Giuseppe
Emeritus
Authors? reply. Virological analysis of fatal influenza cases in the United Kingdom during the early wave of influenza in winter 2010/11 (Euro Surveill., extract, edited)
[Source: Eurosurveillance, full text: <cite cite="http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19773">Eurosurveillance - View Article</cite>. Extract, edited.]
Eurosurveillance, Volume 16, Issue 4, 27 January 2011
Letters
Authors? reply. Virological analysis of fatal influenza cases in the United Kingdom during the early wave of influenza in winter 2010/11
J Ellis 1, M Galiano 1, R Pebody 1, A Lackenby 1, CI Thompson 1, A Bermingham 1, E McLean 1, H Zhao 1, S Bolotin 1, O Dar 1, J M Watson 1, M Zambon 1
1. Health Protection Agency, Centre for Infections, London United Kingdom
Citation style for this article: Ellis J, Galiano M, Pebody R, Lackenby A, Thompson C, Bermingham A, McLean E, Zhao H, Bolotin S, Dar O, Watson JM, Zambon M. Authors? reply. Virological analysis of fatal influenza cases in the United Kingdom during the early wave of influenza in winter 2010/11. Euro Surveill. 2011;16(4)
ii=19773. Available online: http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19773
Date of submission: 27 January 2011
To the editors:
Our Italian colleagues provide commentary on an important question, as yet unresolved, regarding the relationship between pathogenesis of influenza A(H1N1)2009 infection and mutation in particular viral genes contributing to virulence. Viral haemagglutinin (HA) is the key virulence determining gene for influenza in birds, and a major determinant for host cell tropism in mammalian influenza [1]. The link between cell tropism and virulence in humans remains unclear; many different approaches to this question conclude that virulence is associated with multiple viral genes, including genes determining replication efficiency (polymerase genes) and non-structural genes governing the interaction with the host immune response. The emergence of animal viruses into the human population is associated with adaptive mutations [2-3] and tracking substitutions at residues known to be associated with such adaptive changes is an important surveillance function. The commentary highlights the opportunities arising from surveillance to develop and apply hypothesis generating questions from observational data sets.
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[Source: Eurosurveillance, full text: <cite cite="http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19773">Eurosurveillance - View Article</cite>. Extract, edited.]
Eurosurveillance, Volume 16, Issue 4, 27 January 2011
Letters
Authors? reply. Virological analysis of fatal influenza cases in the United Kingdom during the early wave of influenza in winter 2010/11
J Ellis 1, M Galiano 1, R Pebody 1, A Lackenby 1, CI Thompson 1, A Bermingham 1, E McLean 1, H Zhao 1, S Bolotin 1, O Dar 1, J M Watson 1, M Zambon 1
1. Health Protection Agency, Centre for Infections, London United Kingdom
Citation style for this article: Ellis J, Galiano M, Pebody R, Lackenby A, Thompson C, Bermingham A, McLean E, Zhao H, Bolotin S, Dar O, Watson JM, Zambon M. Authors? reply. Virological analysis of fatal influenza cases in the United Kingdom during the early wave of influenza in winter 2010/11. Euro Surveill. 2011;16(4)
Date of submission: 27 January 2011
To the editors:
Our Italian colleagues provide commentary on an important question, as yet unresolved, regarding the relationship between pathogenesis of influenza A(H1N1)2009 infection and mutation in particular viral genes contributing to virulence. Viral haemagglutinin (HA) is the key virulence determining gene for influenza in birds, and a major determinant for host cell tropism in mammalian influenza [1]. The link between cell tropism and virulence in humans remains unclear; many different approaches to this question conclude that virulence is associated with multiple viral genes, including genes determining replication efficiency (polymerase genes) and non-structural genes governing the interaction with the host immune response. The emergence of animal viruses into the human population is associated with adaptive mutations [2-3] and tracking substitutions at residues known to be associated with such adaptive changes is an important surveillance function. The commentary highlights the opportunities arising from surveillance to develop and apply hypothesis generating questions from observational data sets.
(...)
-
-----