Human liver chimeric mice provide a model for hepatitis B and C virus infection and treatment

A paucity of versatile small animal models of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection has been an impediment to both furthering understanding of virus biology and testing antiviral therapies. We recently described a regulatable system for repopulating the liver of immunodeficie...

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Published inThe Journal of clinical investigation Vol. 120; no. 3; pp. 924 - 930
Main Authors Bissig, Karl-Dimiter, Wieland, Stefan F., Tran, Phu, Isogawa, Masanori, Le, Tam T., Chisari, Francis V., Verma, Inder M.
Format Journal Article
LanguageEnglish
Published United States American Society for Clinical Investigation 01.03.2010
Subjects
Animal models in research
Animals
Antiviral agents
Biomedical research
Disease Models, Animal
Drug testing
Genetic aspects
Genomes
Health aspects
Hepacivirus
Hepatitis B
Hepatitis B - pathology
Hepatitis B - therapy
Hepatitis B - virology
Hepatitis B virus
Hepatitis C
Hepatitis C - pathology
Hepatitis C - therapy
Hepatitis C - virology
Hepatitis C virus
Hepatitis viruses
Hepatocytes - pathology
Hepatocytes - transplantation
Hepatocytes - virology
Humans
Infections
Liver - pathology
Liver - virology
Liver cancer
Mice
Mice, Knockout
Monkeys & apes
Pathogens
RNA polymerase
Technical Advance
Toxicity
Transplantation Chimera
Transplantation, Heterologous
Viral infections
Viruses
United States
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Abstract A paucity of versatile small animal models of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection has been an impediment to both furthering understanding of virus biology and testing antiviral therapies. We recently described a regulatable system for repopulating the liver of immunodeficient mice (specifically mice lacking fumaryl acetoacetate hydrolase [Fah], recombination activating gene 2 [Rag2], and the gamma-chain of the receptor for IL-2 [Il-2rgamma]) with human hepatocytes. Here we have shown that a high transplantation dose (3 x 106 to 5 x 106 human hepatocytes/mouse) generates a higher rate of liver chimerism than was previously obtained in these mice, up to 95% human hepatocyte chimerism. Mice with a high level of human liver chimerism propagated both HBV and HCV, and the HCV-infected mice were responsive to antiviral treatment. This human liver chimeric mouse model will expand the experimental possibilities for studying HBV and HCV infection, and possibly other human hepatotropic pathogens, and prove useful for antiviral drug testing.
AbstractList A paucity of versatile small animal models of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection has been an impediment to both furthering understanding of virus biology and testing antiviral therapies. We recently described a regulatable system for repopulating the liver of immunodeficient mice (specifically mice lacking fumaryl acetoacetate hydrolase [Fah], recombination activating gene 2 [Rag2], and the gamma-chain of the receptor for IL-2 [Il-2rgamma]) with human hepatocytes. Here we have shown that a high transplantation dose (3 x 106 to 5 x 106 human hepatocytes/mouse) generates a higher rate of liver chimerism than was previously obtained in these mice, up to 95% human hepatocyte chimerism. Mice with a high level of human liver chimerism propagated both HBV and HCV, and the HCV-infected mice were responsive to antiviral treatment. This human liver chimeric mouse model will expand the experimental possibilities for studying HBV and HCV infection, and possibly other human hepatotropic pathogens, and prove useful for antiviral drug testing.A paucity of versatile small animal models of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection has been an impediment to both furthering understanding of virus biology and testing antiviral therapies. We recently described a regulatable system for repopulating the liver of immunodeficient mice (specifically mice lacking fumaryl acetoacetate hydrolase [Fah], recombination activating gene 2 [Rag2], and the gamma-chain of the receptor for IL-2 [Il-2rgamma]) with human hepatocytes. Here we have shown that a high transplantation dose (3 x 106 to 5 x 106 human hepatocytes/mouse) generates a higher rate of liver chimerism than was previously obtained in these mice, up to 95% human hepatocyte chimerism. Mice with a high level of human liver chimerism propagated both HBV and HCV, and the HCV-infected mice were responsive to antiviral treatment. This human liver chimeric mouse model will expand the experimental possibilities for studying HBV and HCV infection, and possibly other human hepatotropic pathogens, and prove useful for antiviral drug testing.
A paucity of versatile small animal models of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection has been an impediment to both furthering understanding of virus biology and testing antiviral therapies. We recently described a regulatable system for repopulating the liver of immunodeficient mice (specifically mice lacking fumaryl acetoacetate hydrolase [Fah], recombination activating gene 2 [Rag2], and the gamma-chain of the receptor for IL-2 [Il-2rgamma]) with human hepatocytes. Here we have shown that a high transplantation dose (3 x 106 to 5 x 106 human hepatocytes/mouse) generates a higher rate of liver chimerism than was previously obtained in these mice, up to 95% human hepatocyte chimerism. Mice with a high level of human liver chimerism propagated both HBV and HCV, and the HCV-infected mice were responsive to antiviral treatment. This human liver chimeric mouse model will expand the experimental possibilities for studying HBV and HCV infection, and possibly other human hepatotropic pathogens, and prove useful for antiviral drug testing.
