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RESEARCH PRODUCT

Inhibitory effect of nonviable preparations from human immunodeficiency virus 1 on inositol phospholipid metabolism

Werner E.g. MüllerPetra ReuterYoshiyuki KuchinoHeinz C. SchröderJan Van Rooyen

subject

Inositol PhosphatesInositol 145-TrisphosphateBiologyPhospholipasePhosphatidylinositolsBiochemistrychemistry.chemical_compoundCytosolCyclic AMPPhosphatidylinositol phosphorylationHumansInositolLymphocytesPhosphorylationPhytohemagglutininsInositol phosphateProtein kinase AProtein Kinase CProtein kinase Cchemistry.chemical_classificationCell MembraneVirionBiological TransportInositol trisphosphateMolecular biologyCytosolchemistryBiochemistryType C PhospholipasesHIV-1Sugar PhosphatesCell Division

description

Previously it was established [Pahwa, S., Pahwa, R., Saxinger, C., Gallo, R. C. & Good, R. A. (1985) Proc. Natl Acad. Sci. USA 82, 8198] that nonviable preparations of human immunodeficiency virus 1 (HIV-1) abolish the proliferative response of human lymphocytes to phytohemagglutinin A. Now we describe that this effect might be, at least partially, due to an impairment of the function of phospholipase C. It was found that addition of HIV-1 preparation to lymphocytes diminished the stimulation of phosphatidylinositol phosphorylation caused by phytohemagglutinin A. Moreover, this preparation completely abolished the phytohemagglutinin-A-stimulated release of inositol trisphosphate and prevented a translocation of protein kinase C from cytosol to membranes. From this data we conclude that nonviable HIV-1 preparations inhibit the intracellular signalling pathway, leading to a reduced mitogenic response to phytohemagglutinin A, at the level of protein kinase C.

https://doi.org/10.1111/j.1432-1033.1989.tb14940.x