Journal
CELL REPORTS
Volume 5, Issue 4, Pages 909-917Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2013.10.012
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Funding
- NIH [AI063434]
- NIAID award through the Rocky Mountain Regional Center of Excellence [U54 AI-065357]
- United States Air Force AFIT/CIP Program
- USDA NIFA NNF training grant [2010-38420-20367]
- ASM undergraduate fellowship
- NIFA [581234, 2010-38420-20367] Funding Source: Federal RePORTER
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The impact of RNA viruses on the posttranscriptional regulation of cellular gene expression is unclear. Sindbis virus causes a dramatic relocalization of the cellular HuR protein from the nucleus to the cytoplasm in infected cells. This is to the result of the expression of large amounts of viral RNAs that contain high-affinity HuR binding sites in their 30 UTRs effectively serving as a sponge for the HuR protein. Sequestration of HuR by Sindbis virus is associated with destabilization of cellular mRNAs that normally bind HuR and rely on it to regulate their expression. Furthermore, significant changes can be observed in nuclear alternative polyadenylation and splicing events on cellular pre-mRNAs as a result of sequestration of HuR protein by the 3' UTR of transcripts of this cytoplasmic RNA virus. These studies suggest a molecular mechanism of virus-host interaction that probably has a significant impact on virus replication, cytopathology, and pathogenesis.
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