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小鼠巨细胞病毒肺部感染中病毒复制与间质性肺炎的关系。

The relation of viral replication to interstitial pneumonitis in murine cytomegalovirus lung infection.

作者信息

Shanley J D, Pesanti E L

出版信息

J Infect Dis. 1985 Mar;151(3):454-8. doi: 10.1093/infdis/151.3.454.

Abstract

Using a murine model of murine cytomegalovirus (MCMV) interstitial pneumonitis, we examined the relation between the virus content of the lung and lung disease. While MCMV alone does not cause lung disease, interstitial pneumonitis was present in all mice receiving both MCMV and a single dose of cyclophosphamide. In this case the severity of disease, judged by increases in wet weight of the lung, was proportional to the virus content of the lung. Although both acyclovir (50 mg/kg per day) and passive antibody administration reduced the MCMV titers in lung tissues by greater than 90%, histological evidence of interstitial pneumonitis was present in all animals. However, both virus inhibitors reduced the severity of interstitial pneumonitis in treated mice. While transient alterations in host immunity are necessary to induce interstitial pneumonitis after MCMV infection, the severity of interstitial pneumonitis seems to reflect the burden of virus replication. Reduction of virus growth does not prevent, but may moderate, MCMV interstitial pneumonitis.

摘要

利用小鼠巨细胞病毒(MCMV)间质性肺炎的小鼠模型,我们研究了肺内病毒含量与肺部疾病之间的关系。虽然单独的MCMV不会引起肺部疾病,但在所有接受MCMV和单剂量环磷酰胺的小鼠中均出现了间质性肺炎。在这种情况下,通过肺湿重增加判断的疾病严重程度与肺内病毒含量成正比。尽管阿昔洛韦(每天50mg/kg)和被动给予抗体均可使肺组织中的MCMV滴度降低90%以上,但所有动物均有间质性肺炎的组织学证据。然而,两种病毒抑制剂均降低了治疗小鼠中间质性肺炎的严重程度。虽然宿主免疫的短暂改变是MCMV感染后诱发间质性肺炎所必需的,但间质性肺炎的严重程度似乎反映了病毒复制的负荷。病毒生长的减少并不能预防MCMV间质性肺炎,但可能会使其减轻。

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