Journal article

MHC class I expression in intestinal cells is reduced by rotavirus infection and increased in bystander cells lacking rotavirus antigen

Gavan Holloway, Fiona E Fleming, Barbara S Coulson



Detection of viral infection by host cells leads to secretion of type I interferon, which induces antiviral gene expression. The class I major histocompatibility complex (MHCI) is required for viral antigen presentation and subsequent infected cell killing by cytotoxic T lymphocytes. STAT1 activation by interferon can induce NLRC5 expression, promoting MHCI expression. Rotavirus, an important pathogen, blocks interferon signalling through inhibition of STAT1 nuclear translocation. We assessed MHCI expression in HT-29 intestinal epithelial cells following rotavirus infection. MHCI levels were upregulated in a partially type I interferon-dependent manner in bystander cells lacking rotavirus an..

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University of Melbourne Researchers


Awarded by National Health and Medical Research Council of Australia

Funding Acknowledgements

We are most grateful to John Patton for SA11-4F and SA11-5S rotaviruses, Koki Taniguchi for A5-16 rotavirus, Izabel Julien Martini Di Fiore for amplifying, purifying and titrating rotavirus strains, and staff of the Flow Cytometry Platform, Department of Microbiology and Immunology, The University of Melbourne, for their assistance with cell sorting. Microscopy was performed using the facilities of the Biological Optical Microscopy Platform at The University of Melbourne. This work was supported by Project Grant APP1023786 and Senior Research Fellowship ID628319 awarded to B.S.C. from the National Health and Medical Research Council of Australia, and a Faculty of Medicine, Dentistry and Health Sciences Research Fellowship awarded to B.S.C. from The University of Melbourne.