MAVS-dependent host species range and pathogenicity of human hepatitis A virus

Asuka Hirai-Yuki, Lucinda Hensley, David R. McGivern, Olga González-López, Anshuman Das, Hui Feng, Lu Sun, Justin E. Wilson, Fengyu Hu, Zongdi Feng, William Lovell, Ichiro Misumi, Jenny P.Y. Ting, Stephanie Montgomery, John Cullen, Jason K. Whitmire, Stanley M. Lemon

Research output: Contribution to journalArticlepeer-review

71 Scopus citations


Hepatotropic viruses are important causes of human disease, but the intrahepatic immune response to hepatitis viruses is poorly understood because of a lack of tractable small-animal models. We describe a murine model of hepatitis A virus (HAV) infection that recapitulates critical features of type A hepatitis in humans. We demonstrate that the capacity of HAV to evade MAVS-mediated type I interferon responses defines its host species range. HAV-induced liver injury was associated with interferon-independent intrinsic hepatocellular apoptosis and hepatic inflammation that unexpectedly resulted from MAVS and IRF3/7 signaling. This murine model thus reveals a previously undefined link between innate immune responses to virus infection and acute liver injury, providing a new paradigm for viral pathogenesis in the liver.

Original languageEnglish (US)
Pages (from-to)1541-1545
Number of pages5
Issue number6307
StatePublished - Sep 30 2016
Externally publishedYes

ASJC Scopus subject areas

  • General


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