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Updated: Aug 24, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Inhibition of the gamma interferon response by a Sendai virus C protein mutant with no STAT1-binding ability
Bin Gotoh1, Kenji Takeuchi, Takayuki Komatsu
1Microbiology Section, Department of Pathological Sciences, Faculty of Medical Sciences, University of Fukui, Shimoaizuki 23-3, Matsuoka-cho, Yoshida-gun, Fukui 910-1193, Japan. bin@fmsra.fukui-med.ac.jp
Abstract:
Sendai virus C protein interacts with the signal transducer and activator of transcription (STAT) 1. This interaction is believed to be essential for the Sendai virus inhibition of the interferon (IFN) response. We here analyzed C(F170S) (a C protein mutant with the F170S mutation) with no STAT1-binding ability. C(F170S) lacked the ability to inhibit the IFN-alpha response, but retained the ability to inhibit the IFN-gamma response. IFN-gamma stimulation caused STAT1 phosphorylation, formation of the gamma-activated factor capable of binding to a gamma-activated sequence DNA probe, and STAT1 nuclear translocation, even in the presence of C(F170S). These results suggest that C protein has the STAT1-binding-independent anti-IFN-gamma mechanism, which targets processes after the STAT1 nuclear translocation event.
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