Journal
JOURNAL OF VIROLOGY
Volume 83, Issue 18, Pages 9602-9607Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01078-09
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Funding
- United Kingdom Medical Research Council [G0601169, G0400808]
- MRC [G0400808, G0601169] Funding Source: UKRI
- Medical Research Council [G0400808, G0601169] Funding Source: researchfish
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The M141 protein of myxoma virus (MYXV) is a viral CD200 homolog (also called vOX-2) that inhibits macrophage activation in infected rabbits. Here, we show that murine myeloid RAW 264.7 cells became activated when infected with MYXV in which the M141 gene was deleted (vMyx-M141KO) but not with the parental wild-type MYXV. Moreover, transcript and protein levels of tumor necrosis factor and granulocyte colony-stimulating factor were rapidly upregulated in an NF-kappa B-dependent fashion in the RAW 264.7 cells infected with vMyx-M141KO. M141 protein is present in the virion and counteracts this NF-kappa B activation pathway upon infection with the wild-type MYXV. Our data suggest that upregulation of these classic macrophage-related proinflammatory cytokine markers following infection of myeloid cells with the M141-knockout MYXV is mediated via the rapid activation of the cellular NF-kappa B pathway.
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