Enterovirus 71 blocks selectively type I interferon production through the 3C viral protein in mice

Yi Ping Lee, Ya Fang Wang, Jen Ren Wang, Szu Wei Huang, Chun Keung Yu

研究成果: Article同行評審

23 引文 斯高帕斯(Scopus)

摘要

Type I interferons (IFNs) represent an essential innate defense mechanism for controlling enterovirus 71 (EV 71) infection. Mice inoculated with EV 71 produced a significantly lower amount of type I IFNs than those inoculated with poly (I:C), adenovirus type V, or coxsackievirus B3 (CB3). EV 71 infection, however, mounted a proinflammatory response with a significant increase in the levels of serum and brain interleukin (IL)-6, monocyte chemoattractant protein-1, tumor necrosis factor, and IFN-γ. EV 71 infection abolished both poly (I:C)- and CB3-induced type I IFN production of mice. Such effect was not extended to other enteroviruses including coxsackievirus A24, B2, B3, and echovirus 9, as mice infected with these viruses retained type I IFN responsiveness upon poly (I:C) challenge. In addition, EV 71-infected RAW264.7 cells produced significantly lower amount of type I IFNs than non-infected cells upon poly (I:C) stimulation. The inhibitory effect of EV 71 on type I IFN production was attributed to the viral protein 3C, which was confirmed using over-expression systems in both mice and RAW264.7 cells. The 3C over-expression, however, did not interfere with poly (I:C)-induced proinflammatory cytokine production. These findings indicate that EV 71 can hamper the host innate defense by blocking selectively type I IFN synthesis through the 3C viral protein.

原文English
頁(從 - 到)1779-1789
頁數11
期刊Journal of Medical Virology
84
發行號11
DOIs
出版狀態Published - 2012 11月

All Science Journal Classification (ASJC) codes

  • 病毒學
  • 傳染性疾病

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