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Hirai-Yuki, Asuka; Hensley, Lucinda; McGivern, David R.; González-López, Olga; Das, Anshuman; Feng, Hui; Sun, Lu; Wilson, Justin E.; Hu, Fengyu; Feng, Zongdi; Lovell, William; Misumi, Ichiro; Ting, Jenny P.-Y.; Montgomery, Stephanie; Cullen, John; Whitmire, Jason K.; Lemon, Stanley M.
Science (American Association for the Advancement of Science), 09/2016, Letnik: 353, Številka: 6307Journal Article
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 smallanimal 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.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Vir: Osebne bibliografije
in: SICRIS
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