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M94A2544.TXT
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Document 2544
DOCN M94A2544
TI Suppression of HIV replication by the interleukin-1 receptor antagonist.
DT 9412
AU Poli G; Kinter AL; Fox LM; Turchetto L; Vicenzi E; Fauci AS; San
Raffaele Institute, Milano, Italy.
SO Int Conf AIDS. 1994 Aug 7-12;10(1):28 (abstract no. 087A). Unique
Identifier : AIDSLINE ICA10/94370031
AB OBJECTIVE: To investigate the potential role of the natural antagonist
of interleukin-1 (IL-1) receptor (IL-1ra), on cells infected with the
human immunodeficiency virus (HIV). METHODS: Peripheral blood
mononuclear cells (PBMC) of HIV seronegative donors were maintained in
culture with medium enriched of IL-2 and infected with different
laboratory-adapted and primary isolates of HIV type-1 in the presence or
absence of different concentrations of IL-1ra. The chronically infected
promonocytic cell line U1, a previously described model of HIV latency
and induction of viral expression, was stimulated by different
cytokines, including IL-1 alpha and IL-1 beta, in the presence or
absence of different concentrations of IL-1ra. HIV production was
monitored by reverse transcriptase (RT) activity. RESULTS: IL-1ra
suppressed consistently HIV replication in several cultures of PBMC
maintained in IL-2-enriched medium, as determined by the levels of RT
activity measured in the culture supernatants. Similar effects were
obtained with both anti-IL-1 beta, but not anti-IL-1 alpha, antibodies
(Ab) and with Ab directed to the type I, but not the type II, IL-1
receptor. In addition, IL-1ra blocked the induction of HIV expression in
U1 cells stimulated with either IL-1 alpha or IL-1 beta, but did not
interfere with the stimulatory activity of cytokines other than IL-1,
including tumor necrosis factor alpha and IL-6. DISCUSSION AND
CONCLUSIONS: IL-1 induces HIV replication in vitro. IL-1ra, whose only
known function is the inhibition of IL-1 signal transduction via binding
of the cytokine receptors, exerts suppressive effects on HIV replication
derived by endogenously secreted IL-1 (as in the case of IL-2-stimulated
PBMC) or virus expression induced by exogenously added IL-1 (as seen in
U1 cells). These in vitro studies serve as the basis for the formulation
of novel therapeutic strategies aimed at limiting the spreading of the
virus in vivo by blocking the production or effects of HIV-inductive
cytokines, such as IL-1.
DE Cells, Cultured Cytokines/PHARMACOLOGY Human HIV-1/*DRUG
EFFECTS/PHYSIOLOGY Interleukin-1/*PHARMACOLOGY Recombinant
Proteins/PHARMACOLOGY Reverse Transcriptase/METABOLISM
Sialoglycoproteins/*PHARMACOLOGY Virus Replication/*DRUG EFFECTS
MEETING ABSTRACT
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).