Objective We examined the virological, biochemical and pathological features of two compositemouse models of hepatitis B fibrosis. Methods Mice were transfected with rAAV8-1. 3HBV adeno-associated virus andC57BL/6 N-Tg(1. 28HBV) / Vst type hepatitis B virus transgenic mice, combined with CCl₄ to induce hepatitis B liverfibrosis in mice. The mice were divided into the following groups: wild-type control group ( WT), rAAV8-1. 3HBVtransfection control group (rAAV), CCl₄ control group (CCl₄ ), rAAV8-1. 3HBV transfection with CCl₄ model group(rAAV+CCl₄), C57BL/6 N-Tg (1. 28HBV) / Vst hepatitis B virus transgenic control group (Tg), and HBV transgenic complex CCl₄ model group (Tg+CCl₄ ).After 12 weeks,the levels of HBsAg and HBeAg were measured by ELISA. TheHBV-DNA load was detected by PCR. The expression of HBsAg and HBcAg in the liver tissue was observed byimmunohistochemical staining. Serum ALT, AST and AKP were determined by a biochemical kit, and hydroxyproline(Hyp) content was detected by hydrochloric acid hydrolysis method. HE staining and Sirius red staining were used toobserve the pathological changes. Results ELISA result showed positive serum HBsAg and HBeAg,meanwhile the PCRexamined the HBV-DNA load was higher than 1. 0×10⁴ IU/ mL in all the groups except for the WT and CCl₄ group. TheHBsAg and HBeAg content in the Tg+CCl₄ group was higher than in the rAAV+CCl₄ group. The levels of HBV-DNA in therAAV and rAAV+CCl₄ groups were higher than those in the Tg and Tg+CCl₄ groups. Immunohistochemistry showed positiveHBsAg and HBcAg in the liver tissues in all groups except the WT group and CCl₄ group. The expression of HBsAg wasdecreased but HBcAg was significantly increased in the rAAV+group compared with the Tg group. No significant differencewas detected in HBsAg between the Tg+CCl₄ group and rAAV+CCl₄ group, but the HBcAg positive expression wasobviously increased in the latter group. The levels of ALT, AST and liver Hyp were significantly increased in the CCl₄group, Tg+CCl₄ group and rAAV+CCl₄ group. The Hyp content in the Tg+CCl₄ group was higher than in the rAAV+CCl₄group. The biopsy showed that there were significantly increased inflammation reaction and collagen deposition in the CCl₄group, Tg+CCl₄ group and rAAV+CCl₄ group. The Tg+CCl₄ group collagen deposition was higher than in the rAAV+CCl₄group. Conclusions The two composite mouse models conform to the hepatits B liver fibrosis model and the differences areconcentrated in virological indicators and pathological changes. The rAAV + CCl₄ group has an advantage in HBV-DNA load, and the Tg + CCl₄ group was more obvious in fibrosis progress.