Melanoma differentiation-associated protein-5 (MDA-5) limits early viral replication but is not essential for the induction of type 1 interferons after Coxsackievirus infection

Michael H. Hühn, Stephen A. McCartney, Katharina Lind, Emma Svedin, Marco Colonna, Malin Flodström-Tullberg

Research output: Contribution to journalArticlepeer-review

42 Scopus citations

Abstract

Coxsackievirus infections are associated with severe diseases such as myocarditis, meningitis and pancreatitis. To study the contribution of the intracellular viral sensor melanoma differentiation-associated protein-5 (MDA-5) in the host immune response to Coxsackievirus B3 (CVB3) we infected C57BL/6 and 129/SvJ mice lacking mda-5. Mice deficient in MDA-5 showed a dramatically increased susceptibility to CVB3 infection. The loss of MDA-5 allowed the virus to replicate faster, resulting in increased liver and pancreas damage and heightened mortality. MDA-5 was not absolutely required for the induction of type 1 interferons (IFNs), but essential for the production of maximal levels of systemic IFN-α early after infection. Taken together, our findings indicate that MDA-5 plays an important role in the host immune response to CVB3 by preventing early virus replication and limiting tissue pathology.

Original languageEnglish
Pages (from-to)42-48
Number of pages7
JournalVirology
Volume401
Issue number1
DOIs
StatePublished - May 2010

Keywords

  • Coxsackievirus
  • Diabetes
  • Enterovirus
  • Hepatitis
  • Innate immunity
  • Interferon
  • Melanoma differentiation-associated gene-5
  • Pancreatitis

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