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.
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Authors | Hongxia Hu, Xian Zhang, Hansong Zhang, Guilan Wen, Qianqian Zhang, Xiaoliang Li, Weihuan Fang |
Journal | Veterinary immunology and immunopathology
(Vet Immunol Immunopathol)
Vol. 156
Issue 1-2
Pg. 135-40
(Nov 15 2013)
ISSN: 1873-2534 [Electronic] Netherlands |
PMID | 24148827
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2013 Elsevier B.V. All rights reserved. |
Chemical References |
- Interferon Regulatory Factor-3
- Interferon-beta
- Poly I-C
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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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