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

• Published in: Frontiers in microbiology Vol. 10; p. 2680
• Main Authors: Li, Xiangrong, Ma, Ruixian, Li, Qian, Li, Shengjun, Zhang, Haixia, Xie, Jingying, Bai, Jialin, Idris, Adi, Feng, Ruofei
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Media S.A 29.11.2019
• Subjects: ATG7; autophagy; encephalomyocarditis virus; Microbiology; replication; transmembrane protein 39A; replication; encephalomyocarditis virus; autophagy; transmembrane protein 39A; ATG7
• ISSN: 1664-302X; 1664-302X
• DOI: 10.3389/fmicb.2019.02680

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 autophagy. Overall, we show that TMEM39A plays a positive regulatory role in EMCV proliferation and that TMEM39A expression is dependent on the autophagy pathway.