The activation of c-jun N-terminal kinases (JNK) was previously shown to be required for efficient influenza A virus replication, although a detailed mechanism has not been reported. In this study, we found that replication of H5N1 influenza virus was influenced by the JNK inhibitor SP600125. The results of time course experiments suggested that SP600125 inhibited an early post-entry step of viral infection but did not affect nucleocytoplasmic trafficking of the viral ribonucleoprotein complex. The levels of influenza virus genomic RNA (vRNA), but not the corresponding cRNA or mRNA, were specifically reduced by SP600125 in virus-infected cells, indicating that the JNK protein is intimately involved in vRNA synthesis. Additionally, SP600125 affected H5N1 virus protein synthesis, because NS1, PB1, PB2, HA and M1 protein production was impaired. Thus, our data demonstrated a critical role of the JNK protein in the regulation of vRNA and protein synthesis during virus infection. This enhances our understanding of the complicated signal transduction network involved in influenza A virus replication.
Archives of Virology – Springer Journals
Published: Feb 1, 2016
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