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Degradation of nuclear factor kappa B during foot-and-mouth disease virus infection

Teresa de Los Santos1, Fayna Diaz-San Segundo, Marvin J Grubman

  • 1Plum Island Animal Disease Center, ARS, NAA, USDA, P.O. Box 848, Greenport, NY 11944, USA.

Journal of Virology
|September 21, 2007
PubMed

Insights

Foot-and-mouth disease virus leader proteinase (L(pro)) disrupts the innate immune response by degrading nuclear factor kappaB (NF-kappaB). This viral protein interferes with key cellular defenses against infection.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Foot-and-mouth disease virus (FMDV) leader proteinase (L(pro)) previously shown to inhibit interferon production.
  • Innate immune response relies on signaling pathways like NF-kappaB.

Purpose of the Study:

  • Investigate the role of FMDV L(pro) in regulating NF-kappaB activity.
  • Elucidate the mechanism by which FMDV antagonizes cellular antiviral responses.

Main Methods:

  • Reporter gene assays in BHK-21 cells to assess NF-kappaB-dependent gene expression.
  • Analysis of endogenous NF-kappaB-dependent gene expression in primary porcine cells.
  • Western blot analysis to examine p65/RelA protein levels and localization.

Main Results:

  • Wild-type FMDV infection, unlike a mutant lacking L(pro), significantly inhibited NF-kappaB reporter gene expression.
  • Expression of NF-kappaB target genes (TNF-alpha, RANTES) was reduced in WT FMDV-infected cells.
  • L(pro) caused degradation of the p65/RelA subunit of NF-kappaB, not mRNA reduction or impaired nuclear translocation.

Conclusions:

  • FMDV L(pro) directly targets and degrades the p65/RelA subunit of NF-kappaB.
  • This degradation of NF-kappaB is a key mechanism for FMDV to suppress innate immunity and inflammation.
  • L(pro) antagonizes cellular antiviral defenses through disruption of the NF-kappaB pathway.

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