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Porcine reproductive and respiratory syndrome virus inhibition of interferon-β transcription by IRF3-independent mechanisms in MARC-145 cells in early infection.

Abstract
Interferon β is an important antiviral molecule whose expression is triggered through recognition of viral components by pattern recognition receptors via a cascade of signaling molecules, while viruses could target these molecules to evade from innate immunity. IFN regulatory factor 3 (IRF3) plays a crucial role in innate immune responses. Here, we demonstrate that PRRSV infection did not induce IFN-β gene transcription in MARC-145 cells, but inhibited poly (I:C) stimulated IFN-β gene transcription instead. Such inhibition is time-dependent with the progression of PRRSV infection. We also show that the inhibition of IFN-β transcription in the early stage of infection could not be due to inhibition of phosphorylation and nuclear translocation of IRF3, though significant decrease of p-IRF3 and its nuclear translocation in PRRSV-infected and poly (I:C) cells was observed later at 48 h post-infection. The different patterns of inhibition for IFN-β transcription and IRF3 phosphorylation have important implications as to the mechanism(s) by which PRRSV suppresses the type I IFN signaling at early stage of infection. There could be mechanism(s) other than effecting on IRF3 or molecules upstream that require further investigation.
AuthorsHongxia Hu, Xian Zhang, Hansong Zhang, Guilan Wen, Qianqian Zhang, Xiaoliang Li, Weihuan Fang
JournalVeterinary immunology and immunopathology (Vet Immunol Immunopathol) Vol. 156 Issue 1-2 Pg. 135-40 (Nov 15 2013) ISSN: 1873-2534 [Electronic] Netherlands
PMID24148827 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2013 Elsevier B.V. All rights reserved.
Chemical References
  • Interferon Regulatory Factor-3
  • Interferon-beta
  • Poly I-C
Topics
  • Animals
  • Interferon Regulatory Factor-3 (physiology)
  • Interferon-beta (genetics)
  • Poly I-C (pharmacology)
  • Porcine Reproductive and Respiratory Syndrome (immunology)
  • Porcine respiratory and reproductive syndrome virus (pathogenicity)
  • Swine
  • Transcription, Genetic

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