Journal article

Innate immune responses to rotavirus infection in macrophages depend on MAVS but involve neither the NLRP3 inflammasome nor JNK and p38 signaling pathways

Izabel JM Di Fiore, Gavan Holloway, Barbara S Coulson



Rotavirus infection is a major cause of life-threatening infantile gastroenteritis. The innate immune system provides an immediate mechanism of suppressing viral replication and is necessary for an effective adaptive immune response. Innate immunity involves host recognition of viral infection and establishment of a powerful antiviral state through the expression of pro-inflammatory cytokines such as type-1 interferon (IFN). Macrophages, the front-line cells of innate immunity, produce IFN and other cytokines in response to viral infection. However, the role of macrophages during rotavirus infection is not well defined. We demonstrate here that RRV rotavirus triggers the production of proinf..

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University of Melbourne Researchers


Awarded by National Health and Medical Research Council of Australia

Funding Acknowledgements

We thank Douglas Golenbock and Ashley Mansell for advice and provision of the immortalized BMM cell lines, and Carl Kirkwood for the MA104 cells. This work was supported by the National Health and Medical Research Council of Australia (Project Grant APP1023786). B. S. C. is a Senior Research Fellow of the National Health and Medical Research Council (ID628319).