肿瘤坏死因子可拮抗叠氮胸苷在体外对人类免疫缺陷病毒（HIV）复制的抑制作用。

Tumor necrosis factor antagonizes inhibitory effect of azidothymidine on human immunodeficiency virus (HIV) replication in vitro.

作者信息

Ito M, Baba M, Mori S, Hirabayashi K, Sato A, Shigeta S, De Clercq E

机构信息

Department of Bacteriology, Fukushima Medical College, Japan.

出版信息

Biochem Biophys Res Commun. 1990 Feb 14;166(3):1095-101. doi: 10.1016/0006-291x(90)90979-w.

DOI:10.1016/0006-291x(90)90979-w

PMID:1689569

Abstract

Tumor necrosis factor alpha (TNF-alpha) completely reverses the activity of azidothymidine (AZT) against human immunodeficiency virus type 1 (HIV-1) in MOLT-4 cell cultures. The 50% effective concentration of AZT, required to protect MOLT-4 cells against the cytopathic effect of HIV-1, increased from 5.8 nM in the absence of TNF-alpha to greater than 125 microM in the presence of TNF-alpha (100 U/ml). TNF-alpha also antagonized the anti-HIV-1 activity of dideoxycytidine but did not markedly affect the anti-HIV-1 activity of dextran sulfate. The intracellular phosphorylation pattern of AZT was not changed upon the presence of TNF-alpha.

摘要

肿瘤坏死因子α（TNF-α）在MOLT-4细胞培养物中完全逆转了叠氮胸苷（AZT）对1型人类免疫缺陷病毒（HIV-1）的活性。保护MOLT-4细胞免受HIV-1细胞病变效应所需的AZT的50%有效浓度，在不存在TNF-α时为5.8 nM，在存在TNF-α（100 U/ml）时增加至大于125 μM。TNF-α还拮抗了双脱氧胞苷的抗HIV-1活性，但对硫酸葡聚糖的抗HIV-1活性没有明显影响。在存在TNF-α的情况下，AZT的细胞内磷酸化模式没有改变。