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.
journal_name
Front Microbioljournal_title
Frontiers in microbiologyauthors
Li X,Ma R,Li Q,Li S,Zhang H,Xie J,Bai J,Idris A,Feng Rdoi
10.3389/fmicb.2019.02680subject
Has Abstractpub_date
2019-11-29 00:00:00pages
2680issn
1664-302Xjournal_volume
10pub_type
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