tetano
Editor, Senior Moderator
Eurosurveillance, Volume 20, Issue 18, 07 May 2015
Research articles
Haemagglutinin mutations and glycosylation changes shaped the 2012/13 influenza A(H3N2) epidemic, Houston, Texas
K M Stucker[SUP]1[/SUP], S A Schobel[SUP]2[/SUP][SUP],3[/SUP], R J Olsen[SUP]4[/SUP], H L Hodges[SUP]1[/SUP][SUP],5[/SUP], X Lin[SUP]1[/SUP], R A Halpin[SUP]1[/SUP], N Fedorova[SUP]1[/SUP], T B Stockwell[SUP]2[/SUP], A Tovchigrechko[SUP]6[/SUP], S R Das[SUP]1[/SUP], D E Wentworth (
)[SUP]1[/SUP][SUP],7[/SUP], J M Musser (
)[SUP]4[/SUP]
Citation style for this article: Stucker KM, Schobel SA, Olsen RJ, Hodges HL, Lin X, Halpin RA, Fedorova N, Stockwell TB, Tovchigrechko A, Das SR, Wentworth DE, Musser JM. Haemagglutinin mutations and glycosylation changes shaped the 2012/13 influenza A(H3N2) epidemic, Houston, Texas. Euro Surveill. 2015;20(18)
ii=21122. Available online: http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=21122
Date of submission: 30 October 2014
[SIZE=+0]While the early start and higher intensity of the 2012/13 influenza A virus (IAV) epidemic was not unprecedented, it was the first IAV epidemic season since the 2009 H1N1 influenza pandemic where the H3N2 subtype predominated. We directly sequenced the genomes of 154 H3N2 clinical specimens collected throughout the epidemic to better understand the evolution of H3N2 strains and to inform the H3N2 vaccine selection process. Phylogenetic analyses indicated that multiple co-circulating clades and continual antigenic drift in the haemagglutinin (HA) of clades 5, 3A, and 3C, with the evolution of a new 3C subgroup (3C-2012/13), were the driving causes of the epidemic. Drift variants contained HA substitutions and alterations in the potential N-linked glycosylation sites of HA. Antigenic analysis demonstrated that viruses in the emerging subclade 3C.3 and subgroup 3C-2012/13 were not well inhibited by antisera generated against the 3C.1 vaccine strains used for the 2012/13 (A/Victoria/361/2011) or 2013/14 (A/Texas/50/2012) seasons. Our data support updating the H3N2 vaccine strain to a clade 3C.2 or 3C.3-like strain or a subclade that has drifted further. They also underscore the challenges in vaccine strain selection, particularly regarding HA and neuraminidase substitutions derived during laboratory passage that may alter antigenic testing accuracy.?
full article[/SIZE]
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=21122
Research articles
Haemagglutinin mutations and glycosylation changes shaped the 2012/13 influenza A(H3N2) epidemic, Houston, Texas
K M Stucker[SUP]1[/SUP], S A Schobel[SUP]2[/SUP][SUP],3[/SUP], R J Olsen[SUP]4[/SUP], H L Hodges[SUP]1[/SUP][SUP],5[/SUP], X Lin[SUP]1[/SUP], R A Halpin[SUP]1[/SUP], N Fedorova[SUP]1[/SUP], T B Stockwell[SUP]2[/SUP], A Tovchigrechko[SUP]6[/SUP], S R Das[SUP]1[/SUP], D E Wentworth (
- Virology Group, J. Craig Venter Institute, Rockville, Maryland, United States
- Bioinformatics Group, J. Craig Venter Institute, Rockville, Maryland, United States
- Center for Bioinformatics and Computational Biology, University of Maryland, College Park, Maryland, United States
- Department of Pathology and Genomic Medicine, Houston Methodist Hospital, and Center for Molecular and Translational Human Infectious Diseases Research, Houston Methodist Research Institute, Houston, Texas, United States
- Current address: Department of Chemistry, University of Wisconsin-Madison, Madison, Wisconsin, United States
- Genomic Medicine Group, J. Craig Venter Institute, Rockville, Maryland, United States
- Current address: Virology Surveillance and Diagnosis Branch, Influenza Division, Centers for Disease Control and Prevention, Atlanta, Georgia, United States
Citation style for this article: Stucker KM, Schobel SA, Olsen RJ, Hodges HL, Lin X, Halpin RA, Fedorova N, Stockwell TB, Tovchigrechko A, Das SR, Wentworth DE, Musser JM. Haemagglutinin mutations and glycosylation changes shaped the 2012/13 influenza A(H3N2) epidemic, Houston, Texas. Euro Surveill. 2015;20(18)
ii=21122. Available online: http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=21122Date of submission: 30 October 2014
[SIZE=+0]While the early start and higher intensity of the 2012/13 influenza A virus (IAV) epidemic was not unprecedented, it was the first IAV epidemic season since the 2009 H1N1 influenza pandemic where the H3N2 subtype predominated. We directly sequenced the genomes of 154 H3N2 clinical specimens collected throughout the epidemic to better understand the evolution of H3N2 strains and to inform the H3N2 vaccine selection process. Phylogenetic analyses indicated that multiple co-circulating clades and continual antigenic drift in the haemagglutinin (HA) of clades 5, 3A, and 3C, with the evolution of a new 3C subgroup (3C-2012/13), were the driving causes of the epidemic. Drift variants contained HA substitutions and alterations in the potential N-linked glycosylation sites of HA. Antigenic analysis demonstrated that viruses in the emerging subclade 3C.3 and subgroup 3C-2012/13 were not well inhibited by antisera generated against the 3C.1 vaccine strains used for the 2012/13 (A/Victoria/361/2011) or 2013/14 (A/Texas/50/2012) seasons. Our data support updating the H3N2 vaccine strain to a clade 3C.2 or 3C.3-like strain or a subclade that has drifted further. They also underscore the challenges in vaccine strain selection, particularly regarding HA and neuraminidase substitutions derived during laboratory passage that may alter antigenic testing accuracy.?
full article[/SIZE]
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=21122