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M9480002.TXT
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1994-08-09
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Document 0002
DOCN M9480002
TI Inhibition of 3'azido-3'deoxythymidine-resistant HIV-1 infection by
dehydroepiandrosterone in vitro.
DT 9410
AU Yang JY; Schwartz A; Henderson EE; Department of Microbiology and
Immunology, Temple University; School of Medicine, Philadelphia 19140.
SO Biochem Biophys Res Commun. 1994 Jun 30;201(3):1424-32. Unique
Identifier : AIDSLINE MED/94296419
AB Human immunodeficiency virus type 1 (HIV-1) isolated from patients with
acquired immunodeficiency syndrome (AIDS) shows resistance to
3'azido-3'deoxythymidine (AZT) after one or two years of treatment. AZT
also has significant toxic side effects, further limiting its use in the
therapy of HIV-1-infected individuals. Dehydroepiandrosterone (DHEA) has
been shown to have a broad spectrum of biological functions, to be
bioavailable orally and to be relatively nontoxic. Epidemiological
studies provide evidence that reduced serum levels of DHEA are related
to the progression of AIDS in HIV-1 infection. DHEA has also been shown
to inhibit HIV-1 replication in vitro and block HIV-1 reactivation from
chronically infected cell lines. However, there have been no reports on
the ability of DHEA to inhibit the replication of AZT-resistant strains
of HIV-1. We investigated whether DHEA treatment could inhibit
replication of AZT-resistant strains of HIV-1. Addition of DHEA to MT-2
cell cultures infected with either AZT-sensitive or AZT-resistant
isolates of HIV-1 resulted in dose-dependent inhibition of HIV-1-induced
cytopathic effect and suppression of HIV-1 replication as measured by
accumulation of reverse transcriptase activity. At a concentration as
low as 50 microM, DHEA reduced AZT-resistant HIV-1 replication over 50
percent as measured by cytopathic effect and accumulation of reverse
transcriptase activity. This study provides evidence that DHEA can
inhibit the replication of AZT-resistant as well as wild-type HIV-1.
Since the main targets for DHEA are metabolic and cellular signaling
pathways leading to HIV-1 replication-activation, DHEA should be
effective against multidrug-resistant strains of HIV-1. Combined with
recently discovered immunoregulatory properties, the finding that DHEA
is able to inhibit replication of both wild-type and AZT-resistant HIV-1
suggests that in vivo DHEA may have a much broader spectrum of action
than originally anticipated.
DE Cytopathogenic Effect, Viral Drug Resistance, Microbial Human HIV
Infections/*PREVENTION & CONTROL HIV-1/*DRUG EFFECTS/GROWTH &
DEVELOPMENT In Vitro Prasterone/*PHARMACOLOGY Support, U.S. Gov't,
P.H.S. Tumor Cells, Cultured Virus Replication/DRUG EFFECTS
Zidovudine/*PHARMACOLOGY JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).