Study on Regulatory Effects of TRIM21 in Encephalomyocarditis Virus Proliferation

ZHAO Kexue^1,2 , XU Shujuan^1,2, GENG Jinjing^1,2, LIU Yang^1,2, LI Qiongyi^2*, FENG Ruofei^1*

(¹Key Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Biomedical Research Center, Northwest Minzu University, Lanzhou 730030, China; ²Life Science and Engineering College of Northwest Minzu University, Lanzhou 730030, China)

Abstract:

TRIM21, a member of the TRIM (tripartite motif) family proteins, is associated with replication and proliferation of diverse viruses. However, the relationship between TRIM21 and EMCV (encephalomyocarditis virus) infection is still unclear. In order to study the potential involvement of TRIM21 in EMCV replication, the eukaryotic expression plasmid pcDNA3.1-TRIM21 and small RNA interference sequence were transfected into cells by lipofectamine mediated transfection. The effect of TRIM21 on proliferation of EMCV as well as its mechanism was studied. EMCV replication significantly decreased compared to control group when TRIM21 overexpressed in HeLa and HEK293 cells. Virus infectivity increased when TRIM21 was downregulated by specific siRNAs. The mechanism study suggested that overexpression of TRIM21 not only positively regulated the transcription of IFN II,but also increased the expression of pro-inflammatory factors IL-6. This study firstly demonstrated that TRIM21 restricted EMCV replication in HeLa and HEK293 cells in a type II interferon and IL-6 dependent manner.

CSTR: 32200.14.cjcb.2019.12.0005