MDA5 and MAVS mediate type I interferon responses to coxsackie B virus

Jennifer P. Wang, Anna Cerny, Damon R. Asher, Evelyn A. Kurt-Jones, Roderick T. Bronson, Robert W. Finberg

Research output: Contribution to journalArticlepeer-review

113 Scopus citations

Abstract

Coxsackie B viruses (CVB) are enteroviruses that have been associated with a variety of human diseases, including myocarditis. In the present study, we found that MDA5 and its adaptor molecule MAVS are critical for type I interferon responses to CVB, since the absence of either MAVS or MDA5 leads to deficient type I interferon production and early mortality in mice infected with CVB. Pancreatic and hepatic necrosis were observed on histopathological examination of MAVS and MDA5 knockout mice infected with CVB. Inflammatory cytokine production in response to systemic CVB infection was independent of MAVS. Surprisingly, virus titers were not elevated in MAVS-deficient mice, despite significant reductions in type I interferon levels. These data highlight the importance of type I interferon in host defense and provide insight on the mechanisms of innate immune responses following coxsackievirus infection.

Original languageEnglish
Pages (from-to)254-260
Number of pages7
JournalJournal of Virology
Volume84
Issue number1
DOIs
StatePublished - Jan 2010
Externally publishedYes

Fingerprint

Dive into the research topics of 'MDA5 and MAVS mediate type I interferon responses to coxsackie B virus'. Together they form a unique fingerprint.

Cite this