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Classical swine fever virus inhibits nitric oxide production in infected macrophages

K M Zaffuto1, M E Piccone1, T G Burrage1

  • 1Plum Island Animal Disease Center, USDA-ARS, PO Box 848, Greenport, NY 11944, USA.

The Journal of General Virology
|October 20, 2007
PubMed

Insights

Classical swine fever virus (CSFV) alters macrophage gene expression, suppressing nitric oxide production. This interaction involves increased arginase activity and specific gene upregulation in infected cells.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Classical swine fever virus (CSFV) is a significant pathogen affecting swine populations.
  • Macrophage immune responses are critical in controlling viral infections.
  • Understanding host-pathogen interactions at the molecular level is crucial for disease management.

Purpose of the Study:

  • To investigate the transcriptional responses of macrophages upon infection with Classical swine fever virus.
  • To identify specific genes modulated by CSFV during macrophage infection.
  • To elucidate the mechanisms by which CSFV influences macrophage function, particularly nitric oxide production.

Main Methods:

  • Macrophage cell cultures were infected with Classical swine fever virus.
  • Transcriptional responses were analyzed using microarray technology.
  • Nitric oxide levels and arginase activity were measured in infected and uninfected macrophages.

Main Results:

  • Eleven genes showed significantly increased mRNA levels (>2.5-fold, P<0.05) in CSFV-infected macrophages.
  • Upregulated genes included arginase-1 (an inhibitor of nitric oxide production), phosphoinositide 3-kinase, chemokine receptor 4, and interleukin-1beta.
  • CSFV-infected macrophages exhibited lower nitric oxide levels and increased arginase activity.

Conclusions:

  • CSFV infection modulates host gene expression in macrophages.
  • The observed changes suggest a viral strategy to suppress nitric oxide production via arginase-1 upregulation.
  • These findings provide insights into the molecular mechanisms of CSFV pathogenesis and immune evasion.

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