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J Microbiol Biotechnol. 2018 Sep 28;28(9):1554-1562. doi: 10.4014/jmb.1808.08058.

Hepatitis E Virus Methyltransferase Inhibits Type I Interferon Induction by Targeting RIG-I.

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Korea Zoonosis Research Institute and Genetic Engineering Research Institute, Chonbuk National University, Jeonju 54896, Republic of Korea.
Department of Food and Nutrition, Chung-Ang University, Anseong 17546, Republic of Korea.
Department of Infectious Disease, College of Veterinary Medicine, Konkuk University, Seoul 05029, Republic of Korea.
Biological Disaster Analysis Group, Korea Basic Science Research Institute, Daejeon 34133, Republic of Korea.
World Institute of Kimchi, Gwangju 61755, Republic of Korea.
Food and Bio-industry Research Institute, Kyungpook National University, Daegu 41566, Republic of Korea.
Center for Convergent Research of Emerging Virus Infection, Korea Research Institute of Chemical Technology, Daejeon 34114, Republic of Korea.


The type I interferons (IFNs) play a vital role in activation of innate immunity in response to viral infection. Accordingly, viruses have evolved to employ various survival strategies to evade innate immune responses induced by type I IFNs. For example, HEV encoded papainlike cysteine protease (PCP) has been shown to inhibit IFN activation signaling by suppressing K63-linked de-ubiquitination of retinoic acid-inducible gene I (RIG-I) and TANK-binding kinase 1 (TBK1), thus effectively inhibiting down-stream activation of IFN signaling. In present study, we demonstrated that hepatitis E virus (HEV) inhibits poly inosinicpolycytidylic acid (poly(I:C))-induced IFN-β transcriptional induction. Moreover, by using reporter assay with individual HEV-encoded gene, we showed that HEV methyltransferase (MeT), a non-structural protein, significantly decreases RIG-I-induced IFN-β induction and NF-κB signaling activities in a dose-dependent manner. Taken together, we report here that MeT, along with PCP, is responsible for the inhibition of RIG-I-induced activation of type I IFNs, expanding the list of HEV-encoded antagonists of the host innate immunity.


Hepatitis E virus; RIG-I; methyltransferase

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