目的:建立新生BALB/c小鼠巨细胞病毒肝炎模型。方法:小鼠巨细胞病毒经腹腔注射感染新生BALB/c小鼠,建立肝炎小鼠模型。结果:感染小鼠肝炎发病率为100.00%,死亡高峰在感染后3~5天,死亡率为10.00%。MCMV感染小鼠生长发育缓慢,7、14天时体重低于未感染小鼠(P<0.05)。HE染色可见3天时炎性细胞浸润,肝细胞肿胀变性,表现为体积变大、胞浆空淡,肝细胞点状坏死;7天时病变加重达高峰,可见大泡性脂肪变,大量炎性细胞浸润,肝细胞片状坏死;第14天病理损害仍保持较高水平。MCMV感染新生小鼠与对照组相比,在第3、7、14天ALT明显升高(P<0.05),ALT的高峰是在第7天。PCR检测MCMV感染新生小鼠肝脏组织内MCMV DNA为阳性,7天时肝脏病毒滴度最高。结论:新生小鼠巨细胞病毒肝炎动物模型为探讨先天性HCMV肝炎的发病机制、转归及抗病毒药物的筛选提供了有力的工具。 Objective: To establish a neonatal BALB / c mouse model of cytomegalovirus hepatitis. Methods: Mouse cytomegalovirus was injected into neonatal BALB / c mice via intraperitoneal injection to establish a mouse model of hepatitis. Results: The incidence of hepatitis in infected mice was 100.00%. The peak of death was 3 to 5 days after infection with a mortality rate of 10.00%. Mice infected with MCMV grew slowly and had weaker body weights at 7 and 14 days than those without infection (P <0.05). Hematoxylin-eosin staining showed inflammatory cell infiltration and hepatocellular swelling and degeneration at 3 days. The volume increased, the cytoplasm became pale, and the hepatocytes became necrotic. At 7 days, the lesions reached the peak, and the macroscopic steatosis, a large number of inflammatory cells Infiltration, hepatocellular necrosis; pathological lesions on the 14th day remained at a high level. Compared with the control group, the ALT in MCMV-infected neonatal mice was significantly increased (P <0.05) on the 3rd, 7th and 14th days, and the peak of ALT was on the 7th day. PCR detection MCMV infection of neonatal mouse liver tissue MCMV DNA was positive, the highest hepatic virus titer at 7 days. Conclusion: The animal model of neonatal cytomegalovirus hepatitis provides a powerful tool for exploring the pathogenesis, prognosis and screening of antiviral drugs for congenital HCMV hepatitis.