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Cytocidal effect of tumor necrosis factor on cells chronically infected with human immunodeficiency virus (HIV): enhancement of HIV replication.

机译:肿瘤坏死因子对慢性感染人免疫缺陷病毒(HIV)的细胞的杀细胞作用:增强HIV复制。

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摘要

Tumor necrosis factor (TNF), a monokine initially described as a tumoricidal agent, facilitated the replication of human immunodeficiency virus (HIV) in vitro. The viability of human T-cell line MOLT-4/HIV, chronically infected with HIV, was affected by the addition of a low dose (10 ng/ml) of recombinant TNF-alpha (rTNF-alpha), while uninfected MOLT-4 cells were resistant to treatment with rTNF-alpha at concentrations up to 1,000 ng/ml. A marked increase in the level of HIV-specific RNA was detected in MOLT-4/HIV cells as early as 1 h after exposure to rTNF-alpha and reached almost maximum level within 6 h. Production of HIV particles from MOLT-4/HIV was also increased at 6 h after treatment with rTNF-alpha. Nearly identical phenomena were observed in CCRF-CEM/HIV, Jurkat/HIV, and H9/HIV cells, although the sensitivity of these cell lines to rTNF-alpha varied. A human T-lymphotropic virus type 1-infected cell line, MT-4, was insensitive to treatment with rTNF-alpha.
机译:肿瘤坏死因子(TNF),一种最初被描述为杀肿瘤剂的单因子,促进了人类免疫缺陷病毒(HIV)在体外的复制。长期感染HIV的人T细胞系MOLT-4 / HIV的生存力受到低剂量(10 ng / ml)重组TNF-α(rTNF-alpha)的影响,而未感染的MOLT-4细胞对浓度高达1,000 ng / ml的rTNF-α的治疗具有抗性。最早在接触rTNF-α后1小时,在MOLT-4 / HIV细胞中检测到HIV特异性RNA的水平显着增加,并在6小时内达到几乎最高水平。用rTNF-α治疗后6小时,来自MOLT-4 / HIV的HIV颗粒的产生也增加了。在CCRF-CEM / HIV,Jurkat / HIV和H9 / HIV细胞中观察到几乎相同的现象,尽管这些细胞系对rTNF-alpha的敏感性有所不同。人类T淋巴病毒1型感染的细胞系MT-4对rTNF-α的治疗不敏感。

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