期刊
FASEB JOURNAL
卷 30, 期 5, 页码 1757-1766出版社
FEDERATION AMER SOC EXP BIOL
DOI: 10.1096/fj.15-281410
关键词
Aphthovirus; innate immunity; pathogen
资金
- National Natural Science Foundation of China [31402179, 31302118]
- Gansu Science Foundation for Distinguished Young Scholars [145RJDA328]
- National Science and Technology [2015BAD12B04]
- Key Technologies Research and Development Program of Gansu Province [1302NKDA027]
Foot-and-mouth disease is a frequently occurring disease of cloven-hoofed animals that is caused by infection with the foot-and-mouth virus (FMDV). FMDV circumvents the type-I IFN response by expressing proteins that antagonize cellular innate immunity, such as leader protease and 3C protease. We identified the FMDV structural protein VP3 as a negative regulator of the virus-triggered IFN-beta signaling pathway. Expression of FMDV VP3 inhibited the Sendai virus-triggered activation of IFN regulatory factor-3 and the expression of retinoic acid-inducible gene-I/melanoma differentiation-associated protein-5. Transient transfection and coimmunoprecipitation confirmed that the structural protein VP3 interacts with virus-induced signaling adapter (VISA), which is dependent on the C-terminal aa 111-220 of VP3. In addition, we found that FMDV VP3 inhibits the expression of VISA by disrupting its mRNA. Taken together, our findings reveal a novel strategy used by the structural VP3 protein of FMDV to evade host innate immunity.-Li, D., Yang, W., Yang, F., Liu, H., Zhu, Z., Lian, K., Lei, C., Li, S., Liu, X., Zheng, H., Shu, H. The VP3 structural protein of foot-andmouth disease virus inhibits the IFN-beta signaling pathway.
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