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Original Research ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Microbiol. | doi: 10.3389/fmicb.2019.02680

Transmembrane protein 39A promotes the replication of encephalomyocarditis virus via autophagy pathway

 Ruofei FENG1*, Xiangrong Li1, Ruixian Ma1, 2, Shengjun Li1, 2, Qian Li1, 2, Haixia Zhang1, Jingying Xie3 and Jialin Bai1
  • 1Biomedical Research Center, Northwest University for Nationalities, China
  • 2College of Life Science and Engineering, Northwest University for Nationalities, China
  • 3College of Veterinary Medicine, Gansu Agricultural University, China

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 remains 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: TMEM39A 1, EMCV 2, replication 3, ATG7 4, autophagy 5

Received: 25 Aug 2019; Accepted: 05 Nov 2019.

Copyright: © 2019 FENG, Li, Ma, Li, Li, Zhang, Xie and Bai. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Ruofei FENG, Biomedical Research Center, Northwest University for Nationalities, Lanzhou, China,