Inhibition of HIV infection of H9 cells by chlorpromazine derivatives

被引：16

作者：

Hewlett, I

Lee, S

Molnar, J

Weaver, JL

Aszalos, A

机构：

[1] US FDA,CTR DRUG EVALUAT & RES,DIV RES & TESTING,LAUREL,MD 20705

[2] US FDA,CTR BIOL EVALUAT & RES,BETHESDA,MD

[3] ALBERT SZENT GYORGYI MED UNIV,H-6701 SZEGED,HUNGARY

来源：

JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY | 1997年 / 15卷 / 01期

关键词：

anti-Leu3a binding; syncytia formation; HIV infectivity; dioxo-chlorpromazine;

D O I：

10.1097/00042560-199705010-00003

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The binding between the HIV surface protein. gp120, and the CD4 coreceptor is known to be initiated by electrostatic interactions. Because of the ability of chlorpromazine to interact with proteins by charge transfer, we tested several derivatives for their ability to block binding of HIV to CD4(+) cells. We have shown that 7,8-dioxo-chlorpromazine blocks binding of fluorescein isothiocyanate-labeled anti-Leu3a and rgp120 to peripheral human blood T4 cells and blocks syncytia formation between gp120- and CD4-expressing cells. We also found that 7,8-dioxo-chlorpromazine blocks HIV infectivity of H9 cells and acts synergistically with zidovudine.

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页码：16 / 20

页数：5

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