Sendai virus blocks alpha interferon signaling to signal transducers and activators of transcription
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Updated: Jul 30, 2026

Rescue of Recombinant Newcastle Disease Virus from cDNA
Published on: October 11, 2013
T Komatsu1, K Takeuchi, J Yokoo
1Department of Microbiology, Fukui Medical University School of Medicine, Yoshida-gun, Fukui 910-1193, Japan. koma@fmsrsa.fukui-med.ac.jp
Abstract:
We demonstrate here that Sendai virus (SeV) blocks alpha interferon (IFN-alpha) signaling to signal transducers and activators of transcription (STATs) in HeLa cells. IFN-alpha-stimulated tyrosine phosphorylation of STATs and subsequent formation of the IFN-stimulated gene factor 3 transcription complex were inhibited in SeV-infected cells, resulting in inefficient induction of IFN-stimulated gene products. None of the components of the signaling pathway-type I IFN receptor subunits Jak1, Tyk2, Stat1, Stat2, and p48-was degraded. Moreover, tyrosine phosphorylation of Jak1 in response to IFN-alpha was unaffected at the early phase of infection, suggesting that oligomerization of the receptor subunits proceeded normally. In contrast to Jak1, IFN-alpha-stimulated tyrosine phosphorylation of Tyk2 was partially inhibited. Therefore, this partial inhibition of activation of Tyk2 probably contributes to the subsequent failure in the activation of STATs.
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