MAVS-dependent host species range and pathogenicity of human hepatitis A virus.
Science
; 353(6307): 1541-1545, 2016 09 30.
Article
em En
| MEDLINE
| ID: mdl-27633528
ABSTRACT
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.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Vírus da Hepatite A
/
Proteínas Adaptadoras de Transdução de Sinal
/
Modelos Animais de Doenças
/
Interações Hospedeiro-Patógeno
/
Hepatite A
/
Fígado
/
Camundongos
Tipo de estudo:
Prognostic_studies
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Science
Ano de publicação:
2016
Tipo de documento:
Article