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10.1016/j.virusres.2003.08.007

http://scihub22266oqcxt.onion/10.1016/j.virusres.2003.08.007
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14602203!ä!14602203

suck abstract from ncbi


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pmid14602203      Virus+Res 2003 ; 97 (2): 117-26
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  • Active and inactive influenza virus induction of tumor necrosis factor-alpha and nitric oxide in J774 1 murine macrophages: modulation by interferon-gamma and failure to induce apoptosis #MMPMID14602203
  • McKinney LC; Galliger SJ; Lowy RJ
  • Virus Res 2003[Nov]; 97 (2): 117-26 PMID14602203show ga
  • Infection of J774.1 murine macrophages by influenza A virus (IAV) induces two major responses, production of host defense molecules and death by apoptosis. We investigated whether induction of two cytotoxic compounds, tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO), directly caused IAV-induced apoptosis, and whether induction could be modulated by interferon-gamma (IFN-gamma) or the replication competence of the virus. Live IAV potently induced production of both TNF-alpha and NO, but UV inactivated virus was a poor inducer of both molecules. When cells were pre-treated with IFN-gamma, inactive IAV became as effective an inducer of NO, but not TNF-alpha, as live IAV. Amantadine, which antagonizes viral entry and replication, partly inhibited TNF-alpha and NO production in unprimed cells, but did not inhibit NO in IFN-gamma primed cells. IAV-induced cytotoxicity was not due to the induction of TNF-alpha or NO. Cells were insensitive to either TNF-alpha-containing supernatants or to recombinant TNF-alpha. Anti-TNF-alpha antibody did not protect cells from IAV-induced cell death, and anti-oxidants that inhibited TNF-alpha production also failed to increase cell survival. Inhibitors of NO production did not protect from IAV-induced cell death, either alone or in combination with superoxide dismutase (SOD). We conclude that, even though IAV was a potent inducer of TNF-alpha and NO in macrophages, IAV-induced apoptosis was not mediated directly by them. Importantly, viral replication was not required for the induction of TNF-alpha or NO, and the action of inactive IAV could be potentiated by IFN-gamma.
  • |*Apoptosis[MESH]
  • |Amantadine/pharmacology[MESH]
  • |Animals[MESH]
  • |Antibodies/immunology[MESH]
  • |Antioxidants/pharmacology[MESH]
  • |Antiviral Agents/pharmacology[MESH]
  • |Cell Line[MESH]
  • |Culture Media, Conditioned[MESH]
  • |Influenza A virus/immunology/*physiology[MESH]
  • |Interferon-gamma/*pharmacology[MESH]
  • |Macrophages/immunology/metabolism/physiology/*virology[MESH]
  • |Mice[MESH]
  • |Nitric Oxide Synthase Type II[MESH]
  • |Nitric Oxide Synthase/metabolism[MESH]
  • |Nitric Oxide/*biosynthesis[MESH]
  • |Recombinant Proteins/pharmacology[MESH]
  • |Superoxide Dismutase/metabolism[MESH]
  • |Tumor Necrosis Factor-alpha/*biosynthesis/immunology/metabolism/pharmacology[MESH]
  • |Up-Regulation[MESH]
  • |Virus Inactivation/radiation effects[MESH]


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