Pathogenesis of avian flu H5N1 and SARS

• Main Author: Peiris, M
• Format: Conference Object
• Language: English
• Published: United Kingdom 2006
• Subjects: Sars Virus - Pathogenicity - Physiology; Severe Acute Respiratory Syndrome - Pathology - Virology; Animals; Humans; Influenza A Virus; H5n1 Subtype - Pathogenicity - Physiology; Influenza; Human - Pathology - Virology; Avian flu
• Online Access: https://doi.org/10.1002/9780470035399.ch5; http://hdl.handle.net/10722/179846

Symposium on Innate Immunity to Pulmonary Infection, University of Cape Town Medical School, South Africa, 28-30 November 2005 Novartis Foundation Symposium, v.279 entitled as: Innate immunity to pulmonary infection Avian influenza A (H5N1) and severe acute respiratory syndrome (SARS) coronavirus are infections that cause a severe viral pneumonia leading to acute respiratory dysfunction syndrome and carry a high case-fatality rate. We have investigated innate immune responses to both viruses using primary human macrophages and respiratory epithelial cells as in vitro models. In contrast to human influenza A H1N1 viruses, the H5N1 viruses hyper-induce cytokines (tumour necrosis factor [TNF]α, interferon β) and chemokines (IP10, MIP1α, MCP) in in vitro cultures of primary human macrophages. A similar differential effect is observed in primary human bronchial epithelial cells and in type 2 pneumocytes although TNFα is not induced in respiratory epithelial cells. The cell signalling pathways responsible for this differential effect remain to be explored. Preliminary data suggest that such differential signalling involves p38 MAP kinase rather than NF-κB. SARS coronavirus infection of primary human macrophages is associated with a strong induction of chemokines without an associated type 1 interferon response. These observations may be relevant in disease pathogenesis. Copyright © Novartis Foundation 2006. link_to_subscribed_fulltext