Inhibition of hepatitis B virus replication by MyD88 is mediated by nuclear factor-kappaB activation

Shanshan Lin, Min Wu, Yang Xu, Wei Xiong, Zhigang Yi, Xiaonan Zhang, Yuan Zhenghong

Research output: Contribution to journalArticlepeer-review

Abstract

In our previous paper, we reported that myeloid differential primary response protein (MyD88), a key adaptor in the signaling cascade of the innate immune response, inhibits hepatitis B virus (HBV) replication. The MyD88 activated nuclear factor-kappaB (NF-kappaB) signaling pathway and the intracellular upregulation of NF-kappaB signaling can induce an antiviral effect. Therefore, the association between the inhibition of HBV replication by MyD88 and NF-kappaB activation was investigated further. The results show that NF-kappaB activation was moderately increased after MyD88 expression. The strong activation of NF-kappaB by the IkappaB kinase complex IKKalpha/IKKbeta dramatically suppressed HBV replication; the MyD88 dominant negative mutant that abrogated NF-kappaB activity did not inhibit HBV replication. Furthermore, the IkappaBalpha dominant negative mutant restored the inhibition of HBV replication by MyD88. These results support a role for NF-kappaB activation in the inhibition of HBV replication and suggest a novel mechanism for the inhibition of HBV replication by MyD88 protein.

Original languageEnglish
Pages (from-to)1150-1157
Number of pages8
JournalBiochimica et Biophysica Acta: international journal of biochemistry and biophysics
Volume1772
Issue number10
DOIs
Publication statusPublished - Oct 2007
Externally publishedYes

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