Journal
VIRAL IMMUNOLOGY
Volume 16, Issue 4, Pages 447-460Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/088282403771926283
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Funding
- NIAID NIH HHS [AI44458] Funding Source: Medline
- NIDDK NIH HHS [DK52194] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI044458] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK052194] Funding Source: NIH RePORTER
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Prostaglandins are lipid mediators, generated by cyclooxygenase (COX), that have been shown to participate in the regulation of virus replication and the modulation of inflammatory responses following infection. A number of studies support a role for PGE(2) in the modulation of virus replication and virulence in a cell type and virus selective manner. 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. This review will focus on the mechanisms by which proinflammatory prostaglandin production regulates virus replication and virulence. In addition, the signaling pathways that are activated during a virus infection, and that regulate proinflammatory gene expression in macrophages will be reviewed. Specific attention will be placed on the ability of virus infection to activate multiple signaling cascades (such as PKR, MAPK, iPLA(2), NF-kappaB) and how these pathways are integrated in the regulation of individual target gene expression.
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