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单核因子介导的人类免疫缺陷病毒1型在慢性感染的前单核细胞和T细胞系中的表达增加。

Monokine-mediated increase in human immunodeficiency virus type 1 expression in chronically infected promonocyte- and T-cell-derived lines.

作者信息

Ho W Z, Tomassini N, Cherukuri R, Shun-D G, Song L, Lee H R, Douglas S D

机构信息

Department of Pediatrics, Children's Hospital of Philadelphia, University of Pennsylvania Medical School 19104, USA.

出版信息

Clin Diagn Lab Immunol. 1994 Sep;1(5):517-25. doi: 10.1128/cdli.1.5.517-525.1994.

DOI:10.1128/cdli.1.5.517-525.1994
PMID:8556495
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC368326/
Abstract

The ACH-2 cell clone derived from a human T-cell line and chronically infected with human immunodeficiency virus 1 (HIV-1) and the U1 cell clone derived from a human promonocyte cell line and also chronically infected with HIV-1 produce HIV-1 in a response to stimulation with monokine-enriched supernatants prepared from highly purified populations of peripheral blood-derived human monocytes. Monokine-mediated expression of HIV-1 in these cell lines resulted in augmented virus production reflected by increases in reverse transcriptase (RT) activity, production of p24 antigen, and synthesis of major viral proteins. Examination of the cells by electron microscopy revealed numerous HIV-1 virions in the cells treated with the supernatants. This stimulation of virus production by monokine-enriched supernatants resulted in approximately 100-fold increases in RT activity and p24 antigen expression in comparison with those in untreated U1 and ACH-2 cells. Absorption of monokine-enriched supernatants with rabbit anti-tumor necrosis factor alpha antibody removed most, but not all, of the induced HIV-1 RT activity and p24 antigen expression in U1 and ACH-2 cell lines, suggesting that tumor necrosis factor alpha in the monokine-enriched supernatants is a major factor in the induction of HIV-1 expression in these cells.

摘要

源自人T细胞系并长期感染人免疫缺陷病毒1(HIV-1)的ACH-2细胞克隆,以及源自人原单核细胞系且同样长期感染HIV-1的U1细胞克隆,在用从高度纯化的外周血来源的人单核细胞群体制备的富含单核因子的上清液刺激后会产生HIV-1。单核因子介导的HIV-1在这些细胞系中的表达导致病毒产生增加,这通过逆转录酶(RT)活性的增加、p24抗原的产生以及主要病毒蛋白的合成得以体现。通过电子显微镜检查细胞发现,用上清液处理的细胞中有大量HIV-1病毒颗粒。与未处理的U1和ACH-2细胞相比,富含单核因子的上清液对病毒产生的这种刺激导致RT活性和p24抗原表达增加约100倍。用兔抗肿瘤坏死因子α抗体吸收富含单核因子的上清液后,U1和ACH-2细胞系中大部分(但并非全部)诱导的HIV-1 RT活性和p24抗原表达被去除,这表明富含单核因子的上清液中的肿瘤坏死因子α是诱导这些细胞中HIV-1表达的主要因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29cb/368326/a62039eff566/cdli00005-0048-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29cb/368326/0987ee22c6e6/cdli00005-0044-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29cb/368326/4ccf232c77a4/cdli00005-0045-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29cb/368326/d7e5751bfb1b/cdli00005-0046-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29cb/368326/b9b8cea8fba3/cdli00005-0047-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29cb/368326/a62039eff566/cdli00005-0048-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29cb/368326/0987ee22c6e6/cdli00005-0044-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29cb/368326/4ccf232c77a4/cdli00005-0045-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29cb/368326/d7e5751bfb1b/cdli00005-0046-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29cb/368326/b9b8cea8fba3/cdli00005-0047-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29cb/368326/a62039eff566/cdli00005-0048-a.jpg

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