期刊
ANTIVIRAL RESEARCH
卷 124, 期 -, 页码 43-53出版社
ELSEVIER
DOI: 10.1016/j.antiviral.2015.09.016
关键词
Enterovirus 71; Autophagy; miR-30a; Beclin-1; Viral replication
资金
- Major Research and Development Project from National Health and Family Planning Commission [2012ZX10001-007-009-001, 2013ZX10001005-003]
- Jiangsu National Science Foundation [BK20130591]
Enterovirus 71 (EV71), the etiological agent of hand-foot-and-mouth disease, has increasingly become a public health challenge around the world. Previous studies reported that EV71 infection can induce autophagic machinery to enhance viral replication in vitro and in vivo, but did not address the underlying mechanisms. Increasing evidence suggests that autophagy, in a virus-specific manner, may function to degrade viruses or facilitate viral replication. In this study, we reported that EV71 infection of human epidermoid carcinoma (Hep2) and African green monkey kidney cells (Vero) induced autophagy, which is beneficial for viral replication. Our investigation of the mechanisms revealed that EV71 infection resulted in the reduction of cellular miR-30a, which led to the inhibition of Beclin-1, a key autophagy-promoting gene that plays important roles at the early phase of autophagosome formation. We provided further evidence that by modulating cellular miR-30a level through either overexpression or inhibition, one can inhibit or promote EV71 replication, respectively, through regulating autophagic activity. (C) 2015 Elsevier B.V. All rights reserved.
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