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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Organ-specific roles for transcription factor NF-kappaB in reovirus-induced apoptosis and disease.

Reovirus induces apoptosis in cultured cells and in vivo. In cell culture models, apoptosis is contingent upon a mechanism involving reovirus-induced activation of transcription factor NF-kappaB complexes containing p50 and p65/RelA subunits. To explore the in vivo role of NF-kappaB in this process, we tested the capacity of reovirus to induce apoptosis in mice lacking a functional nfkb1/ p50 gene. The genetic defect had no apparent effect on reovirus replication in the intestine or dissemination to secondary sites of infection. In comparison to what was observed in wild-type controls, apoptosis was significantly diminished in the CNS of p50-null mice following reovirus infection. In sharp contrast, the loss of p50 was associated with massive reovirus-induced apoptosis and uncontrolled reovirus replication in the heart. Levels of IFN-beta mRNA were markedly increased in the hearts of wild-type animals but not p50-null animals infected with reovirus. Treatment of p50-null mice with IFN-beta substantially diminished reovirus replication and apoptosis, which suggests that IFN-beta induction by NF-kappaB protects against reovirus-induced myocarditis. These findings reveal an organ-specific role for NF-kappaB in the regulation of reovirus-induced apoptosis, which modulates encephalitis and myocarditis associated with reovirus infection.[1]


  1. Organ-specific roles for transcription factor NF-kappaB in reovirus-induced apoptosis and disease. O'Donnell, S.M., Hansberger, M.W., Connolly, J.L., Chappell, J.D., Watson, M.J., Pierce, J.M., Wetzel, J.D., Han, W., Barton, E.S., Forrest, J.C., Valyi-Nagy, T., Yull, F.E., Blackwell, T.S., Rottman, J.N., Sherry, B., Dermody, T.S. J. Clin. Invest. (2005) [Pubmed]
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