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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
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Inhibition of macrophage activation by the myxoma virus M141 protein (vCD200)

Leiliang Zhang1, Marianne Stanford, Jia Liu

  • 1Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, 32610, USA.

Journal of Virology
|July 3, 2009
PubMed

Insights

Myxoma virus M141 protein prevents macrophage activation. Deleting the M141 gene in the virus (vMyx-M141KO) activates myeloid cells via the NF-kappaB pathway, increasing inflammatory markers.

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Myxoma virus (MYXV) M141 protein is a viral CD200 homolog (vOX-2).
  • M141 inhibits macrophage activation in infected rabbits.
  • The role of M141 in myeloid cell activation during MYXV infection is unclear.

Purpose of the Study:

  • To investigate the role of MYXV M141 protein in myeloid cell activation.
  • To determine the mechanism by which M141 influences inflammatory responses.

Main Methods:

  • Infection of murine RAW 264.7 myeloid cells with wild-type MYXV and a M141 gene-deleted mutant (vMyx-M141KO).
  • Analysis of cellular activation markers, including tumor necrosis factor and granulocyte colony-stimulating factor.
  • Assessment of the NF-kappaB signaling pathway activation.

Main Results:

  • RAW 264.7 cells infected with vMyx-M141KO showed activation, unlike cells infected with wild-type MYXV.
  • vMyx-M141KO infection led to rapid upregulation of tumor necrosis factor and granulocyte colony-stimulating factor.
  • This upregulation was dependent on the NF-kappaB pathway.
  • M141 protein, present in wild-type MYXV virions, counteracts NF-kappaB activation.

Conclusions:

  • The M141 protein of myxoma virus suppresses myeloid cell activation.
  • Deletion of M141 allows for rapid NF-kappaB pathway activation in infected myeloid cells.
  • This leads to the upregulation of pro-inflammatory cytokine markers, suggesting a key role for M141 in MYXV immune evasion.

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