Division of Virology, National Institute of Cholera and Enteric Diseases, P-33, C.I.T. Road Scheme-XM, Beliaghata, Kolkata 700010, West Bengal, India.
Virology. 2013 Sep;444(1-2):41-4. doi: 10.1016/j.virol.2013.07.003. Epub 2013 Jul 23.
TNF receptor associated factor 2 (TRAF2) plays a very important role in cellular innate immune as well as inflammatory responses. Previous studies have reported TRAF2 mediated regulation of TNF and Interferon (IFN) induced canonical and non-canonical activation of NFκB. In this study, we show that rotavirus NSP1 targets TRAF2 to regulate IFN induced non-canonical NFκB activation. Here we found that rotavirus Non-Structural Protein-1 (NSP1) interacts with TRAF2 and degrades it in a proteasome dependent manner. C-terminal part of NSP1 was sufficient for interacting with TRAF2 but it alone could not degrade TRAF2. This inhibition of interferon mediated non-canonical NFκB activation by NSP1 may modulate inflammatory cytokine production after rotavirus infection to help the virus propagation.
肿瘤坏死因子受体相关因子 2（TRAF2）在细胞固有免疫和炎症反应中起着非常重要的作用。先前的研究报告称 TRAF2 介导了 TNF 和干扰素（IFN）诱导的 NFκB 的经典和非经典激活的调节。在这项研究中，我们表明轮状病毒 NSP1 靶向 TRAF2 以调节 IFN 诱导的非经典 NFκB 激活。在这里，我们发现轮状病毒非结构蛋白 1（NSP1）与 TRAF2 相互作用，并以蛋白酶体依赖的方式使其降解。NSP1 的 C 端部分足以与 TRAF2 相互作用，但它本身不能降解 TRAF2。NSP1 通过这种抑制干扰素介导的非经典 NFκB 激活可能会调节轮状病毒感染后炎症细胞因子的产生，以帮助病毒传播。
