Infectious bursal disease virus-induced activation of JNK signaling pathway is required for virus replication and correlates with virus-induced apoptosis.

The Jun NH2-terminal kinase (JNK) which serves as an important component of cellular signal transduction pathways has been shown to regulate many viral infections. The present study demonstrated for the first time that infectious bursal disease virus (IBDV), the causative agent of a highly contagious disease in chickens, can activate JNK1/2 pathway in IBDV-infected cells dependent upon viral replication. IBDV-induced JNK1/2 activation causes its downstream target c-Jun phosphorylation, which kinetically paralleled JNK1/2 activation. Investigations into the mechanism of JNK1/2 regulation revealed that inhibition of JNK1/2 activation leads to reduced viral progeny release, which is associated with decreased viral transcription and lower virus protein expression, and thereby limiting apoptotic cell death as evidenced by blockage of Bax activation, cytochrome c release, and caspase activation. These data suggest that the JNK pathway plays an important role in the IBDV replication and contributes to virus-mediated changes in host cells.

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