Transmembrane Protein 39A Promotes the Replication of Encephalomyocarditis Virus via Autophagy Pathway

Front Microbiol. 2019 Nov 29;10:2680. doi: 10.3389/fmicb.2019.02680.

Xiangrong Li ¹ ², Ruixian Ma ¹ ³, Qian Li ¹ ³, Shengjun Li ¹ ³, Haixia Zhang ¹ ², Jingying Xie ⁴, Jialin Bai ¹ ², Adi Idris ⁵, Ruofei Feng ¹ ²

Affiliations

1 Key Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Biomedical Research Center, Northwest Minzu University, Lanzhou, China.
2 Gansu Tech Innovation Center of Animal Cell, Biomedical Research Center, Lanzhou, China.
3 Life Science and Engineering College, Northwest Minzu University, Lanzhou, China.
4 College of Veterinary Medicine, Gansu Agricultural University, Lanzhou, China.
5 School of Medical Science, Menzies Health Institute Queensland, Griffith University, Gold Coast, QLD, Australia.

PMID: 31849860 DOI: 10.3389/fmicb.2019.02680

Abstract

Encephalomyocarditis virus (EMCV) causes encephalitis, myocarditis, neuropathy, reproductive disorders, and diabetes in Animals. EMCV is known to induce cell autophagy; however, the molecular mechanisms underlying this remain unclear. Here, we show that the type III-transmembrane protein, transmembrane protein 39A (TMEM39A), plays a critical role in EMCV replication. We showed that EMCV GS01 strain Infection upregulated TMEM39A expression. Importantly, EMCV induced Autophagy in a range of host cells. The Autophagy chemical inhibitor, 3-MA, inhibited EMCV replication and reduced TMEM39A expression. This is the first study demonstrating TMEM39A promoting the replication of EMCV via Autophagy. Overall, we show that TMEM39A plays a positive regulatory role in EMCV proliferation and that TMEM39A expression is dependent on the Autophagy pathway.

Keywords

ATG7; autophagy; encephalomyocarditis virus; replication; transmembrane protein 39A.

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