., Ferreon, J.C., Nakamura, M., Ferreon, A.C., Ikeda, M., Ray, S.C., Gale Jr., M. and Lemon, S.M. (2005) Immune evasion by hepatitis C virus NS3/4A protease-mediated cleavage of the Toll-like receptor 3 adaptor protein TRIF. Proceedings of the National Academy of Sciences of the United States of America, 102, 2992-2997. doi:10.1073/pnas.0408824102

has been cited by the following article:

• TITLE: Rethinking cytokine function during hepatitis A and hepatitis C infections

  AUTHORS: Nora A. Fierro, Flor P. Castro-Garcia, Arturo Panduro

  KEYWORDS: Hepatitis A Virus; Hepatitis C Virus; Cytokines

  JOURNAL NAME: Advances in Bioscience and Biotechnology, Vol.4 No.7A, July 16, 2013

  ABSTRACT: Hepatitis A virus (HAV) and hepatitis C virus (HCV) are both viruses with hepatotropic lifestyles. HAV induces an acute infection that results in the elimination of the virus by the host whereas HCV is typically able to establish a persistent infection that may result in cirrhosis and hepatocellular carcinoma. The mechanisms responsible for this difference are unknown. However, given HAV and HCV are both non-cytophatic viruses, the observed symptoms and liver injury during the infections are the result of specific immune responses under the control of cytokines. Thus, the production of cytokines during hepatotropic viral infections may constitute a mechanism leading to different outcomes. Therefore, understanding the differences in the cytokine patterns induced in response to HAV and HCV is likely to provide important insights into the cytokine-mediated mechanisms underlying the long-term persistence of HCV, the broad spectrum of clinical manifestations induced by HAV and the resolution of HAV infection during the acute phase. Herein, we focus on discoveries that hold promise in identifying cytokines as therapeutic targets for the treatment of viral hepatitis.