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Animal Models of Chronic Hepatitis Delta Virus Infection Host–Virus Immunologic Interactions

Gene Therapy and Regulation of Gene Expression Program, Centro de Investigación Médica Aplicada (CIMA), Universidad de Navarra (UNAV), Pamplona 31008, Spain
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Academic Editor: Moriya Tsuji
Pathogens 2015, 4(1), 46-65; https://doi.org/10.3390/pathogens4010046
Received: 12 November 2014 / Accepted: 5 February 2015 / Published: 12 February 2015
(This article belongs to the Special Issue Animal Model to Study Viral Immunity)
Hepatitis delta virus (HDV) is a defective RNA virus that has an absolute requirement for a virus belonging to the hepadnaviridae family like hepatitis B virus (HBV) for its replication and formation of new virions. HDV infection is usually associated with a worsening of HBV-induced liver pathogenesis, which leads to more frequent cirrhosis, increased risk of hepatocellular carcinoma (HCC), and fulminant hepatitis. Importantly, no selective therapies are available for HDV infection. The mainstay of treatment for HDV infection is pegylated interferon alpha; however, response rates to this therapy are poor. A better knowledge of HDV–host cell interaction will help with the identification of novel therapeutic targets, which are urgently needed. Animal models like hepadnavirus-infected chimpanzees or the eastern woodchuck have been of great value for the characterization of HDV chronic infection. Recently, more practical animal models in which to perform a deeper study of host virus interactions and to evaluate new therapeutic strategies have been developed. Therefore, the main focus of this review is to discuss the current knowledge about HDV host interactions obtained from cell culture and animal models. View Full-Text
Keywords: hepatitis delta virus; HDV animal models; liver damage; antiviral treatment; vaccines hepatitis delta virus; HDV animal models; liver damage; antiviral treatment; vaccines
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Aldabe, R.; Suárez-Amarán, L.; Usai, C.; González-Aseguinolaza, G. Animal Models of Chronic Hepatitis Delta Virus Infection Host–Virus Immunologic Interactions. Pathogens 2015, 4, 46-65.

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