Interferon type I response in porcine reproductive and respiratory syndrome virus-infected MARC-145 cells

Arch Virol. 2004 Dec;149(12):2453-63. doi: 10.1007/s00705-004-0377-9. Epub 2004 Aug 27.

Abstract

Infection by porcine reproductive and respiratory syndrome virus (PRRSV) results in a weak induction of the innate immune response. There are many genes that collectively comprise this response and the extent to which each gene responds to PRRSV infection is unclear and warrants further investigation. To this end, we have utilized real-time PCR using SYBR Green I dye-based detection to quantify transcript abundance of the type I interferons (IFN-alpha and -beta) and IFN-beta transcriptional enhanceasome genes. In MARC-145 cells, both IFN-alpha and -beta transcript abundance were unaffected by PRRSV infection. However, stimulation of MARC-145 cells by exogenous double-stranded RNA, resulted in significant increases in transcript abundance of both IFN-alpha and -beta as well as IFN-beta enhanceasome components, indicating that a type I IFN response could be induced in these cells. The double-stranded RNA induction of type I IFN transcription was significantly inhibited by dual-exposure with PRRSV. These results suggest that PRRSV infection directly interferes with type I IFN transcriptional activation early in its pathway, at the level of IFN-beta gene transcription.

MeSH terms

  • Animals
  • Cell Line
  • Gene Expression Regulation / immunology
  • Interferon-alpha / biosynthesis*
  • Interferon-alpha / genetics
  • Interferon-beta / biosynthesis*
  • Interferon-beta / genetics
  • Porcine respiratory and reproductive syndrome virus / immunology*
  • RNA, Messenger / metabolism
  • Swine
  • Transcription Factors / metabolism

Substances

  • Interferon-alpha
  • RNA, Messenger
  • Transcription Factors
  • Interferon-beta