Journal article

Rotavirus inhibits IFN-induced STAT nuclear translocation by a mechanism that acts after STAT binding to importin-alpha

Gavan Holloway, Vi T Dang, David A Jans, Barbara S Coulson



The importance of innate immunity to rotaviruses is exemplified by the range of strategies evolved by rotaviruses to interfere with the IFN response. We showed previously that rotaviruses block gene expression induced by type I and II IFNs, through a mechanism allowing activation of signal transducer and activator of transcription (STAT) 1 and STAT2 but preventing their nuclear accumulation. This normally occurs through activated STAT1/2 dimerization, enabling an interaction with importin α5 that mediates transport into the nucleus. In rotavirus-infected cells, STAT1/2 inhibition may limit the antiviral actions of IFN produced early in infection. Here we further analysed the block to STAT1/2..

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University of Melbourne Researchers


Awarded by National Health and Medical Research Council of Australia (NHMRC)

Funding Acknowledgements

Rotaviruses were kindly provided by John Patton (SA11-5S, SA11-30-1A), Koki Taniguchi (A5-16) and Ian H. Holmes (Ty-1 and B223). We thank Christopher Basler for plasmids expressing FLAG-IMP alpha 5 and FLAG-IMP alpha 1. This work was supported by the National Health and Medical Research Council of Australia (NHMRC; project grant 1023786). B. S. C. is a Senior Research Fellow and D. A. J. is a Senior Principal Research Fellow of the NHMRC.