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染色体外1型人类免疫缺陷病毒DNA可引发HL-60细胞的播散性感染。

Extrachromosomal human immunodeficiency virus type-1 DNA can initiate a spreading infection of HL-60 cells.

作者信息

Butera S T, Perez V L, Besansky N J, Chan W C, Wu B Y, Nabel G J, Folks T M

机构信息

Retrovirus Diseases Branch, Centers for Disease Control, Atlanta, Georgia 30333.

出版信息

J Cell Biochem. 1991 Apr;45(4):366-73. doi: 10.1002/jcb.240450410.

DOI:10.1002/jcb.240450410
PMID:2045430
Abstract

In this report, we describe a human immunodeficiency virus type-1 (HIV-1)-infected promyelocytic cell line, OM, derived from HL-60 cells. Although the OM cell line was biologically cloned twice, the pattern of HIV-1 expression during culture appeared analogous to a classical acute spreading infection and was inhibited by both azidothymidine and recombinant soluble CD4 treatment. The number of OM cells actually expressing HIV-1 at the beginning of culture was 0%, reached a peak of nearly 100% at 6 weeks, and then fell to less than 10% HIV-1+ cells by 10 weeks. Clonal analysis of the surviving cells verified that stable HIV-1+ OM cells resulted from the spreading infection. Southern analysis confirmed the transmission of HIV-1 through these OM cultures and the occurrence of stable clones which resulted. The initial percentage of OM cells actually harboring the HIV-1 genome was less than 0.1%, indicating nonfaithful transmission of an unintegrated HIV-1 genome during clonal expansion. These results demonstrate that extrachromosomal HIV-1 DNA can contribute to the spread of HIV-1 infection and give rise to cells which have stably integrated HIV-1 provirus.

摘要

在本报告中,我们描述了一种源自HL - 60细胞的人免疫缺陷病毒1型(HIV - 1)感染的早幼粒细胞系OM。尽管OM细胞系经过了两次生物学克隆,但培养过程中HIV - 1的表达模式类似于典型的急性播散性感染,且齐多夫定和重组可溶性CD4处理均能抑制其表达。培养开始时实际表达HIV - 1的OM细胞数量为0%,6周时达到近100%的峰值,到10周时HIV - 1阳性细胞降至不到10%。对存活细胞的克隆分析证实,稳定的HIV - 1阳性OM细胞源于播散性感染。Southern分析证实了HIV - 1在这些OM培养物中的传播以及由此产生的稳定克隆的出现。最初实际携带HIV - 1基因组的OM细胞百分比不到0.1%,这表明在克隆扩增过程中未整合的HIV - 1基因组存在非忠实传递。这些结果表明,染色体外HIV - 1 DNA可促进HIV - 1感染的传播,并产生已稳定整合HIV - 1前病毒的细胞。

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