Pathogenesis of avian flu H5N1 and SARS.
Identifieur interne : 003D87 ( Main/Exploration ); précédent : 003D86; suivant : 003D88Pathogenesis of avian flu H5N1 and SARS.
Auteurs : Malik Peiris [Hong Kong]Source :
- Novartis Foundation symposium [ 1528-2511 ] ; 2006.
Descripteurs français
- KwdFr :
- Animaux, Grippe humaine (anatomopathologie), Grippe humaine (virologie), Humains, Sous-type H5N1 du virus de la grippe A (pathogénicité), Sous-type H5N1 du virus de la grippe A (physiologie), Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (pathogénicité), Virus du SRAS (physiologie).
- MESH :
- anatomopathologie : Grippe humaine, Syndrome respiratoire aigu sévère.
- pathogénicité : Sous-type H5N1 du virus de la grippe A, Virus du SRAS.
- physiologie : Sous-type H5N1 du virus de la grippe A, Virus du SRAS.
- virologie : Grippe humaine, Syndrome respiratoire aigu sévère.
- Animaux, Humains.
English descriptors
- KwdEn :
- Animals, Humans, Influenza A Virus, H5N1 Subtype (pathogenicity), Influenza A Virus, H5N1 Subtype (physiology), Influenza, Human (pathology), Influenza, Human (virology), SARS Virus (pathogenicity), SARS Virus (physiology), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (virology).
- MESH :
- pathogenicity : Influenza A Virus, H5N1 Subtype, SARS Virus.
- pathology : Influenza, Human, Severe Acute Respiratory Syndrome.
- physiology : Influenza A Virus, H5N1 Subtype, SARS Virus.
- virology : Influenza, Human, Severe Acute Respiratory Syndrome.
- Animals, Humans.
Abstract
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 H1NI viruses, the H5N1 viruses hyper-induce cytokines (tumour necrosis factor [TNF]alpha, interferon beta) and chemokines (IP10, MIP1alpha, 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 TNFalpha 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-kappaB. 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.
PubMed: 17278385
Affiliations:
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Le document en format XML
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wicri:level="1"><nlm:affiliation>Department of Microbiology, The University of Hong Kong, University Pathology Building, Queen Mary Hospital Compound, Pokfulam, Hong Kong.</nlm:affiliation><country xml:lang="fr">Hong Kong</country><wicri:regionArea>Department of Microbiology, The University of Hong Kong, University Pathology Building, Queen Mary Hospital Compound, Pokfulam</wicri:regionArea><wicri:noRegion>Pokfulam</wicri:noRegion></affiliation></author></analytic><series><title level="j">Novartis Foundation symposium</title><idno type="ISSN">1528-2511</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Humans</term><term>Influenza A Virus, H5N1 Subtype (pathogenicity)</term><term>Influenza A Virus, H5N1 Subtype (physiology)</term><term>Influenza, Human (pathology)</term><term>Influenza, Human (virology)</term><term>SARS Virus 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Virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Sous-type H5N1 du virus de la grippe A</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Influenza, Human</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Sous-type H5N1 du virus de la grippe A</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Influenza A Virus, H5N1 Subtype</term><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Grippe humaine</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Influenza, Human</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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 H1NI viruses, the H5N1 viruses hyper-induce cytokines (tumour necrosis factor [TNF]alpha, interferon beta) and chemokines (IP10, MIP1alpha, 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 TNFalpha 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-kappaB. 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.</div></front></TEI><affiliations><list><country><li>Hong Kong</li></country></list><tree><country name="Hong Kong"><noRegion><name sortKey="Peiris, Malik" sort="Peiris, Malik" uniqKey="Peiris M" first="Malik" last="Peiris">Malik Peiris</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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