Activation of human immunodeficiency virus long terminal repeat by arachidonic acid.
Arachidonic acid is the precursor of highly reactive mediators, including prostaglandins and leukotrienes, and the most abundant n-6 polyunsaturated fatty acid in mammalian cell membranes. It is released from phospholipids upon many inflammatory stimuli. In this study, a chloramphenicol acyltransferase reporter gene, under control of the human immunodeficiency virus-1 long terminal repeat, was strongly induced upon treating human promonocytes with arachidonic acid. The n-3 fatty acid eicosapentenoic, found in abundance in fish oil, had no effect. HIV-1 long terminal repeat activation by arachidonic acid was suppressed by inhibitors of both lipoxygenase and cyclooxygenase pathways, suggesting that metabolites, rather than arachidonic acid itself, mediated the stimulatory effect. This is the first report linking HIV-1 expression to the metabolism of arachidonic acid.
Carini
R
R
Department of Experimental Medicine and Oncology, University of Torino, Italy.
Leonarduzzi
G
G
Camandola
S
S
Musso
T
T
Varesio
L
L
Baeuerle
P A
PA
Poli
G
G
D000704:Analysis of Variance; D016718:Arachidonic Acid / Q000494:pharmacology*; D002460:Cell Line; D003470:Culture Media; D015118:Eicosapentaenoic Acid / Q000494:pharmacology*; D005227:Fatty Acids / Q000494:pharmacology; D016679:Genome, Viral; D016325:HIV Long Terminal Repeat / Q000187:drug effects*; D006801:Humans; D009000:Monocytes / Q000187:drug effects* / Q000378:metabolism; D014158:Transcription, Genetic / Q000187:drug effects*
D003470:Culture Media; D005227:Fatty Acids; D016718:Arachidonic Acid; D015118:Eicosapentaenoic Acid