Porcine reproductive and respiratory syndrome virus (PRRSV) could be sensed by professional beta interferon-producing system and had mechanisms to inhibit this action in MARC-145 cells

Virus Res. 2010 Oct;153(1):151-6. doi: 10.1016/j.virusres.2010.07.028. Epub 2010 Aug 6.

Abstract

Porcine reproductive and respiratory syndrome virus (PRRSV) causes an economically important disease in swine-producing area, and interferon beta (IFN-beta) is the first responder against the animal virus infection. However, whether PRRSV could induce the production of IFN-beta is controversial. In this paper, we first time found that PRRSV could phosphorylate IFN-regulatory factor 3 (IRF-3) and weakly activate the IFN-beta promoter in MARC-145 cells in early infection, but the activations of IRF-3 and IFN-beta promoter were rapidly inhibited in the following infection. Furthermore, which components or products of the invading PRRSV cause PRRSV to inhibit IFN-beta promoter activity attracted our attentions. The obtained results showed that PRRSV nsp1 could inhibit Poly(I:C)-induced IFN-beta promoter activity in MARC-145 cells by down-regulating the protein level of IRF-3 and inhibiting the phosphorylation of IRF-3. In conclusion, our results suggested that PRRSV could be sensed by professional IFN-beta-producing system and had mechanisms to inhibit this action in MARC-145 cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Immune Evasion*
  • Interferon Regulatory Factor-3 / metabolism
  • Interferon-beta / antagonists & inhibitors*
  • Phosphorylation
  • Porcine respiratory and reproductive syndrome virus / immunology*
  • Porcine respiratory and reproductive syndrome virus / pathogenicity*
  • Swine
  • Viral Proteins / metabolism*
  • Virulence Factors / metabolism*

Substances

  • Interferon Regulatory Factor-3
  • Viral Proteins
  • Virulence Factors
  • Interferon-beta