Predominance of influenza A(H1N1)pdm09 virus genetic subclade 6B.1 and influenza B/Victoria lineage viruses at the start of the 2015/16 influenza season in Europe

Broberg, Eeva; Melidou, Angeliki; Prosenc, Katarina; Bragstad, Karoline; Hungnes, Olav

doi:10.2807/1560-7917.es.2016.21.13.30184

Cited by 39 publications

(39 citation statements)

References 10 publications

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“…Accordingly, the total number of amino acid mutations (14 common, 1 less common, and 11 rare) in the 2015‐2016 season was higher than of the previously reported by Guldemir et al The 90%‐100% of our isolates carried 14 common mutations (P83S, S84N, D97N, S162N, K163Q, S185T, S203T, I216T, A256T, K283E, I321V in HA1 and E47K, S124N, E172K in HA2). These mutations have been previously reported from different parts of the world in isolates of the same period . A less common S185P mutation was seen instead of S185T in 10% of our isolates, and we also identified rare mutations (C4S, T72A, I96V, N260D, I266F, L314M, S326F in HA1 and I45V, V66A, R106K, F140L in HA2) in individual isolates.…”

Section: Discussionsupporting

confidence: 87%

“…Regarding the 2015‐2016 season, subclades 6B.1 and 6B.2 appeared as new clusters in clade 6B. In Turkey, all studied influenza A(H1N1)pdm09 isolates of this season belonged only to 6B.1 as detected in studies by Komissarov et al, Korsun et al, Clark et al, Puig‐Barberà et al, Mohebbi et al Cocirculation of 6B.1 and 6B.2 isolates was also observed in some other studies …”

Section: Discussionsupporting

confidence: 64%

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Molecular characterization of the influenza A(H1N1)pdm09 isolates collected in the 2015‐2016 season and comparison of HA mutations detected in Turkey since 2009

Güldemir

Coşkun-Ari

Altaş

et al. 2019

Journal of Medical Virology

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Influenza A(H1N1)pdm09 pandemic virus causing the 2009 global outbreak moved into the post‐pandemic period, but its variants continued to be the prevailing subtype in the 2015‐2016 influenza season in Europe and Asia. To determine the molecular characteristics of influenza A(H1N1)pdm09 isolates circulating during the 2015‐2016 season in Turkey, we identified mutations in the hemagglutinin (HA) genes and investigated the presence of H275Y alteration in the neuraminidase genes in the randomly selected isolates. The comparison of the HA nucleotide sequences revealed a very high homology (>99.5%) among the studied influenza A(H1N1)pdm09 isolates, while a relatively low homology (96.6%‐97.2%), was observed between Turkish isolates and the A/California/07/2009 vaccine virus. Overall 14 common mutations were detected in HA sequences of all 2015‐2016 influenza A(H1N1)pdm09 isolates with respect to the A/California/07/2009 virus, four of which located in three different antigenic sites. Eleven rare mutations in 12 HA sequences were also detected. Phylogenetic analysis revealed that all characterized influenza A(H1N1)pdm09 isolates formed a single genetic cluster, belonging to the genetic subclade 6B.1, defined by HA amino acid substitutions S84N, S162N, and I216T. Furthermore, all isolates showed an oseltamivir‐sensitive genotype, suggesting that Tamiflu (Oseltamivir) could still be the drug of choice in Turkey.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionsupporting

confidence: 64%

Molecular characterization of the influenza A(H1N1)pdm09 isolates collected in the 2015‐2016 season and comparison of HA mutations detected in Turkey since 2009

Güldemir

Coşkun-Ari

Altaş

et al. 2019

Journal of Medical Virology

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“…All 6B clade viruses in our analysis contained the amino acid variations that define this clade: D97N, K163Q, S185T, S203T, A256T and K283E (Table 1) [15–17]. Additional mutations included S84N, S162N and I216T in the 6B.1 clade and V152T, V173I, E491G, D501E in the 6B.2 clade [18].…”

