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人泡沫病毒对造血细胞的持续性增殖性感染。

Productive persistent infection of hematopoietic cells by human foamy virus.

作者信息

Yu S F, Stone J, Linial M L

机构信息

Division of Basic Sciences, Fred Hutchinson Cancer Center, Seattle, Washington 98104-2092, USA.

出版信息

J Virol. 1996 Feb;70(2):1250-4. doi: 10.1128/JVI.70.2.1250-1254.1996.

Abstract

Human foamy virus can establish persistent infections in human hematopoietic cell lines, such as H92.1.7 (erythroblastoid cells), Jurkat (CD4+ T cells), and U937 (myeloid-monocytic cells). The infection is characterized by constant production of infectious viruses (for > 2 1/2 years) with no cytopathic effects on the host cells. Electron microscopy of the infected cells showed a viral morphology similar to that observed for particles produced after acute infection. We have detected, in addition to the full-length form of bel1, a previously described deletion in the bel1 gene of the proviral DNA in these cells. RNA containing this 301-bp deletion, which mapped to the splice donor and acceptor sites of the intron of the bet gene, was also found in encapsidated virion RNA. However, the presence of this defective provirus harboring the deletion in bel1 does not prevent productive persistence in these chronically infected cells, since the virus titer does not decrease during cultivation.

摘要

人泡沫病毒可在人造血细胞系中建立持续感染,如H92.1.7(成红细胞样细胞)、Jurkat(CD4 + T细胞)和U937(髓单核细胞)。这种感染的特征是持续产生传染性病毒(超过2年半),且对宿主细胞无细胞病变效应。对感染细胞的电子显微镜检查显示,病毒形态与急性感染后产生的颗粒所观察到的相似。除了全长形式的bel1外,我们在这些细胞的前病毒DNA的bel1基因中检测到了先前描述的缺失。在衣壳化的病毒体RNA中也发现了含有这种301bp缺失的RNA,该缺失定位于bet基因内含子的剪接供体和受体位点。然而,这种在bel1中携带缺失的缺陷前病毒的存在并不妨碍在这些慢性感染细胞中的有效持续感染,因为在培养过程中病毒滴度不会降低。

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