Paramyxovirus strategies for evading the interferon response.
Two genera, the Respirovirus (Sendai virus (SeV) and human parainfluenza virus (hPIV3) and the Rubulavirus (simian virus (SV) 5, SV41, mumps virus and hPIV2), of the three in the subfamily Paramyxovirinae inhibit interferon (IFN) signalling to circumvent the IFN response. The viral protein responsible for the inhibition is the C protein for respirovirus SeV and the V protein for the rubulaviruses, both of which are multifunctional accessory proteins expressed from the P gene. SeV suppresses IFN-stimulated tyrosine phosphorylation of signal transducers and activators of transcription (STATs) at an early phase of infection and further inhibits the downstream signalling without degrading any of the signalling components in most cell lines. On the contrary, the Rubulavirus V protein targets Stat1 or Stat2 for degradation. Proteasome-mediated degradation appears to be involved in most cases. Studies on the molecular mechanisms by which paramyxoviruses evade the IFN response will offer important information for modulating the JAK-STAT pathway, designing novel antiviral drugs and recombinant live vaccines, and improving paramyxovirus expression vectors for gene therapy.[1]References
- Paramyxovirus strategies for evading the interferon response. Gotoh, B., Komatsu, T., Takeuchi, K., Yokoo, J. Rev. Med. Virol. (2002) [Pubmed]
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