Abstract
A selective cyclooxygenase-2 (COX-2) inhibitor has been previously shown to suppress the hyper-induced pro-inflammatory responses in H5N1 infected primary human cells. Here, we demonstrate that COX-2 inhibitors suppress H5N1 virus replication in human macrophages suggesting that H5N1 virus replication (more so than seasonal H1N1 virus) is dependent on activation of COX-2 dependent signaling pathways in host cells. COX-2 and its downstream signaling pathways deserve detailed investigation as a novel therapeutic target for treatment of H5N1 disease.
Copyright © 2011 Elsevier B.V. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antiviral Agents / pharmacology
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Birds
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Cells, Cultured
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Cyclooxygenase 2 / genetics
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Cyclooxygenase 2 / metabolism*
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Cyclooxygenase 2 Inhibitors / pharmacology
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Dose-Response Relationship, Drug
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Humans
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Influenza A Virus, H1N1 Subtype / drug effects
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Influenza A Virus, H1N1 Subtype / physiology
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Influenza A Virus, H5N1 Subtype / drug effects*
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Influenza A Virus, H5N1 Subtype / physiology
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Influenza in Birds / drug therapy
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Influenza in Birds / virology
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Influenza, Human / drug therapy*
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Influenza, Human / virology
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Macrophages / cytology
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Macrophages / drug effects*
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Macrophages / virology
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Reverse Transcriptase Polymerase Chain Reaction
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Signal Transduction / drug effects*
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Sulfonamides / pharmacology*
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Viral Proteins / genetics
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Viral Proteins / metabolism*
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Virus Replication / drug effects
Substances
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Antiviral Agents
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Cyclooxygenase 2 Inhibitors
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Sulfonamides
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Viral Proteins
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Cyclooxygenase 2
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PTGS2 protein, human
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nimesulide