Section: Resultsmentioning

confidence: 99%

“…Mutations K163Q, S185T, S203T (clade 6B) are respectively located on Sa, Sb and Ca1 antigenic sites. In addition, we found that S162N (clade 6B.1) located in Sa site [21] and V173I (clade 6B.2) in Ca1 site [15]. …”

Section: Resultsmentioning

confidence: 99%

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A(H1N1)pdm09 influenza infection: vaccine inefficiency

et al. 2017

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The last influenza pandemic, caused by the swine A(H1N1)pdm09 influenza virus, began in North America at 2009. Since then, the World Health Organization (WHO) recommended integration of the swine-based virus A/California/07/2009 strain in yearly vaccinations. Yet, infections with A(H1N1)pdm09 have continued in subsequent years. The reasons for this are currently unknown. During the 2015–2016 influenza season, we noted an increased prevalence of A(H1N1)pdm09 influenza virus infection in Israel. Our phylogenetic analysis indicated that the circulating A(H1N1)pdm09 strains belonged to 6B.1 and 6B.2 clades and differed from the vaccinating strain, with approximately 18 amino acid differences found between the circulating strains and the immunizing A/California/07/2009 strain. Hemmaglutination inhibition (HI) assays demonstrated higher antibodies titer against the A/California/07/2009 vaccinating strain as compared to the circulating Israeli strains. We thus suggest that the current vaccination was not sufficiently effective and propose inclusion of the current circulating A(H1N1)pdm09 influenza viruses in the annual vaccine composition.

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Antigenic drift of hemagglutinin and neuraminidase in seasonal H1N1 influenza viruses from Saudi Arabia in 2014 to 2015

Naeem

Elbakkouri

AlFaiz

et al. 2020

Journal of Medical Virology

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Antigenic drift of the hemagglutinin (HA) and neuraminidase (NA) proteins of the influenza virus cause a decrease in vaccine efficacy. Since the information about the evolution of these viruses in Saudi is deficient so we investigated the genetic diversity of circulating H1N1 viruses. Nasopharyngeal aspirates/swabs collected from 149 patients hospitalized with flu‐like symptoms during 2014 and 2015 were analyzed. Viral RNA extraction was followed by a reverse transcription‐polymerase chain reaction and genetic sequencing. We analyzed complete gene sequences of HA and NA from 80 positive isolates. Phylogenetic analysis of HA and NA genes of 80 isolates showed similar topologies and co‐circulation of clades 6b. Genetic diversity was observed among circulating viruses belonging to clade 6B.1A. The amino acid residues in the HA epitope domain were under purifying selection. Amino acid changes at key antigenic sites, such as position S101N, S179N (antigenic site‐Sa), I233T (antigenic site‐Sb) in the head domain might have resulted in antigenic drift and emergence of variant viruses. For NA protein, 36% isolates showed the presence of amino acid changes such as V13I (n = 29), I314M (n = 29) and 12% had I34V (n = 10). However, H257Y mutation responsible for resistance to neuraminidase inhibitors was missing. The presence of amino acid changes at key antigenic sites and their topologies with structural mapping of residues under purifying selection highlights the importance of antigenic drift and warrants further characterization of recently circulating viruses in view of vaccine effectiveness. The co‐circulation of several clades and the predominance of clade 6B.1 suggest multiple introductions in Saudi.

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Predominance of influenza A(H1N1)pdm09 virus genetic subclade 6B.1 and influenza B/Victoria lineage viruses at the start of the 2015/16 influenza season in Europe

Cited by 39 publications

References 10 publications

Molecular characterization of the influenza A(H1N1)pdm09 isolates collected in the 2015‐2016 season and comparison of HA mutations detected in Turkey since 2009

Molecular characterization of the influenza A(H1N1)pdm09 isolates collected in the 2015‐2016 season and comparison of HA mutations detected in Turkey since 2009

A(H1N1)pdm09 influenza infection: vaccine inefficiency

Antigenic drift of hemagglutinin and neuraminidase in seasonal H1N1 influenza viruses from Saudi Arabia in 2014 to 2015

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