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Fatty liver reduces hepatitis B virus replication in a genotype B hepatitis B virus transgenic mice model
Author(s) -
Zhang Zheng,
Pan Qin,
Duan XiaoYan,
Liu Qiang,
Mo GuoYu,
Rao GuiRong,
Fan JianGao
Publication year - 2012
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.2012.07268.x
Subject(s) - hbsag , hbeag , hepatitis b virus , fatty liver , medicine , steatosis , virology , liver function , hepatitis b , orthohepadnavirus , immunology , hepadnaviridae , genetically modified mouse , virus , transgene , biology , disease , gene , biochemistry
Background and Aim Non‐alcoholic fatty liver disease ( NAFLD ) overlapping with chronic hepatitis B virus ( HBV ) infection is undergoing a rapid increase in C hina. Therefore, the establishment and character of an animal model with both NAFLD and chronic HBV infection has become an urgent task. Methods Mice with chronic HBV genotype B infection were established with a microinjection of oocytes. Transgenic and nontransgenic mice were then randomized into groups of NAFLD + HBV , HBV , NAFLD , and control and were treated with high‐fat diets or common forage. At 8, 16, and 24 weeks, characteristics of NAFLD were evaluated by physical indices, liver function tests, glycolipid metabolism, and histopathological scoring. Viral dynamics were also analyzed by HBV‐DNA and HBV ‐related antigens. Results Hepatitis B surface antigen ( HBsAg ) and hepatitis B e antigen ( HBeAg ) were expressed, and HBV‐DNA was replicated in HBV transgenic mice at different stages in the serum and liver. Hepatic steatosis was only induced after exposure of the mice to high‐fat diets, and no obvious pathological changes occurred in the HBV group from 8 to 24 weeks. Compared to mice with HBV alone, significant reductions in serum levels of HBV‐DNA , HBsAg and HBeAg occurred in the NAFLD + HBV group after 24 weeks (all P < 0.05). Nevertheless, the NAFLD and NAFLD + HBV groups shared comparable physical and metabolic disorders and similar steatotic, inflammatory and fibrotic characteristics in the liver. Conclusion High‐fat diets and transgenic operations on the HBV genotype B induced a rodent model of NAFLD overlapping with chronic HBV infection, and this model reduces the HBV viral factors but not the metabolic and histologic features.