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巨细胞病毒感染的发病机制。I. 体外同种异体反应激活骨髓来源淋巴细胞中的病毒。

Pathogenesis of of cytomegalovirus infection. I. Activation of virus from bone marrow-derived lymphocytes by in vitro allogenic reaction.

作者信息

Olding L B, Jensen F C, Oldstone M B

出版信息

J Exp Med. 1975 Mar 1;141(3):561-72. doi: 10.1084/jem.141.3.561.

DOI:10.1084/jem.141.3.561
PMID:163887
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2189707/
Abstract

After infection in utero or at birth with a cell culture adapted strain of mouse cytomegalovirus (MCMV), several mouse strains developed a latent virus infection in the presence of specific antiviral antibodies. Up to 5 mo after infection, MCMV could be activated and recovered from spleen lymphocytes of the infected animals that were co-cultivated with histoincompatible (H-2 foreign) mouse embryo cells from uninfected animals. In contrast, co-cultivation of lymphoid cells from infected mice with mouse embryo cells from syngeneic, histocompatible (H-2 similar) donors did not activate MCMV. Similarly, MCMV was not recovered from sonicated lymphoid cells. Virus was activated by treating viable lymphoid cells with lipopolysaccharide, a B-cell mitogen, but was not activated by a variety of other mitogens such as phytohemagglutinin, concanavalin A, or pokeweed mitogen. Subsequent purification of lymphoid cells from the infected mice by a variety of techniques indicated that MCMV was harbored in the B-lymphocyte population.

摘要

在子宫内或出生时感染了细胞培养适应株的小鼠巨细胞病毒(MCMV)后,几种小鼠品系在存在特异性抗病毒抗体的情况下发生了潜伏病毒感染。感染后长达5个月,MCMV可从与未感染动物的组织不相容(H-2异源)小鼠胚胎细胞共培养的感染动物的脾淋巴细胞中被激活并回收。相比之下,将感染小鼠的淋巴细胞与同基因、组织相容(H-2相似)供体的小鼠胚胎细胞共培养不会激活MCMV。同样,从超声处理的淋巴细胞中未回收MCMV。用B细胞有丝分裂原脂多糖处理活淋巴细胞可激活病毒,但多种其他有丝分裂原如植物血凝素、刀豆球蛋白A或商陆有丝分裂原不会激活病毒。随后通过多种技术从感染小鼠中纯化淋巴细胞表明,MCMV存在于B淋巴细胞群体中。

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