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• W2039947003 abstract "Background & AimsLittle is known about the direct cytopathic effect of hepatitis B virus (HBV) and its association with particular viral genotypes or genetic mutations. We investigate HBV genotype–related differences in viral replication, antigen expression, and histopathology in severe combined immunodeficiency transgenic with urokinase-type plasminogen activator mice harboring human hepatocytes.MethodsMice were inoculated with wild-type of different genotype strains (3 for each HBV/A2, B1, and C2) recovered from preinfected-mice sera or patient sera.ResultsHistologic analysis of mice infected with HBV/C2 for 22–25 weeks showed abundant ground-glass appearance of the hepatocytes and fibrosis in the humanized part of the murine liver owing to the activation of hepatic stellate cells mediated by oxidative stress through transforming growth factor-β1 signaling, whereas neither was observed with HBV/A2 and B1. The HBV-DNA level in sera was the highest in mice infected with HBV/C2 compared with those with HBV/A2 and HBV/B1 (109, 107, and 104 log copies/mL, respectively, P < .05) during 6–8 weeks postinoculation. HB core-related antigen excretion had a similar trend among the genotypes, whereas secretion of HB surface antigen was more pronounced for HBV/A2 followed by HBV/C2 and much less for HBV/B1. Introduction of precore stop-codon mutation in the HBV/B1 caused a significant increase in viral replication, antigen expression, and a histopathologic picture similar to HBV/C2.ConclusionsBy using a humanized in vivo model, we show that different HBV genotypes and even particular mutations resulted in different virologic and histopathologic outcomes of infection, indicating that particular genetic variants of HBV may be directly cytopathic in immunosuppressive conditions. Little is known about the direct cytopathic effect of hepatitis B virus (HBV) and its association with particular viral genotypes or genetic mutations. We investigate HBV genotype–related differences in viral replication, antigen expression, and histopathology in severe combined immunodeficiency transgenic with urokinase-type plasminogen activator mice harboring human hepatocytes. Mice were inoculated with wild-type of different genotype strains (3 for each HBV/A2, B1, and C2) recovered from preinfected-mice sera or patient sera. Histologic analysis of mice infected with HBV/C2 for 22–25 weeks showed abundant ground-glass appearance of the hepatocytes and fibrosis in the humanized part of the murine liver owing to the activation of hepatic stellate cells mediated by oxidative stress through transforming growth factor-β1 signaling, whereas neither was observed with HBV/A2 and B1. The HBV-DNA level in sera was the highest in mice infected with HBV/C2 compared with those with HBV/A2 and HBV/B1 (109, 107, and 104 log copies/mL, respectively, P < .05) during 6–8 weeks postinoculation. HB core-related antigen excretion had a similar trend among the genotypes, whereas secretion of HB surface antigen was more pronounced for HBV/A2 followed by HBV/C2 and much less for HBV/B1. Introduction of precore stop-codon mutation in the HBV/B1 caused a significant increase in viral replication, antigen expression, and a histopathologic picture similar to HBV/C2. By using a humanized in vivo model, we show that different HBV genotypes and even particular mutations resulted in different virologic and histopathologic outcomes of infection, indicating that particular genetic variants of HBV may be directly cytopathic in immunosuppressive conditions." @default.
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• W2039947003 date "2009-02-01" @default.
• W2039947003 modified "2023-10-14" @default.
• W2039947003 title "Direct Cytopathic Effects of Particular Hepatitis B Virus Genotypes in Severe Combined Immunodeficiency Transgenic With Urokinase-Type Plasminogen Activator Mouse With Human Hepatocytes" @default.
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• W2039947003 doi "https://doi.org/10.1053/j.gastro.2008.10.048" @default.
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