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

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.

Isolation, molecular and phylogenetic analysis of porcine encephalomyocarditis virus strain HLJ in China

“…The virus can cause acute myocarditis or even acute death in piglets with a mortality rate of 100% [10]. In mice, EMCV caused mainly myocarditis, neurovirulence, and diabetes [11][12][13].…”