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

A critical role of interferon-induced protein IFP35 in the type I interferon response in cells... 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

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

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Publisher
Springer Vienna
Copyright
Copyright © 2014 by Springer-Verlag Wien
Subject
Biomedicine; Virology; Medical Microbiology; Infectious Diseases
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s00705-014-2147-7
Publisher site
See Article on Publisher Site

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.

Journal

Archives of VirologySpringer Journals

Published: Nov 1, 2014

References

  • Amino-terminal region of poliovirus 2C protein is sufficient for membrane binding
    Echeverri, A; Banerjee, R; Dasgupta, A
  • A critical role of N-myc and STAT interactor (Nmi) in foot-and-mouth disease virus (FMDV) 2C-induced apoptosis
    Wang, J; Wang, Y; Liu, J; Ding, L; Zhang, Q
  • Expression of type I interferon-induced antiviral state and pro-apoptosis markers during experimental infection with low or high virulence bovine viral diarrhea virus in beef calves
    Palomares, RA; Walz, HG; Brock, KV
  • Engagement of soluble resistance-related calcium binding protein (sorcin) with foot-and-mouth disease virus (FMDV) VP1 inhibits type I interferon response in cells
    Li, X; Wang, J; Liu, J; Li, Z; Wang, Y
  • The PH domain containing protein CKIP-1 binds to IFP35 and Nmi and is involved in cytokine signaling
    Zhang, L; Tang, Y; Tie, Y; Tian, C; Wang, J
  • IFP 35 forms complexes with B-ATF, a member of the AP1 family of transcription factors
    Wang, X; Johansen, LM; Tae, HJ; Taparowsky, EJ

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