PMID: 8989205Jan 1, 1997Paper

Tenidap inhibits replication of the human immunodeficiency virus-1 in cultured cells

Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology : Official Publication of the International Retrovirology Association
B J DezubeR W Finberg

Abstract

Interleukin-6 (IL-6) may be important in the pathogenesis of HIV-1 because of its ability to induce HIV-1 expression in infected cells in vitro. Tenidap, a structurally and functionally novel antirheumatic drug affecting diverse biologic processes, has been shown to reduce IL-6 production by peripheral blood mononuclear cells stimulated with lipopolysaccharide. Tenidap also inhibits the activity of chloride-bicarbonate exchangers and causes acidification of the cytoplasmic compartment that is similar to the effect of the anion transport inhibitor UK5099. Furthermore, tenidap inhibits the cyclooxygenase-mediated pathway of arachidonic acid metabolism as do the nonsteroidal antiinflammatory drugs (NSAIDs). Here we show that tenidap decreased HIV-1 replication as measured by p24 core antigen in the acutely infected CD4+ T-lymphocyte lines H9 and Jurkat, in the acutely infected monocyte line U937, and in its chronically infected subclone U1.8/HIV. These effects were seen at concentrations in the range of 3 to 15 microM, well below those toxic to cells. The antiviral effects of tenidap may be independent of its ability to reduce IL-6 production based on the observations that these effects were as prominent in IL-6 nonresponsive line...Continue Reading

References

Oct 23, 1992·Science·T KishimotoT Taga
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