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[Life Sciences Seminar]
▶Subject: Cytokine-mediated Suppression of Hepatitis B Virus
▶Speaker: Prof. Kyun-Hwan Kim (Konkuk University)
▶Place: Auditorium(1F), Postech Biotech Center
Cytokines are involved in the early host defense against pathogen infections. In particular, tumor necrosis factor alpha (TNF-α) and interferon gamma (IFN-?) are known to play a critical role in the non-cytopatic elimination of HBV in hepatocytes. Numerous studies have reported that TNF- α and IFN-? inhibit HBV gene expression and replication in vitro and in vivo, however, the molecular mechanism and mediator molecules are unclear.
Cellular FLICE-inhibitory protein (c-FLIP), an anti-apoptotic protein, is known to be induced by TNF-a. We recently showed that p22-FLIP, a newly discovered c-FLIP variant, is constitutively generated in hepatocytes and interacts with HBx. In this study, we found that p22-FLIP inhibits the replication of HBV. Furthermore, we found that p22-FLIP is generated through the processing of c-FLIP by the TNF-α/NF-κB pathway, and that it is involved in the TNF-α-mediated inhibition of HBV. A mechanistic study revealed that p22-FLIP inhibits HBV replication through the dysregulation of hepatocyte nuclear factor 3 beta (HNF3b) and 4 alpha (HNF4a). Finally, p22-FLIP was found to potently inhibit the replication of HBV in a mouse model of HBV infection. These findings suggest that the anti-apoptotic p22-FLIP exerts a novel function in hepatocytes as a natural inhibitor against HBV infection and may provide a novel mechanism to explain the TNF-α-mediated suppression of HBV.
▶Inquiry: Prof. Gho, Yong Song (279-2345)
* This seminar will be given in Korean.
please refrain from taking photos during seminars. *