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Usage Information

Organ-specific roles for transcription factor NF-κB in reovirus-induced apoptosis and disease
Sean M. O’Donnell, … , Barbara Sherry, Terence S. Dermody
Sean M. O’Donnell, … , Barbara Sherry, Terence S. Dermody
Published September 1, 2005
Citation Information: J Clin Invest. 2005;115(9):2341-2350. https://doi.org/10.1172/JCI22428.
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Research Article Virology

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

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Abstract

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-κB complexes containing p50 and p65/RelA subunits. To explore the in vivo role of NF-κB 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-β 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-β substantially diminished reovirus replication and apoptosis, which suggests that IFN-β induction by NF-κB protects against reovirus-induced myocarditis. These findings reveal an organ-specific role for NF-κB in the regulation of reovirus-induced apoptosis, which modulates encephalitis and myocarditis associated with reovirus infection.

Authors

Sean M. O’Donnell, Mark W. Hansberger, Jodi L. Connolly, James D. Chappell, Melissa J. Watson, Janene M. Pierce, J. Denise Wetzel, Wei Han, Erik S. Barton, J. Craig Forrest, Tibor Valyi-Nagy, Fiona E. Yull, Timothy S. Blackwell, Jeffrey N. Rottman, Barbara Sherry, Terence S. Dermody

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Usage data is cumulative from May 2024 through May 2025.

Usage JCI PMC
Text version 522 27
PDF 153 21
Figure 492 25
Citation downloads 74 0
Totals 1,241 73
Total Views 1,314
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Usage information is collected from two different sources: this site (JCI) and Pubmed Central (PMC). JCI information (compiled daily) shows human readership based on methods we employ to screen out robotic usage. PMC information (aggregated monthly) is also similarly screened of robotic usage.

Various methods are used to distinguish robotic usage. For example, Google automatically scans articles to add to its search index and identifies itself as robotic; other services might not clearly identify themselves as robotic, or they are new or unknown as robotic. Because this activity can be misinterpreted as human readership, data may be re-processed periodically to reflect an improved understanding of robotic activity. Because of these factors, readers should consider usage information illustrative but subject to change.

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