Pathogenesis of avian flu H5N1 and SARS
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 ar...
Main Author: | |
---|---|
Format: | Conference Object |
Language: | English |
Published: |
United Kingdom
2006
|
Subjects: | |
Online Access: | https://doi.org/10.1002/9780470035399.ch5 http://hdl.handle.net/10722/179846 |
id |
ftunivhongkonghu:oai:hub.hku.hk:10722/179846 |
---|---|
record_format |
openpolar |
spelling |
ftunivhongkonghu:oai:hub.hku.hk:10722/179846 2023-05-15T15:34:29+02:00 Pathogenesis of avian flu H5N1 and SARS Peiris, M 2006 https://doi.org/10.1002/9780470035399.ch5 http://hdl.handle.net/10722/179846 eng eng United Kingdom Novartis Foundation Symposium http://www.scopus.com/mlt/select.url?eid=2-s2.0-33847694909&selection=ref&src=s&origin=recordpage Novartis Foundation Symposium, 2006, v. 279, p. 56-60 doi:10.1002/9780470035399.ch5 60 134622 1528-2511 17278385 eid_2-s2.0-33847694909 56 http://hdl.handle.net/10722/179846 279 Sars Virus - Pathogenicity - Physiology Severe Acute Respiratory Syndrome - Pathology - Virology Animals Humans Influenza A Virus H5n1 Subtype - Pathogenicity - Physiology Influenza Human - Pathology - Virology Conference_Paper 2006 ftunivhongkonghu https://doi.org/10.1002/9780470035399.ch5 2023-01-14T15:54:58Z 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 Conference Object Avian flu University of Hong Kong: HKU Scholars Hub 56 65 |
institution |
Open Polar |
collection |
University of Hong Kong: HKU Scholars Hub |
op_collection_id |
ftunivhongkonghu |
language |
English |
topic |
Sars Virus - Pathogenicity - Physiology Severe Acute Respiratory Syndrome - Pathology - Virology Animals Humans Influenza A Virus H5n1 Subtype - Pathogenicity - Physiology Influenza Human - Pathology - Virology |
spellingShingle |
Sars Virus - Pathogenicity - Physiology Severe Acute Respiratory Syndrome - Pathology - Virology Animals Humans Influenza A Virus H5n1 Subtype - Pathogenicity - Physiology Influenza Human - Pathology - Virology Peiris, M Pathogenesis of avian flu H5N1 and SARS |
topic_facet |
Sars Virus - Pathogenicity - Physiology Severe Acute Respiratory Syndrome - Pathology - Virology Animals Humans Influenza A Virus H5n1 Subtype - Pathogenicity - Physiology Influenza Human - Pathology - Virology |
description |
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 |
format |
Conference Object |
author |
Peiris, M |
author_facet |
Peiris, M |
author_sort |
Peiris, M |
title |
Pathogenesis of avian flu H5N1 and SARS |
title_short |
Pathogenesis of avian flu H5N1 and SARS |
title_full |
Pathogenesis of avian flu H5N1 and SARS |
title_fullStr |
Pathogenesis of avian flu H5N1 and SARS |
title_full_unstemmed |
Pathogenesis of avian flu H5N1 and SARS |
title_sort |
pathogenesis of avian flu h5n1 and sars |
publisher |
United Kingdom |
publishDate |
2006 |
url |
https://doi.org/10.1002/9780470035399.ch5 http://hdl.handle.net/10722/179846 |
genre |
Avian flu |
genre_facet |
Avian flu |
op_relation |
Novartis Foundation Symposium http://www.scopus.com/mlt/select.url?eid=2-s2.0-33847694909&selection=ref&src=s&origin=recordpage Novartis Foundation Symposium, 2006, v. 279, p. 56-60 doi:10.1002/9780470035399.ch5 60 134622 1528-2511 17278385 eid_2-s2.0-33847694909 56 http://hdl.handle.net/10722/179846 279 |
op_doi |
https://doi.org/10.1002/9780470035399.ch5 |
container_start_page |
56 |
op_container_end_page |
65 |
_version_ |
1766364863234310144 |