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M9650557.TXT
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1996-03-09
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Document 0557
DOCN M9650557
TI Interferon-gamma-induced downregulation of CD4 inhibits the entry of
human immunodeficiency virus type-1 in primary monocytes.
DT 9605
AU Dhawan S; Heredia A; Wahl LM; Epstein JS; Meltzer MS; Hewlett IK;
Laboratory of Molecular Virology, Food and Drug Administration,;
Rockville, Md., USA.
SO Pathobiology. 1995;63(2):93-9. Unique Identifier : AIDSLINE MED/96108566
AB We have previously shown that the treatment of monocytes with
interferon-gamma (IFN-gamma) prior to exposure with human
immunodeficiency virus type-1 (HIV) results in complete inhibition of
HIV infection of monocytes. In the present report, we have extended this
study to obtain information on the mechanism(s) underlying
IFN-gamma-induced inhibition of HIV infection of monocytes. To examine
the effect of IFN-gamma on HIV entry, the first event in the infectious
cycle of the virus, we amplified HIV-gag sequences in the genomic DNA
and RNA of IFN-gamma treated monocytes, and found no evidence for the
presence of either proviral DNA or HIV RNA sequences. These results were
consistent with the absence of intracellular HIV particles either in the
latent or actively replicating state as determined by flow-cytometric
analysis of these cells. Furthermore, no HIV-induced cytopathic effects,
such as multinucleated giant cell formation or cell death, were observed
in IFN-gamma-treated monocytes after their exposure to HIV. Stimulation
of IFN-gamma-treated monocytes 6 days postinfection with tumor necrosis
factor-alpha (TNF-alpha), which is known to augment HIV replication in
the infected cells, did not result in the induction of the HIV
indicating the absence of latent HIV infection in IFN-gamma-treated
monocytes. Treatment of monocytes with IFN-gamma, TNF-alpha, or with a
combination of the two agents which is known to induce antimicrobial
free radical nitric oxide (NO2- in the murine system did not induce NO2-
production human monocytes suggesting the antiviral activity of
IFN-gamma to be independent of NO2(-)-mediated killing of HIV or
HIV-infected monocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
DE Antigens, CD4/*BIOSYNTHESIS Cells, Cultured Cytopathogenic Effect,
Viral *Down-Regulation (Physiology) Human HIV Core Protein
p24/BIOSYNTHESIS HIV-1/PHYSIOLOGY/*PATHOGENICITY Interferon Type
II/*PHARMACOLOGY Kinetics Monocytes/IMMUNOLOGY/*VIROLOGY Nitric
Oxide/METABOLISM Polymerase Chain Reaction Transfection Tumor
Necrosis Factor/PHARMACOLOGY Virus Replication JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).