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• W2056522394 abstract "Monocytes/macrophages are highly susceptible to an infection with influenza A virus. After infection, de novo virus protein synthesis is detectable but rapidly interrupted before completion of the first viral replication cycle. Within 24–48hours the infected monocytes die by apoptosis. Before cell death, infected monocytes initiate a cell-specific immune response. This includes the transcription and subsequent release of TNF-a (tumor necrosis factor a), IL-1b (Interleukin 1b), IL-6, type I inferferons and CC chemokines. Enhanced cytokine mRNA expression is due to a prolonged mRNA stability and an augmented gene transcription. Activation of transcription factors such as NF-ÍB (nuclear factor ÍB) and AP-1 are involved in activation of cytokine mRNA transcription. Infection of monocytes with influenza A virus induces the selective expression of mononuclear leukocyte attracting chemokines, such as MCP-1 (monocyte chemotactic protein 1), MIP-1a (macrophage inflammatory protein 1a) and RANTES (regulated upon activation, normal T cell expressed and secreted). In striking contrast, the release of the neutrophil-specific chemokines IL-8 (interleukin 8) and GRO-a (growth stimulatory activity a) is entirely suppressed. This differentially regulated chemokine expression may explain the mononuclear cell infiltrate characteristic for virus-infected tissue. Thus, infection of monocytes/macrophages with influenza A virus primes for a rapid proinflammatory reaction and induces an enhanced immigration of mononuclear cells into infected tissue. Taken together, these mechanisms may prepare the infected host for a fast and virus-specific immune response." @default.
• W2056522394 created "2016-06-24" @default.
• W2056522394 creator A5066939454 @default.
• W2056522394 date "2001-01-01" @default.
• W2056522394 modified "2023-09-26" @default.
• W2056522394 title "Defense against Influenza A Virus Infection: Essential Role of the Chemokine System" @default.
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• W2056522394 doi "https://doi.org/10.1078/0171-2985-00099" @default.
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