TRIM52 inhibits Japanese Encephalitis Virus replication by degrading the viral NS2A

Wenchun Fan; Mengge Wu; Suhong Qian; Yun Zhou; Huanchun Chen; Xiangmin Li; Ping Qian

doi:10.1038/srep33698

TRIM52 inhibits Japanese Encephalitis Virus replication by degrading the viral NS2A

Sci Rep. 2016 Sep 26:6:33698. doi: 10.1038/srep33698.

Authors

Wenchun Fan^{1

2}, Mengge Wu^{1

2}, Suhong Qian^{1

2}, Yun Zhou^{1

2}, Huanchun Chen^{1

2}, Xiangmin Li^{1

2

3}, Ping Qian^{1

2

3}

Affiliations

¹ State Key Laboratory of Agriculture Microbiology, Huazhong Agricultural University, Wuhan 430070, P. R. China.
² Division of Animal Infectious Diseases, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China.
³ The Cooperative Innovation Center for Sustainable Pig Production, Huazhong Agricultural University Wuhan 430070, China.

Abstract

The members of tripartite-motif containing (TRIM) protein participate in various cellular processes and play an important role in host antiviral function. TRIM proteins exert their antiviral activity either directly by degrading viral proteins through their E3 ligase activity, or indirectly by promoting host innate immunity. This study demonstrated for the first time that TRIM52 is a novel antiviral TRIM protein against Japanese encephalitis virus (JEV) infection. Overexpression of TRIM52 restricted JEV replication in BHK-21 and 293T cells. In addition, JEV nonstructural protein 2A (NS2A) is a protein that interacts with TRIM52. Their interaction degraded NS2A in a proteasome-dependent manner via the E3 ligase activity of TRIM52. Thus, TRIM52 is a novel antiviral TRIM protein, and it exerted antiviral activity against JEV infection by targeting and degrading viral NS2A.