Levy G A, MacPhee P J, Fung L S, Fisher M M, Rappaport A M
Hepatology. 1983 Nov-Dec;3(6):964-73. doi: 10.1002/hep.1840030614.
Mouse hepatitis virus type 3 infection results in strain-dependent liver disease. The effects of mouse hepatitis virus type 3 on the microcirculation of the liver in both fully susceptible (Balb/cJ) and fully resistant (A/J) mice were studied. In Balb/cJ mice, 6 to 12 hr following infection, abnormalities in liver blood flow were observed which consisted of granular blood flow in both terminal hepatic and terminal portal venules. In addition, sinusoidal microthrombi were present predominantly in periportal areas. By 24 to 48 hr, liver cell edema and small focal lesions were prominent. At 48 hr, thrombi and hepatocellular necrosis were widespread, and blood was shunted from damaged areas into patent sinusoids. In sharp contrast to these abnormal findings, normal streamlined blood flow was present in the resistant A/J animals at all time points following infection. Since large amounts of virus were demonstrated by immunofluorescene in and by recovery and growth from livers of both resistant and susceptible strains, the presence of the virus per se cannot explain the abnormalities observed.
3型小鼠肝炎病毒感染会导致不同品系依赖性的肝脏疾病。研究了3型小鼠肝炎病毒对完全易感(Balb/cJ)和完全抗性(A/J)小鼠肝脏微循环的影响。在Balb/cJ小鼠中,感染后6至12小时,观察到肝脏血流异常,表现为终末肝小静脉和终末门静脉小静脉内的颗粒状血流。此外,窦状微血栓主要出现在门静脉周围区域。到24至48小时,肝细胞水肿和小灶性病变明显。在48小时时,血栓和肝细胞坏死广泛存在,血液从受损区域分流到开放的血窦中。与这些异常发现形成鲜明对比的是,在感染后的所有时间点,抗性A/J动物的肝脏中均存在正常的层流。由于通过免疫荧光以及从抗性和易感品系的肝脏中恢复和生长都证明了大量病毒的存在,因此病毒本身的存在无法解释所观察到的异常现象。