期刊
FASEB JOURNAL
卷 34, 期 3, 页码 4497-4511出版社
WILEY
DOI: 10.1096/fj.201902031RRR
关键词
antiviral protein; HSP60; MAVS
资金
- National Natural Science Fund [31490600]
- Henan Natural Science Foundation [182300410077]
- Henan Normal University Outstanding Youth Science Fund [20170031]
- Henan Province Animal Immunology Key Laboratory Open Project [PKLAI20170605]
- Key Scientific Research Projects of Henan Provincial Institution of Higher Education [17A180006]
- National Foundation of China [31472177]
Previous studies have indicated that inhibition of type I interferon production may be an important reason for porcine reproductive and respiratory syndrome virus (PRRSV) to achieve immune escape, revealing the mechanism of inhibiting the production of type I interferon will help design novel strategies for controlling PRRS. Here, we found that PRRSV infection upregulated the expression of miR-382-5p, which in turn inhibited polyI:C-induced the production of type I interferon by targeting heat shock protein 60 (HSP60), thus facilitating PRRSV replication in MARC-145 cells. Furthermore, we found that HSP60 could interact with mitochondrial antiviral signaling protein (MAVS), an important signal transduction protein for inducing production of type I interferon, and promote polyI:C-mediated the production of type I interferon in a MAVS-dependent manner. Finally, we also found that HSP60 could inhibit PRRSV replication in a MAVS-dependent manner, which indicated that HSP60 was a novel antiviral protein against PRRSV replication. In conclusion, the study demonstrated that miR-382-5p was upregulated during PRRSV infection and may promote PRRSV replication by negatively regulating the production of type I interferon, which also indicated that miR-382-5p and HSP60 might be the potential therapeutic targets for anti-PRRSV.
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