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J Microbiol ; 57(12): 1126-1131, 2019 Dec.
Article in English | MEDLINE | ID: mdl-31758397

ABSTRACT

Hepatitis E virus (HEV) is a causative agent of acute hepatitis and jaundice. The number of human infections is approximated to be over 20 million cases per year. The transmission is mainly via the fecal-oral route and contaminated water and food are considered to be a major source of infection. As a mouse model is not available, a recent development of a cell culture-adapted HEV strain (47832c) is considered as a very important tools for molecular analysis of HEV pathogenesis in cells. Previously, we demonstrated that HEV-encoded methyltransferase (MeT) encoded by the 47832c strain inhibits MDA5- and RIG-I-mediated activation of interferon ß (IFN-ß) promoter. Here, we report that MeT impairs the phosphorylation and activation of interferon regulatory factor 3 and the p65 subunit of NF-κB in a dose-dependent manner. In addition, the MeT encoded by the 47832c, but not that of HEV clinical or field isolates (SAR-55, Mex-14, KC-1, and ZJ-1), displays the inhibitory effect. A deeper understanding of MeTmediated suppression of IFN-ß expression would provide basis of the cell culture adaptation of HEV.


Subject(s)
Hepatitis E virus/physiology , Interferon-Induced Helicase, IFIH1/drug effects , Interferon-Induced Helicase, IFIH1/metabolism , Methyltransferases/antagonists & inhibitors , Methyltransferases/metabolism , Signal Transduction/physiology , Animals , Cell Culture Techniques , DEAD Box Protein 58/drug effects , DEAD Box Protein 58/metabolism , Disease Models, Animal , HEK293 Cells , Hepatitis E/virology , Hepatitis E virus/enzymology , Hepatitis E virus/pathogenicity , Humans , Interferon Regulatory Factor-3/metabolism , Interferon-beta/metabolism , Mice , NF-kappa B/metabolism , Phosphorylation , Receptors, Immunologic
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