Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 108, Issue 29, Pages 12024-12029Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1108926108
Keywords
ion channel; myocarditis; potassium efflux; aging; tolbutamide
Categories
Funding
- Centre National de la Recherche Scientifique, Institut National de la Sante et de la Recherche Medicale, Universite de Strasbourg
- Region Alsace
- National Institute of Health [PO1 AI070167, RO1 HL54732]
- Balzan Foundation
- Centre National de la Recherche Scientifique
- American Heart Association
- Fondation pour la Recherche Medicale
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The effects of the cellular environment on innate immunity remain poorly characterized. Here, we show that in Drosophila ATP-sensitive potassium channels (K-ATP) mediate resistance to a cardiotropic RNA virus, Flock House virus (FHV). FHV viral load in the heart rapidly increases in KATP mutant flies, leading to increased viremia and accelerated death. The effect of K-ATP channels is dependent on the RNA interference genes Dcr-2, AGO2, and r2d2, indicating that an activity associated with this potassium channel participates in this antiviral pathway in Drosophila. Flies treated with the K-ATP agonist drug pinacidil are protected against FHV infection, thus demonstrating the importance of this regulation of innate immunity by the cellular environment in the heart. In mice, the Coxsackievirus B3 replicates to higher titers in the hearts of mayday mutant animals, which are deficient in the Kir6.1 subunit of K-ATP channels, than in controls. Together, our data suggest that K-ATP channel deregulation can have a critical impact on innate antiviral immunity in the heart.
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