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MDA5 Inhibits the Replication of Hepatitis B Virus (108.13)

Hepatitis B virus (HBV) infection causes a wide spectrum of liver diseases; however, the innate immunity against HBV infection has been rarely studied and remains elusive. Here, we investigated the involvement of pattern recognition receptors, RIG-I like receptors (RLRs), in HBV replication. We demo...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2012-05, Vol.188 (1_Supplement), p.108-108.13
Main Authors: Lu, Hsin-Lin, Liao, Fang
Format: Article
Language:English
Online Access:Get full text
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Summary:Hepatitis B virus (HBV) infection causes a wide spectrum of liver diseases; however, the innate immunity against HBV infection has been rarely studied and remains elusive. Here, we investigated the involvement of pattern recognition receptors, RIG-I like receptors (RLRs), in HBV replication. We demonstrated that the expression of MDA5, but not RIG-I, was increased in Huh-7 cells transfected with HBV replicative plasmids. Consistent with the in vitro finding, the expression of MDA5, but not RIG-I, was also increased in mice receiving HBV replicative plasmids through hydrodynamic injection. To further determine the effect of RLRs on HBV replication, we cotransfected MDA5 or RIG-I with HBV replicative plasmids into Huh-7 cells and measured HBV replication. The results showed that with similar protein levels of MDA5 and RIG-I, only MDA5, but not RIG-I, significantly inhibited HBV replication. In line with these results, knockdown of MDA5 by siRNA in cells transfected with HBV replicative plasmids increased HBV replication while knockdown of RIG-I did not have any effect on HBV replication. Interestingly, activation of MDA5 by HBV significantly induces IRF3 phosphorylation and NF-κB translocation. This result suggests that HBV-mediated MDA5 activation may be responsible for the IRF3 and NF-κB activation. In summary, our results demonstrate that MDA5, a known cytosolic sensor for RNA virus, contributes to the innate immune response against HBV infection.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.188.Supp.108.13