The use of cyclosporine, FK506, and SDZ NIM811 to prevent CD25(-) quiescent peripheral blood mononuclear cells from producing human immunodeficiency virus

被引:12
作者
Borvak, J
Chou, CS
VanDyke, G
Rosenwirth, B
Vitetta, ES
Ramilo, O
机构
[1] UNIV TEXAS,SW MED CTR,CTR CANC IMMUNOBIOL,DEPT MICROBIOL,IMMUNOL GRAD PROGRAM,DALLAS,TX 75235
[2] UNIV TEXAS,SW MED CTR,DEPT PEDIAT,DALLAS,TX 75235
[3] BIOMED PRIMATE RES CTR,RIJSWIJK,NETHERLANDS
关键词
D O I
10.1093/infdis/174.4.850
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
It has been shown that the combined use of two pharmacologic agents can inhibit human immunodeficiency virus (HIV) production by peripheral blood mononuclear cells in vitro. One, an anti-CD25 immunotoxin (IT), kills activated T cells that produce virus; the other, the immunosuppressive drug cyclosporine, prevents the quiescent cells, which harbor HIV, from becoming activated. The present study compares the antiviral activities of two agents, SDZ NIM811 and FK506, to that of cyclosporine. In combination with the anti-CD25 IT, these drugs significantly suppressed virus production. In the absence of prior addition of the IT, the ability of the drugs to inhibit virus production was much lower, suggesting that they work effectively in latently infected cells. In the case of SDZ NIM811, the inhibition of virus production was accompanied by a modest inhibition of cell proliferation. In contrast, FK506 exerted strong antiproliferative activity. Cyclosporine was both moderately antiproliferative and a potent antiviral agent.
引用
收藏
页码:850 / 853
页数:4
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