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

Xiangrong Li; Ruixian Ma; Qian Li; Shengjun Li; Haixia Zhang; Jingying Xie; Jialin Bai; Adi Idris; Ruofei Feng

doi:10.3389/fmicb.2019.02680

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. eCollection 2019.

Authors

Xiangrong Li^{1

2}, Ruixian Ma^{1

3}, Qian Li^{1

3}, Shengjun Li^{1

3}, Haixia Zhang^{1

2}, Jingying Xie⁴, Jialin Bai^{1

2}, Adi Idris⁵, 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.

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.