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呼肠孤病毒诱导的严重联合免疫缺陷(SCID)小鼠肝病。一种用于研究病毒感染、发病机制和清除的模型。

Reovirus-induced liver disease in severe combined immunodeficient (SCID) mice. A model for the study of viral infection, pathogenesis, and clearance.

作者信息

George A, Kost S I, Witzleben C L, Cebra J J, Rubin D H

机构信息

Department of Biology, University of Pennsylvania, Philadelphia.

出版信息

J Exp Med. 1990 Mar 1;171(3):929-34. doi: 10.1084/jem.171.3.929.

Abstract

Adult severe combined immunodeficient (SCID) mice can be infected by the oral route with reovirus, and a systemic infection can be established. Infectious virus is recovered from all internal organs, and the mice die in 4-6 wk. Chronic, discrete inflammatory lesions appear in the liver of infected mice, and are associated with hepatocytes containing demonstrable levels of viral antigen. The adoptive transfer of Peyer's patch (PP) cells from congenic mice before infection protects the SCID mice against disease and death. Immune donor PP cells can be distinguished from nonimmune cells by their ability to contain and resolve infection by 1 wk after challenge.

摘要

成年严重联合免疫缺陷(SCID)小鼠可通过口服途径感染呼肠孤病毒,并能建立全身感染。从所有内脏器官中均可分离出传染性病毒,小鼠在4 - 6周内死亡。受感染小鼠的肝脏中会出现慢性、离散的炎性病变,且与含有可检测水平病毒抗原的肝细胞有关。在感染前从同基因小鼠中过继转移派伊尔结(PP)细胞可保护SCID小鼠免于发病和死亡。免疫供体的PP细胞在受到攻击后1周内,可通过其控制和消除感染的能力与非免疫细胞区分开来。

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