THALIDOMIDE INHIBITS THE REPLICATION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1

被引：232
作者：
MAKONKAWKEYOON, S
LIMSONPOBRE, RNR
MOREIRA, AL
SCHAUF, V
KAPLAN, G
机构：
[1] ROCKEFELLER UNIV,CELLULAR PHYSIOL & IMMUNOL,1230 YORK AVE,NEW YORK,NY 10021
[2] CORNELL UNIV,MED CTR,NEW YORK HOSP,DEPT MED,DIV INFECT DIS,NEW YORK,NY 10021
来源：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 1993年 / 90卷 / 13期
关键词：
D O I：
10.1073/pnas.90.13.5974
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
Thalidomide, a selective inhibitor of tumor necrosis factor alpha (TNF-alpha) synthesis, suppresses the activation of latent human immunodeficiency virus type 1 (HIV-1) in a monocytoid (U1) line. The inhibition is dose dependent and occurs after exposure of the cells to recombinant TNF-alpha, phorbol myristate acetate, lipopolysaccharide, and other cytokine combinations. Associated with HIV-1 inhibition is a reduction in agonist-induced TNF-alpha protein and mRNA production. Thalidomide inhibition of virus replication in the phorbol myristate acetate- and recombinant TNF-alpha-stimulated T-cell line ACH-2 is not observed. The presence of thalidomide also inhibits the activation of virus in the peripheral blood mononuclear cells of 16 out of 17 patients with advanced HIV-1 infection and AIDS. These results suggest the use of thalidomide in a dinical setting to inhibit both virus replication and the TNF-alpha-induced systemic toxicity of HIV-1 and opportunistic infections.
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页码：5974 / 5978
页数：5
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