Innate immune responses to influenza A H5N1: friend or foe?
Identifieur interne : 000431 ( Ncbi/Curation ); précédent : 000430; suivant : 000432Innate immune responses to influenza A H5N1: friend or foe?
Auteurs : Jsm Peiris [République populaire de Chine] ; Cy Cheung [République populaire de Chine] ; Cyh Leung [République populaire de Chine] ; Jm Nicholls [République populaire de Chine]Source :
- Trends in immunology [ 1471-4906 ] ; 2009.
Abstract
Avian influenza A H5N1 remains unusual in its virulence for humans. While infection of humans remains inefficient, many of those with H5N1 disease have a rapidly progressing viral pneumonia leading to acute respiratory distress syndrome and death but its pathogenesis remains an enigma. Comparisons in the virology and pathogenesis of human seasonal influenza viruses (H3N2 and H1N1) and H5N1 in patients, animal models and in relevant primary human cell cultures remains instructive. While the direct effects of viral replication and differences in the tropism of the virus for cells in the lower respiratory tract clearly contribute to the pathogenesis, we focus here on the possible contribution of the host innate immune response in the pathogenesis of this disease.
Url:
DOI: 10.1016/j.it.2009.09.004
PubMed: 19864182
PubMed Central: 5068224
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PMC:5068224Le document en format XML
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<front><div type="abstract" xml:lang="en"><p id="P1">Avian influenza A H5N1 remains unusual in its virulence for humans. While infection of humans remains inefficient, many of those with H5N1 disease have a rapidly progressing viral pneumonia leading to acute respiratory distress syndrome and death but its pathogenesis remains an enigma. Comparisons in the virology and pathogenesis of human seasonal influenza viruses (H3N2 and H1N1) and H5N1 in patients, animal models and in relevant primary human cell cultures remains instructive. While the direct effects of viral replication and differences in the tropism of the virus for cells in the lower respiratory tract clearly contribute to the pathogenesis, we focus here on the possible contribution of the host innate immune response in the pathogenesis of this disease.</p>
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