Viral Pathogenesis Laboratory, Department of Biochemistry and Molecular Biology, Monash University, Victoria, Australia.
J Virol. 2013 Jul;87(14):8261-5. doi: 10.1128/JVI.00989-13. Epub 2013 May 22.
Immune evasion by rabies virus depends on targeting of the signal transducers and activator of transcription 1 (STAT1) and STAT2 proteins by the viral interferon antagonist P protein, but targeting of other STAT proteins has not been investigated. Here, we find that P protein associates with activated STAT3 and inhibits STAT3 nuclear accumulation and Gp130-dependent signaling. This is the first report of STAT3 targeting by the interferon antagonist of a virus other than a paramyxovirus, indicating that STAT3 antagonism is important to a range of human-pathogenic viruses.
狂犬病病毒的免疫逃逸依赖于病毒干扰素拮抗剂 P 蛋白对信号转导和转录激活因子 1(STAT1)和 STAT2 蛋白的靶向作用,但其他 STAT 蛋白的靶向作用尚未被研究。在这里,我们发现 P 蛋白与激活的 STAT3 结合,并抑制 STAT3 核积累和 Gp130 依赖性信号转导。这是首例报道除副粘病毒以外的干扰素拮抗剂靶向 STAT3 的报告,表明 STAT3 拮抗作用对一系列人类致病病毒很重要。