| 研究実績の概要 |
Hepatitis B Virus (HBV) is a stealth virus that exhibits only minimal induction of the interferon system that is required for both innate and adaptive immune responses. However, 90% of acutely infected adults can clear the virus, suggesting the presence of additional mechanisms that facilitate viral clearance. Marwa identified Maf bZIP transcription factor F (MafF) to promote host defense against infection with HBV. MafF was found to control HBV-pgRNA levels. Her data showed that silencing of MafF led to 6-fold increase in luciferase activity after HBV/NL infection, induced HBV-pgRNA levels, HBV replication, and the expression of HBV core protein expressed from HBV-pgRNA. Overexpression of MafF reduced HBV core promoter transcriptional activity, which was relieved upon mutating the putative MafF binding region. Marwa found that MafF is induced by famous inflammatory cytokines IL-1b and TNF-a. Analyzing the data from human hepatocytes chimeric mouse infected in-vivo with HBV, or single cell data from primary hepatocytes infected in-vitro with HBV; she found that MafF levels were induced after HBV infection, confirming the induction of MafF levels in response to HBV infection. The anti-viral effect of MafF was also extended to EBV, where MAfF suppressed genes required for activation of EBV infection (BZLF1 gene).
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