Journal
VIRAL IMMUNOLOGY
Volume 21, Issue 1, Pages 78-82Publisher
MARY ANN LIEBERT INC
DOI: 10.1089/vim.2007.0072
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Funding
- Howard Hughes Medical Institute Funding Source: Medline
- NIAID NIH HHS [R01 AI032947, AI070343, N01 AI500031, N01-AI-50031, U01 AI070343-03, N01AI50031, U01 AI070343, U01 AI070343-02, U01 AI070343-01, R01 AI041440] Funding Source: Medline
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West Nile virus (WNV) is a mosquito-borne flavivirus that has spread rapidly throughout the U. S. and there is currently no effective treatment. Understanding the pathogenesis of WNV infection in humans is critical for development of a potent therapy. In this study, we examined the activation of primary human macrophages in response to WNV infection, and showed that WNV interacts with human macrophages at multiple levels. While infection with WNV induced production of interleukin (IL)-8, production of IL-1 beta, and type I interferon was inhibited. Infection with WNV interferes with the downstream JAK/STAT pathway, which is important for macrophage activation. In comparison to other related flaviviruses, the differential response of proinflammatory cytokines is distinct to WNV.
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