新生BALB/c小鼠巨细胞病毒肝炎模型的建立

Establishment of neonatal BALB /c murine viral hepatitis model by cytomegalovirus

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MCMVDNA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 neonatal BALB/c murine viral hepatitis model by cytomegalovirus. Methods： The mouse model of hepatitis was established by transabdominal injection of cytomegalovirus to infect neonatal BALB/c mice. Results： The mortality of hepatitis in infected mice was 100. 00% , the death peak occurred at 3 -5 days after infection, the mortality was 10.00%. The growth and development of cytomegalovirus - infected mice was slow, the body weights at 7 and 14 days were statistically significantly lower than normal mice （ P 〈 0. 05 ） . After HE staining, the changes found at three days included inflammatory cell infiltration, swelling and degeneration of liver cells, which was mainly manifested as increasing size, empty cytoplasm, spotty necrosis of liver cells ; at seven days, the severity of the disease peaked, fatty degeneration, large inflammatory cell infiltration and platy necrosis of liver were observed; at 14 days, the pathological injury maintained at a relatively high level. Compared with control group, ALT levels at 3, 7 and 14 days in model group increased signifi- candy （ P 〈 0.05 ）, the peak time of peak value of ALT was seventh day. Cytomegalovirus DNA in hepatic tissue of cytomegalovirus - infec- ted neonatal mice was positive, the titer of cytomegalovirus in liver at 7 days was the highest. Conclusion： The model provides a effective tool for analyzing mechanism and prognosis of congenital cytomegalovirus - induced hepatitis and screening of antiviral drugs.