F Xavier López-Labrador1, Angels Natividad-Sancho2, Maria Pisareva3, Andrey Komissarov4, Karina Salvatierra5, Artem Fadeev6, Andrés Moya7, Mikhail Grudinin8, Javier Díez-Domingo9, Olga Afanasieva10, Nadezhda Konovalova11, Anna Sominina12, Joan Puig-Barberà13. 1. Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunidad Valenciana (FISABIO), Avda. de Catalunya, 21, 46020 Valencia, Spain; Joint Units of Infection and of Genomics and Health, FISABIO/Cavanilles Institute for Biodiversity and Evolutionary Biology, University of Valencia, Spain; Centro de Investigación Biomédica en Red de Epidemiología y Salud Publica (CIBER-ESP), Instituto de Salud Carlos III, Spain. Electronic address: F.Xavier.Lopez@uv.es. 2. Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunidad Valenciana (FISABIO), Avda. de Catalunya, 21, 46020 Valencia, Spain. Electronic address: angels.natividad@hotmail.co.uk. 3. Research Institute of Influenza, Ministry of Health, Prof. Popov Str. 15/17, St. Petersburg, Russian Federation. Electronic address: pisareva@influenza.spb.ru. 4. Research Institute of Influenza, Ministry of Health, Prof. Popov Str. 15/17, St. Petersburg, Russian Federation. Electronic address: komissarov@influenza.spb.ru. 5. Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunidad Valenciana (FISABIO), Avda. de Catalunya, 21, 46020 Valencia, Spain; Joint Units of Infection and of Genomics and Health, FISABIO/Cavanilles Institute for Biodiversity and Evolutionary Biology, University of Valencia, Spain. Electronic address: kariales@gmail.com. 6. Research Institute of Influenza, Ministry of Health, Prof. Popov Str. 15/17, St. Petersburg, Russian Federation. Electronic address: artem.fadeev@influenza.spb.ru. 7. Joint Units of Infection and of Genomics and Health, FISABIO/Cavanilles Institute for Biodiversity and Evolutionary Biology, University of Valencia, Spain. Electronic address: andres.moya@uv.es. 8. Research Institute of Influenza, Ministry of Health, Prof. Popov Str. 15/17, St. Petersburg, Russian Federation. Electronic address: grudinin@influenza.spb.ru. 9. Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunidad Valenciana (FISABIO), Avda. de Catalunya, 21, 46020 Valencia, Spain. Electronic address: diez_jav@gva.es. 10. Research Institute of Influenza, Ministry of Health, Prof. Popov Str. 15/17, St. Petersburg, Russian Federation. Electronic address: olga-afanaseva57@mail.ru. 11. Research Institute of Influenza, Ministry of Health, Prof. Popov Str. 15/17, St. Petersburg, Russian Federation. Electronic address: konovalova_nadya@mail.ru. 12. Research Institute of Influenza, Ministry of Health, Prof. Popov Str. 15/17, St. Petersburg, Russian Federation. Electronic address: anna@influenza.spb.ru. 13. Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunidad Valenciana (FISABIO), Avda. de Catalunya, 21, 46020 Valencia, Spain. Electronic address: puig_joa@gva.es.
Abstract
BACKGROUND: Continuous surveillance for genetic changes in circulating influenza viruses is needed to guide influenza prevention and control. OBJECTIVES: To compare intra-seasonal influenza genetic diversity of hemagglutinin in influenza A strains isolated from influenza hospital admissions collected at two distinct sites during the same season. STUDY DESIGN: Comparative phylogenetic analysis of full-length hemagglutinin genes from 77 isolated influenza A viruses from the St. Petersburg, Russian Federation and Valencia, Spain sites of the Global Influenza Hospital Surveillance Network (GIHSN) during the 2013/14 season. RESULTS: We found significant variability in A(H3N2) and A(H1N1)pdm09 viruses between the two sites, with nucleotide variation at antigenic positions much lower for A(H1N1)pdm09 than for A(H3N2) viruses. For A(H1N1)pdm09, antigenic sites differed by three to four amino acids from the vaccine strain, two of them common to all tested isolates. For A(H3N2) viruses, antigenic sites differed by six to nine amino acids from the vaccine strain, four of them common to all tested isolates. A fifth amino acid substitution in the antigenic sites of A(H3N2) defined a new clade, 3C.2. For both influenza A subtypes, pairwise amino acid distances between circulating viruses and vaccine strains were significantly higher at antigenic than at non-antigenic sites. Whereas A(H1N1)pdm09 viruses clustered with clade 6B and 94% of A(H3N2) with clade 3C.3, at both study sites A(H3N2) clade 3C.2 viruses emerged towards the end of the season, showing greater pairwise amino acid distances from the vaccine strain compared to the predominant clade 3C.3. CONCLUSIONS: Influenza A antigenic variants differed between St. Petersburg and Valencia, and A(H3N2) clade 3C.2 viruses were characterized by more amino acid differences from the vaccine strain, especially at the antigenic sites. Copyright Â
BACKGROUND: Continuous surveillance for genetic changes in circulating influenza viruses is needed to guide influenza prevention and control. OBJECTIVES: To compare intra-seasonal influenza genetic diversity of hemagglutinin in influenza A strains isolated from influenza hospital admissions collected at two distinct sites during the same season. STUDY DESIGN: Comparative phylogenetic analysis of full-length hemagglutinin genes from 77 isolated influenza A viruses from the St. Petersburg, Russian Federation and Valencia, Spain sites of the Global Influenza Hospital Surveillance Network (GIHSN) during the 2013/14 season. RESULTS: We found significant variability in A(H3N2) and A(H1N1)pdm09 viruses between the two sites, with nucleotide variation at antigenic positions much lower for A(H1N1)pdm09 than for A(H3N2) viruses. For A(H1N1)pdm09, antigenic sites differed by three to four amino acids from the vaccine strain, two of them common to all tested isolates. For A(H3N2) viruses, antigenic sites differed by six to nine amino acids from the vaccine strain, four of them common to all tested isolates. A fifth amino acid substitution in the antigenic sites of A(H3N2) defined a new clade, 3C.2. For both influenza A subtypes, pairwise amino acid distances between circulating viruses and vaccine strains were significantly higher at antigenic than at non-antigenic sites. Whereas A(H1N1)pdm09 viruses clustered with clade 6B and 94% of A(H3N2) with clade 3C.3, at both study sites A(H3N2) clade 3C.2 viruses emerged towards the end of the season, showing greater pairwise amino acid distances from the vaccine strain compared to the predominant clade 3C.3. CONCLUSIONS: Influenza A antigenic variants differed between St. Petersburg and Valencia, and A(H3N2) clade 3C.2 viruses were characterized by more amino acid differences from the vaccine strain, especially at the antigenic sites. Copyright Â