Zinc Finger CCCH-Type Antiviral Protein 1 Restricts the Viral Replication by Positively Regulating Type I Interferon Response

Baoge Zhang; Mohsan Ullah Goraya; Na Chen; Lifeng Xu; Yan Hong; Meiyi Zhu; Ji-Long Chen

doi:10.3389/fmicb.2020.01912

Zinc Finger CCCH-Type Antiviral Protein 1 Restricts the Viral Replication by Positively Regulating Type I Interferon Response

Front Microbiol. 2020 Aug 14:11:1912. doi: 10.3389/fmicb.2020.01912. eCollection 2020.

Authors

Baoge Zhang¹, Mohsan Ullah Goraya¹, Na Chen¹, Lifeng Xu¹, Yan Hong¹, Meiyi Zhu¹, Ji-Long Chen^{1

2

3}

Affiliations

¹ Key Laboratory of Fujian-Taiwan Animal Pathogen Biology, College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou, China.
² State Key Laboratory of Food Safety Technology for Meat Products, Xiamen, China.
³ CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.

Abstract

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 β (IFN-β) induced the ZC3HAV1 expression. Interference with the endogenous expression of ZC3HAV1 enhanced the replication of influenza virus by impairing the production of IFN-β 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-β expression. In addition, ZC3HAV1 also promoted the induction of tumor necrosis factor and interleukin 6. These results suggest that ZC3HAV1 is induced by IFN-β/IFNAR signaling during IAV and Sev infection and involved in positive regulation of IFN-dependent innate antiviral response.

Keywords: ZC3HAV1; host factor; influenza virus; innate immunity; interferon.