A paucity of versatile small animal models of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection has been an impediment to both furthering understanding of virus biology and testing antiviral therapies. We recently described a regulatable system for repopulating the liver of immunodeficient mice (specifically mice lacking fumaryl acetoacetate hydrolase [Fah], recombination activating gene 2 [Rag2], and the g-chain of the receptor for IL-2 [Il-2rg]) with human hepatocytes. Here we have shown that a high transplantation dose (3 x 10 super(6) to 5 x 10 super(6) human hepatocytes/mouse) generates a higher rate of liver chimerism than was previously obtained in these mice, up to 95% human hepatocyte chimerism. Mice with a high level of human liver chimerism propagated both HBV and HCV, and the HCV-infected mice were responsive to antiviral treatment. This human liver chimeric mouse model will expand the experimental possibilities for studying HBV and HCV infection, and possibly other human hepatotropic pathogens, and prove useful for antiviral drug testing.
A paucity of versatile small animal models of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection has been an impediment to both furthering understanding of virus biology and testing antiviral therapies. We recently described a regulatable system for repopulating the liver of immunodeficient mice (specifically mice lacking fumaryl acetoacetate hydrolase [Fah], recombination activating gene 2 [Rag2], and the γ-chain of the receptor for IL-2 [Il-2rγ]) with human hepatocytes. Here we have shown that a high transplantation dose (3 x [10.sup.6] to 5 x [10.sup.6] human hepatocytes/mouse) generates a higher rate of liver chimerism than was previously obtained in these mice, up to 95% human hepatocyte chimerism. Mice with a high level of human liver chimerism propagated both HBV and HCV, and the HCV-infected mice were responsive to antiviral treatment. This human liver chimeric mouse model will expand the experimental possibilities for studying HBV and HCV infection, and possibly other human hepatotropic pathogens, and prove useful for antiviral drug testing.
A paucity of versatile small animal models of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection has been an impediment to both furthering understanding of virus biology and testing antiviral therapies. We recently described a regulatable system for repopulating the liver of immunodeficient mice (specifically mice lacking fumaryl acetoacetate hydrolase [Fah], recombination activating gene 2 [Rag2], and the γ-chain of the receptor for IL-2 [Il-2rγ]) with human hepatocytes. Here we have shown that a high transplantation dose (3 × 10 6 to 5 × 10 6 human hepatocytes/mouse) generates a higher rate of liver chimerism than was previously obtained in these mice, up to 95% human hepatocyte chimerism. Mice with a high level of human liver chimerism propagated both HBV and HCV, and the HCV-infected mice were responsive to antiviral treatment. This human liver chimeric mouse model will expand the experimental possibilities for studying HBV and HCV infection, and possibly other human hepatotropic pathogens, and prove useful for antiviral drug testing.
Audience Academic
Author Bissig, Karl-Dimiter
Verma, Inder M.
Isogawa, Masanori
Tran, Phu
Chisari, Francis V.
Wieland, Stefan F.
Le, Tam T.
AuthorAffiliation 1 The Salk Institute for Biological Studies, Laboratory of Genetics, La Jolla, California, USA. 2 The Scripps Research Institute, Department of Immunology and Microbial Science, La Jolla, California, USA
AuthorAffiliation_xml – name: 1 The Salk Institute for Biological Studies, Laboratory of Genetics, La Jolla, California, USA. 2 The Scripps Research Institute, Department of Immunology and Microbial Science, La Jolla, California, USA
Author_xml – sequence: 1
  givenname: Karl-Dimiter
  surname: Bissig
  fullname: Bissig, Karl-Dimiter
– sequence: 2
  givenname: Stefan F.
  surname: Wieland
  fullname: Wieland, Stefan F.
– sequence: 3
  givenname: Phu
  surname: Tran
  fullname: Tran, Phu
– sequence: 4
  givenname: Masanori
  surname: Isogawa
  fullname: Isogawa, Masanori
– sequence: 5
  givenname: Tam T.
  surname: Le
  fullname: Le, Tam T.
– sequence: 6
  givenname: Francis V.
  surname: Chisari
  fullname: Chisari, Francis V.
– sequence: 7
  givenname: Inder M.
  surname: Verma
  fullname: Verma, Inder M.
BackLink https://www.ncbi.nlm.nih.gov/pubmed/20179355$$D View this record in MEDLINE/PubMed
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Snippet A paucity of versatile small animal models of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection has been an impediment to both furthering...
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SubjectTerms Animal models in research
Animals
Antiviral agents
Biomedical research
Disease Models, Animal
Drug testing
Genetic aspects
Genomes
Health aspects
Hepacivirus
Hepatitis B
Hepatitis B - pathology
Hepatitis B - therapy
Hepatitis B - virology
Hepatitis B virus
Hepatitis C
Hepatitis C - pathology
Hepatitis C - therapy
Hepatitis C - virology
Hepatitis C virus
Hepatitis viruses
Hepatocytes - pathology
Hepatocytes - transplantation
Hepatocytes - virology
Humans
Infections
Liver - pathology
Liver - virology
Liver cancer
Mice
Mice, Knockout
Monkeys & apes
Pathogens
RNA polymerase
Technical Advance
Toxicity
Transplantation Chimera
Transplantation, Heterologous
Viral infections
Viruses
Title Human liver chimeric mice provide a model for hepatitis B and C virus infection and treatment
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