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Molecular mechanisms of interspecies transmission and pathogenicity of influenza viruses: Lessons from the 2009 pandemic

Identifieur interne : 000D31 ( Main/Exploration ); précédent : 000D30; suivant : 000D32

Molecular mechanisms of interspecies transmission and pathogenicity of influenza viruses: Lessons from the 2009 pandemic

Auteurs : Hans D. Klenk [Allemagne] ; Wolfgang Garten [Allemagne] ; Mikhail Matrosovich [Allemagne]

Source :

RBID : ISTEX:78EFEEA43563CF0703E7B85361688C343720DF2B

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English descriptors

Abstract

The emergence of the 2009 H1N1 virus pandemic was unexpected, since it had been predicted that the next pandemic would be caused by subtype H5N1. We also had to learn that a pandemic does not necessarily require the introduction of a new virus subtype into the human population, but that it may result from antigenic shift within the same subtype. The new variant was derived from human and animal viruses by genetic reassortment in the pig, supporting the concept that this animal is the mixing vessel for the generation of new human influenza viruses. Although it is generally believed that the 2009 outbreak was mild, there have been severe cases particularly among the young and the middle‐aged. Pathogenicity and host range are determined to a large extent by the polymerase, the haemagglutinin and the NS1 protein of influenza A viruses. There is evidence that mutations of these proteins may change the pathogenicity of the new virus.
The unexpected emergence of the 2009 H1N1 pandemic showed that an influenza pandemic does not necessarily require the introduction of a new virus subtype into the human population but may also result from antigenic shift within the same subtype.

Url:
DOI: 10.1002/bies.201000118


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<front>
<div type="abstract" xml:lang="en">The emergence of the 2009 H1N1 virus pandemic was unexpected, since it had been predicted that the next pandemic would be caused by subtype H5N1. We also had to learn that a pandemic does not necessarily require the introduction of a new virus subtype into the human population, but that it may result from antigenic shift within the same subtype. The new variant was derived from human and animal viruses by genetic reassortment in the pig, supporting the concept that this animal is the mixing vessel for the generation of new human influenza viruses. Although it is generally believed that the 2009 outbreak was mild, there have been severe cases particularly among the young and the middle‐aged. Pathogenicity and host range are determined to a large extent by the polymerase, the haemagglutinin and the NS1 protein of influenza A viruses. There is evidence that mutations of these proteins may change the pathogenicity of the new virus.</div>
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