Shanley J D, Jordan M C, Cook M L, Stevens J G
Am J Pathol. 1979 Apr;95(1):67-80.
Sixteen weeks after inoculation, murine cytomegalovirus (MCMV) can no longer be detected in the tissues of mice. However, a 2-week course of immunosuppression with antilymphocyte serum and cortisone acetate results in reactivation and dissemination of the latent virus in all animals. In this study of reactivation, MCMV was first detected in the liver, usually during the first week of immunosuppression, and virus replication was shown to be restricted to hepatocytes. Subsequently, a viremia occurred, with spread of infection to other organs. The highest titers of virus were reached in salivary glands in which replication occurred in serous acinar cells. In the lung, virus-specific abnormalities were difficult to detect because of superimposed bacterial and fungal infections. However, interstitial pneumonitis could be produced when cortisone acetate was deleted from the immunosuppressive regimen. Although the site of virus latency has not been defined, this model system will be useful for study of reactivation of latent cytomegalovirus infection.
接种16周后,在小鼠组织中已无法检测到鼠巨细胞病毒(MCMV)。然而,用抗淋巴细胞血清和醋酸可的松进行为期2周的免疫抑制疗程会导致所有动物体内潜伏病毒的重新激活和扩散。在这项关于重新激活的研究中,MCMV通常在免疫抑制的第一周首先在肝脏中被检测到,并且病毒复制被证明局限于肝细胞。随后,出现病毒血症,感染扩散到其他器官。病毒滴度在唾液腺中达到最高,在浆液性腺泡细胞中发生复制。在肺部,由于叠加的细菌和真菌感染,很难检测到病毒特异性异常。然而,当从免疫抑制方案中去除醋酸可的松时,可产生间质性肺炎。尽管病毒潜伏部位尚未明确,但该模型系统将有助于研究潜伏性巨细胞病毒感染的重新激活。