| Literature DB >> 28706073 |
Eva Billerbeck1, Raphael Wolfisberg2, Ulrik Fahnøe2, Jing W Xiao1, Corrine Quirk1, Joseph M Luna1, John M Cullen3, Alex S Hartlage4, Luis Chiriboga5, Kalpana Ghoshal6, W Ian Lipkin7, Jens Bukh2, Troels K H Scheel1,2, Amit Kapoor4, Charles M Rice8.
Abstract
An estimated 71 million people worldwide are infected with hepatitis C virus (HCV). The lack of small-animal models has impeded studies of antiviral immune mechanisms. Here we show that an HCV-related hepacivirus discovered in Norway rats can establish high-titer hepatotropic infections in laboratory mice with immunological features resembling those seen in human viral hepatitis. Whereas immune-compromised mice developed persistent infection, immune-competent mice cleared the virus within 3 to 5 weeks. Acute clearance was T cell dependent and associated with liver injury. Transient depletion of CD4+ T cells before infection resulted in chronic infection, characterized by high levels of intrahepatic regulatory T cells and expression of inhibitory molecules on intrahepatic CD8+ T cells. Natural killer cells controlled early infection but were not essential for viral clearance. This model may provide mechanistic insights into hepatic antiviral immunity, a prerequisite for the development of HCV vaccines.Entities:
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Year: 2017 PMID: 28706073 PMCID: PMC5654634 DOI: 10.1126/science.aal1962
Source DB: PubMed Journal: Science ISSN: 0036-8075 Impact factor: 47.728