Abstract
1. Hyper-induction of cytokines and chemokines was found in human blood macrophages infected with the avian influenza H5N1 and H9N2/G1 viruses, as compared to those infected with human influenza H1N1 virus. 2. IRF3 played a significant role in the hyperinduction of cytokines including IFN-β, IFN-λ1,IFN-α subtypes, MCP-1, and TNF-α, and also played a part in subsequent cytokine-induced cell signalling cascades. 3. Compared with H1N1 viruses, avian influenza viruses including H5N1/97 and its precursors triggered a caspase-mediated but delayed apoptotic response in human macrophages. 4. Therapies that can minimise immunopathology-associated dysregulation of innate immunity without impairing effective host defence may be valuable adjuncts to antiviral therapy.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis*
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Caspase 3 / metabolism
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Cells, Cultured
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Cytokines / biosynthesis
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Cytokines / genetics*
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Gene Expression Regulation
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Humans
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Influenza A Virus, H1N1 Subtype
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Influenza A Virus, H5N1 Subtype*
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Influenza, Human / metabolism*
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Interferon Regulatory Factor-3 / genetics
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Interferon Regulatory Factor-3 / metabolism*
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Interferon-beta / biosynthesis
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Interferon-beta / genetics
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Interferons
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Interleukins / biosynthesis
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Interleukins / genetics
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Macrophages / enzymology
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Macrophages / metabolism*
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Macrophages / virology
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Poly(ADP-ribose) Polymerases / metabolism
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RNA, Messenger / metabolism*
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RNA, Small Interfering
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Transcription Factors / metabolism
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Tumor Necrosis Factor-alpha / biosynthesis
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Tumor Necrosis Factor-alpha / genetics
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Up-Regulation / genetics
Substances
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Cytokines
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interferon-lambda, human
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IRF3 protein, human
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Interferon Regulatory Factor-3
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Interleukins
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RNA, Messenger
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RNA, Small Interfering
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Transcription Factors
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Tumor Necrosis Factor-alpha
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Interferon-beta
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Interferons
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Poly(ADP-ribose) Polymerases
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Caspase 3