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A critical role of interferon-induced protein IFP35 in the type I interferon response in cells induced by foot-and-mouth disease virus (FMDV) protein 2C.

Abstract
Foot-and-mouth disease virus (FMDV) protein 2C is one of the most highly conserved viral proteins among the serotypes of FMDV. However, its effect on host cell response is not very clear. In our previous report, we showed that FMDV protein 2C interacts with cellular protein N-myc and STAT interactor (Nmi), inducing moderate apoptosis in cells. Here, we show that transfection of HEK293T cells with pEGFP-N1-2C or pEGFP-N1-Nmi induces activation of type I interferon promoters, leading to delayed vesicular stomatitis virus (VSV) growth. Using immunoprecipitation and confocal microscopy assays, we found that interferon-induced protein IFP35 interacts with Nmi. Knockdown of IFP35 expression by siRNA abolished pEGFP-N1-2C and pEGFP-N1-Nmi-induced activation of type I interferon promoters and restored VSV growth, suggesting that IFP35 plays a critical role in the type I interferon response induced by FMDV protein 2C. These findings may help to further understand cell responses to FMDV infection.
AuthorsWei Zheng, Xiaying Li, Jianchang Wang, Xiaoqi Li, Hong Cao, Yongqiang Wang, Qinghua Zeng, Shijun J Zheng
JournalArchives of virology (Arch Virol) Vol. 159 Issue 11 Pg. 2925-35 (Nov 2014) ISSN: 1432-8798 [Electronic] Austria
PMID25085622 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • IFI35 protein, human
  • Interferon Type I
  • Intracellular Signaling Peptides and Proteins
  • NMI protein, human
  • Viral Nonstructural Proteins
Topics
  • Animals
  • Foot-and-Mouth Disease (genetics, metabolism, virology)
  • Foot-and-Mouth Disease Virus (genetics, metabolism)
  • Humans
  • Interferon Type I (genetics, metabolism)
  • Intracellular Signaling Peptides and Proteins (genetics, metabolism)
  • Protein Binding
  • Vesicular Stomatitis (virology)
  • Vesicular stomatitis Indiana virus (physiology)
  • Viral Nonstructural Proteins (genetics, metabolism)

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