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

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  • 1Animal Health Research Unit, Roman L. Hruska U.S. Meat Animal Research Center (MARC), ARS, USDA, Clay Center, Nebraska 68933-0166, USA.

Archives of Virology
|September 1, 2004
PubMed

Insights

Porcine reproductive and respiratory syndrome virus (PRRSV) weakens the innate immune response. PRRSV infection inhibits the induction of type I interferons (IFN), crucial for antiviral defense.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Porcine reproductive and respiratory syndrome virus (PRRSV) infection is known to induce a weak innate immune response.
  • The specific genes and mechanisms underlying this suppressed response, particularly concerning type I interferons, remain incompletely understood.

Purpose of the Study:

  • To investigate the impact of PRRSV infection on the transcriptional abundance of type I interferons (IFN-alpha and IFN-beta) and their associated enhanceasome genes.
  • To determine if PRRSV interferes with the induction of type I interferon responses.

Main Methods:

  • Quantitative real-time PCR with SYBR Green I dye-based detection was used.
  • Transcript abundance of IFN-alpha, IFN-beta, and IFN-beta enhanceasome components was measured in MARC-145 cells.
  • Cells were stimulated with exogenous double-stranded RNA (dsRNA) to induce type I IFN response, with and without concurrent PRRSV infection.

Main Results:

  • PRRSV infection alone did not alter IFN-alpha and IFN-beta transcript levels in MARC-145 cells.
  • Stimulation with dsRNA significantly increased IFN-alpha, IFN-beta, and IFN-beta enhanceasome component transcripts.
  • PRRSV co-infection significantly inhibited the dsRNA-induced increase in type I interferon transcription.

Conclusions:

  • PRRSV infection directly interferes with the early stages of type I interferon transcriptional activation.
  • The virus appears to inhibit the IFN-beta gene transcription pathway, contributing to the weak innate immune response observed during PRRSV infection.

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