Viral hepatitis is an important cause of global morbidity but no small animal models replicate human virus-induced liver disease. Hepatitis A (HAV), as with HBV and HCV, is restricted to humans and nonhuman primates as the virus encodes proteinases that degrade MAVS — a molecule involved in the induction of type I interferons that restrict HAV replication. However, because human MAVS sequences are not conserved in small mammals, Hirai-Yuki et al. hypothesized that the restricted host range of HAV stems from an inability to evade MAVS-mediated interferon responses. The researchers show that mice lacking interferon receptors were highly permissive to HAV infection, which accurately recapitulated the features of hepatitis A in humans. Thus, these data provide a tool for studying HAV infection that could be relevant to other hepatotropic viruses.
Hirai-Yuki, A. et al. MAVS-dependent host species range and pathogenicity of human hepatits A virus. Science http://dx.doi.org/10.1126/science.aaf8325 (2016)
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Dickson, I. A mouse model of hepatitis A virus infection. Nat Rev Gastroenterol Hepatol 13, 624 (2016). https://doi.org/10.1038/nrgastro.2016.172