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Suppression of the interferon-mediated innate immune response by pseudorabies virus

Alla Brukman1, L W Enquist

  • 1Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.

Journal of Virology
|June 16, 2006
PubMed

Insights

Pseudorabies virus (PRV) hinders the interferon-beta (IFN-beta) immune response by disrupting STAT1 phosphorylation. This evasion mechanism explains PRV's lethality in many mammal hosts.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Pseudorabies virus (PRV) is an alphaherpesvirus with broad mammalian host range.
  • PRV's mechanisms for evading innate immunity, particularly interferon (IFN)-mediated responses, remain poorly understood.
  • Unlike herpes simplex virus type 1 (HSV-1), PRV's anti-IFN strategies are largely uncharacterized.

Purpose of the Study:

  • To investigate if wild-type PRV can overcome an established beta interferon (IFN-beta)-induced antiviral state in primary rat fibroblasts.
  • To elucidate the molecular mechanisms by which PRV interferes with the IFN-beta signaling pathway.

Main Methods:

  • Utilized microarray analysis to assess gene expression changes in PRV-infected rat fibroblasts treated with IFN-beta.
  • Examined the phosphorylation status of STAT1, a key component of IFN signal transduction.
  • Investigated the role of virion-associated proteins in inhibiting IFN signaling.

Main Results:

  • PRV infection suppressed the induction of a subset of IFN-beta-stimulated genes.
  • Expression of transcripts for MHC class I antigen presentation and NK cell activation was reduced.
  • PRV infection impaired IFN signal transduction, specifically reducing STAT1 phosphorylation.
  • A virion-associated protein was identified as a factor in inhibiting STAT1 tyrosine phosphorylation.

Conclusions:

  • PRV actively disarms the IFN-beta-mediated antiviral response.
  • Impaired STAT1 phosphorylation is a key mechanism for PRV's immune evasion.
  • This ability to inhibit the IFN-beta pathway provides a potential explanation for PRV's high virulence and lethality in nonnatural hosts.

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