Exposure of eukaryotic cells to viruses will activate the host NF-kappaB transcription factor, resulting in proinflammatory and immune protein production. Vaccinia virus (VV), the prototypic orthopoxvirus, expresses products that inhibit this antiviral event. To identify novel mechanisms responsible for this effect, we made use of a VV deletion mutant (MVA) that stimulates NF-kappaBeta activation in infected 293T cells.
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