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Comparative Study
. 1994 Mar;95(3):442-9.
doi: 10.1111/j.1365-2249.1994.tb07016.x.

HIV-1 induces tumour necrosis factor and IL-1 gene expression in primary human macrophages independent of productive infection

G Herbein  1 , S Keshav, M Collin, L J Montaner, S Gordon
Affiliations
Comparative Study

HIV-1 induces tumour necrosis factor and IL-1 gene expression in primary human macrophages independent of productive infection

G Herbein et al. Clin Exp Immunol. 1994 Mar.

Abstract

Cytokines such as tumour necrosis factor-alpha (TNF-alpha) and IL-1 beta may play a role in immunopathogenesis of AIDS. We studied early effects (0.5-48 h) of monocytotropic (ADA) or lymphotropic (IIIB) strains of HIV-1 on TNF-alpha and IL-1 beta mRNA expression in primary human macrophages by a semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) assay. Three-day-old monocyte-derived macrophages were exposed either to tissue culture supernatants containing virus (at multiplicity of infection (m.o.i.) of 0.05) or to control supernatants free of virions and gp120. ADA strain, but not IIIB, replicated in primary tissue culture-differentiated macrophages (TCDM). Soluble CD4 (sCD4) was used to inhibit binding of both strains to macrophages. We found that TNF-alpha and IL-1 beta gene expression was induced by both strains 0.5-3 h after addition of virus, and that enhanced expression of both cytokines was inhibited by sCD4. We conclude that CD4-dependent binding to the cell surface is sufficient to enhance TNF-alpha and IL-1 beta mRNA, whereas productive viral replication in primary human macrophages is not required. Therefore, similar pathways regulate gene expression of TNF-alpha and IL-1 beta by macrophages during initial infection by HIV-1 in vitro.

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References

    1. Science. 1984 May 4;224(4648):497-500 - PubMed
    1. J Exp Med. 1965 May 1;121:835-48 - PubMed
    1. J Exp Med. 1985 Mar 1;161(3):503-13 - PubMed
    1. J Virol. 1986 Apr;58(1):67-74 - PubMed
    1. J Immunol. 1986 Apr 15;136(8):2938-42 - PubMed

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