MDA5 and MAVS mediate type I interferon responses to coxsackie B virus.
Document Type
Article
Publication Date
2010
Keywords
Animals, Coxsackievirus-Infections, Cytokines, DEAD-box-RNA-Helicases, Enterovirus-B-Human, Immunity-Innate, Interferon-Type-I, Mice-Knockout, Viral-Load
First Page
254
Last Page
260
JAX Source
J Virol 2010 Jan; 84(1):254-60.
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.
Recommended Citation
Wang JP,
Cerny A,
Asher DR,
Kurt JE,
Bronson RT,
Finberg RW.
MDA5 and MAVS mediate type I interferon responses to coxsackie B virus. J Virol 2010 Jan; 84(1):254-60.