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Prostaglandins (PG), generated by cyclooxygenase (COX), are a group of lipid mediators formed in response to various stimuli. They include PGD2, PGE2, PGF2alpha, and PGI2. Immediately after synthesis, they are released outside the cell and exert their actions by binding to a G-protein-coupled rhodopsin-type receptor on the surface of target cells. There are seven types of prostaglandin receptors: the PGD receptor, four subtypes of PGE receptor, the PGF receptor, and the PGI receptor. Prostaglandins are involved in host defense against various pathogens. Along with mediating inflammatory symptoms, PGs might suppress some innate immune factors, including nitric oxide (NO) production. These immunomodulatory molecules have been shown to participate in the regulation of virus replication and the modulation of inflammatory responses following infection. Moreover, virus infection also stimulates the expression of a number of proinflammatory gene products, including COX-2, inducible nitric oxide synthase (iNOS) as well as proinflammatory cytokines. An overproduction of PGE2 (as high as 10−4M) is seen in a number of disorders (e.g. allergy, hyper-IgE syndrome, Hodgkin lymphoma, trauma, sepsis, and transplantation), most of which are characterized by elevated Th2 and IgE responses. Elevated levels of PGE2 have also been reported in individuals infected with HIV-1 and it has been postulated that this may contribute to the immunosuppressive state seen in such virally infected patients. The mechanism(s) responsible for the enhanced prostaglandin formation is still undefined. The initial contact between the virus particle and its target cell might represent the crucial step leading to the production of PGE2 by macrophages. This concept is supported by the finding that a significant production of endogenous PGE2 is induced (20to 40-fold increase) following incubation of primary human monocytes with the HIV-1 external envelope glycoprotein gp120. Given that pro-inflammatory molecules such as PGE2 are up-regulated during HIV-1 infection, an imbalance in PGJ2 production is observed in HIV+ individuals. This book chapter will focus on roles of prostaglandins in HIV-1 replication and their potential therapeutic implications. We propose to review mechanisms by which the proinflammatory prostaglandin PGE2 and the anti-inflammatory prostaglandin PGJ2 regulate HIV-1 transcription and replication. Specific attention will be placed on how prostaglandins affect the nuclear translocation of NF-B (nuclear factor kappa B), an essential transcription factor for HIV-1 transcription. In addition, signaling pathways as well as other transcription

Emerging Roles of Prostaglandins in HIV-1 Transcription