Key result
Expression of the FMDV structural protein VP3 inhibited the virus-triggered IFN-β signaling pathway by interacting with and disrupting the mRNA of the virus-induced signaling adapter (VISA).
The FMDV structural protein VP3 evades host innate immunity by interacting with VISA and disrupting its mRNA to inhibit the IFN-β signaling pathway.
Suggests VP3-VISA axis as antiviral target in FMDV; leaves open translation beyond animal models.
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-β 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-and-mouth disease virus inhibits the IFN-β signaling pathway.
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Li et al. (2016) studied Foot-and-mouth disease. FMDV structural protein VP3 was evaluated on IFN-β signaling pathway activation and VISA expression. Expression of the FMDV structural protein VP3 inhibited the virus-triggered IFN-β signaling pathway by interacting with and disrupting the mRNA of the virus-induced signaling adapter (VISA).