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Eurosurveillance, Volume 22, Issue 8, 23 February 2017
Rapid communication
Emergence of a novel subclade of influenza A(H3N2) virus in London, December 2016 to January 2017
H Harvala 1 2 , D Frampton 2 , P Grant 1 , J Raffle 2 , RB Ferns 2 3 , Z Kozlakidis 2 , P Kellam 4 , D Pillay 2 , A Hayward 5 , E Nastouli 1 3 6 , For the ICONIC Consortium 7
+ Author affiliations
1. Department of Clinical Virology, University College London Hospitals NHS Foundation Trust, London, United Kingdom
2. Department of Infection and Immunity, University College of London, London, United Kingdom
3. NIHR UCLH/UCL Biomedical Research Centre, London, United Kingdom
4. Department of Medicine, Imperial College Faculty of Medicine, London, United Kingdom
5. Department of Infectious Disease Informatics, Farr Institute of Health Informatics Research, London, United Kingdom
6. Department of Population, Policy and Practice, UCL GOS Institute of Child Health, London, United Kingdom
7. The members of these networks are listed at the end of the article
Correspondence: Eleni Nastouli (e.nastouli@ucl.ac.uk), Heli Harvala (heli.harvala@uclh.nhs.uk)
Citation style for this article: Harvala H, Frampton D, Grant P, Raffle J, Ferns RB, Kozlakidis Z, Kellam P, Pillay D, Hayward A, Nastouli E, For the ICONIC Consortium. Emergence of a novel subclade of influenza A(H3N2) virus in London, December 2016 to January 2017. Euro Surveill. 2017;22(8):pii=30466. DOI: http://dx.doi.org/10.2807/1560-7917.ES.2017.22.8.30466
Received:13 February 2017; Accepted:23 February 2017
We report the molecular investigations of a large influenza A(H3N2) outbreak, in a season characterised by sharp increase in influenza admissions since December 2016. Analysis of haemagglutinin (HA) sequences demonstrated co-circulation of multiple clades (3C.3a, 3C.2a and 3C.2a1). Most variants fell into a novel subclade (proposed as 3C.2a2); they possessed four unique amino acid substitutions in the HA protein and loss of a potential glycosylation site. These changes potentially modify the H3N2 strain antigenicity.
full article
Rapid communication
Emergence of a novel subclade of influenza A(H3N2) virus in London, December 2016 to January 2017
H Harvala 1 2 , D Frampton 2 , P Grant 1 , J Raffle 2 , RB Ferns 2 3 , Z Kozlakidis 2 , P Kellam 4 , D Pillay 2 , A Hayward 5 , E Nastouli 1 3 6 , For the ICONIC Consortium 7
+ Author affiliations
1. Department of Clinical Virology, University College London Hospitals NHS Foundation Trust, London, United Kingdom
2. Department of Infection and Immunity, University College of London, London, United Kingdom
3. NIHR UCLH/UCL Biomedical Research Centre, London, United Kingdom
4. Department of Medicine, Imperial College Faculty of Medicine, London, United Kingdom
5. Department of Infectious Disease Informatics, Farr Institute of Health Informatics Research, London, United Kingdom
6. Department of Population, Policy and Practice, UCL GOS Institute of Child Health, London, United Kingdom
7. The members of these networks are listed at the end of the article
Correspondence: Eleni Nastouli (e.nastouli@ucl.ac.uk), Heli Harvala (heli.harvala@uclh.nhs.uk)
Citation style for this article: Harvala H, Frampton D, Grant P, Raffle J, Ferns RB, Kozlakidis Z, Kellam P, Pillay D, Hayward A, Nastouli E, For the ICONIC Consortium. Emergence of a novel subclade of influenza A(H3N2) virus in London, December 2016 to January 2017. Euro Surveill. 2017;22(8):pii=30466. DOI: http://dx.doi.org/10.2807/1560-7917.ES.2017.22.8.30466
Received:13 February 2017; Accepted:23 February 2017
We report the molecular investigations of a large influenza A(H3N2) outbreak, in a season characterised by sharp increase in influenza admissions since December 2016. Analysis of haemagglutinin (HA) sequences demonstrated co-circulation of multiple clades (3C.3a, 3C.2a and 3C.2a1). Most variants fell into a novel subclade (proposed as 3C.2a2); they possessed four unique amino acid substitutions in the HA protein and loss of a potential glycosylation site. These changes potentially modify the H3N2 strain antigenicity.
full article