Key result
Silencing of Misshapen NCK-related kinase (MINK) significantly reduced EV71 viral replication by impairing IRES-mediated viral protein translation via the p38 MAPK pathway.
MINK plays a crucial role in the IRES-mediated translation of EV71 viral RNA, presenting a potential target for antiviral therapies against EV71.
MINK silencing reduces EV71 replication in animal models; leaves open whether p38 MAPK pathway targeting offers human antiviral potential.
Human Enterovirus 71 (EV71) commonly causes Hand, Foot and Mouth Disease in young children, and occasional occurrences of neurological complications can be fatal. In this study, a high-throughput cell-based screening on the serine/threonine kinase siRNA library was performed to identify potential antiviral agents against EV71 replication. Among the hits, Misshapen/NIKs-related kinase (MINK) was selected for detailed analysis due to its strong inhibitory profile and novelty. In the investigation of the stage at which MINK is involved in EV71 replication, virus RNA transfection in MINK siRNA-treated cells continued to cause virus inhibition despite bypassing the normal entry pathway, suggesting its involvement at the post-entry stage. We have also shown that viral RNA and protein expression level was significantly reduced upon MINK silencing, suggesting its involvement in viral protein synthesis which feeds into viral RNA replication process. Through proteomic analysis and infection inhibition assay, we found that the activation of MINK was triggered by early replication events, instead of the binding and entry of the virus. Proteomic analysis on the activation profile of p38 Mitogen-activated Protein Kinase (MAPK) indicated that the phosphorylation of p38 MAPK was stimulated by EV71 infection upon MINK activation. Luciferase reporter assay further revealed that the translation efficiency of the EV71 internal ribosomal entry site (IRES) was reduced after blocking the MINK/p38 MAPK pathway. Further investigation on the effect of MINK silencing on heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) localisation demonstrated that cytoplasmic relocalisation of hnRNP A1 upon EV71 infection may be facilitated via the MINK/p38 MAPK pathway which then positively regulates the translation of viral RNA transcripts. These novel findings hence suggest that MINK plays a functional role in the IRES-mediated translation of EV71 viral RNA and may provide a potential target for the development of specific antiviral strategies against EV71 infection.
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Leong et al. (2015) studied Human Enterovirus 71 (EV71) infection. MINK siRNA knockdown and p38 MAPK inhibition vs. Scrambled siRNA or DMSO control was evaluated on EV71 viral replication and protein synthesis. Silencing of Misshapen NCK-related kinase (MINK) significantly reduced EV71 viral replication by impairing IRES-mediated viral protein translation via the p38 MAPK pathway.
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