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Interleukins, Chemokines, and Tumor Necrosis Factor Superfamily Ligands in the Pathogenesis of West Nile Virus Infection

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VIRUSES-BASEL
卷 15, 期 3, 页码 -

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MDPI
DOI: 10.3390/v15030806

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West Nile virus; cytokines; interleukins; chemokines; tumor necrosis factor superfamily ligands; infection model

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This article provides an up-to-date review of cytokine expression patterns in human and experimental animal models of West Nile virus (WNV) infections. Cytokines play a critical role in inflammation and immunity during and after WNV infection, with some offering protection and assisting with viral clearance, while others contributing to neuropathogenesis and immune-mediated tissue damage.
West Nile virus (WNV) is a mosquito-borne pathogen that can lead to encephalitis and death in susceptible hosts. Cytokines play a critical role in inflammation and immunity in response to WNV infection. Murine models provide evidence that some cytokines offer protection against acute WNV infection and assist with viral clearance, while others play a multifaceted role WNV neuropathogenesis and immune-mediated tissue damage. This article aims to provide an up-to-date review of cytokine expression patterns in human and experimental animal models of WNV infections. Here, we outline the interleukins, chemokines, and tumor necrosis factor superfamily ligands associated with WNV infection and pathogenesis and describe the complex roles they play in mediating both protection and pathology of the central nervous system during or after virus clearance. By understanding of the role of these cytokines during WNV neuroinvasive infection, we can develop treatment options aimed at modulating these immune molecules in order to reduce neuroinflammation and improve patient outcomes.

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