期刊
FRONTIERS IN MICROBIOLOGY
卷 11, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fmicb.2020.01912
关键词
ZC3HAV1; interferon; innate immunity; influenza virus; host factor
类别
资金
- National Natural Science Foundation of China [U1805231]
- National Key Research and Development Program of China [2016YFD0500205, 2016YFD0500206]
- National Science Foundation of China [U1305212]
Zinc finger CCCH-type antiviral protein 1 (ZC3HAV1) is a host antiviral factor that can repress translation and promote degradation of specific viral mRNAs. In this study, we found that expression of ZC3HAV1 was significantly induced by infection with influenza A virus (IAV) and Sendai virus (Sev). It was shown that deficiency of IFNAR resulted in a dramatic decrease in the virus-induced expression of ZC3HAV1. Furthermore, transfection with poly(I:C) and treatment with interferon beta (IFN-beta) induced the ZC3HAV1 expression. Interference with the endogenous expression of ZC3HAV1 enhanced the replication of influenza virus by impairing the production of IFN-beta and MxA, following the infection of influenza virus. In contrast, ectopic expression of ZC3HAV1 significantly restricted the replication of influenza virus by increasing the IFN-beta expression. In addition, ZC3HAV1 also promoted the induction of tumor necrosis factor and interleukin 6. These results suggest that ZC3HAV1 is induced by IFN-beta/IFNAR signaling during IAV and Sev infection and involved in positive regulation of IFN-dependent innate antiviral response.
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