A(H1N1)pdm09 influenza infection: vaccine inefficiency

Abstract

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.

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

“…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.…”

“…Antigenic site distribution of the common mutations detected by us was like those of other studies carried out in the same period: S162N and K163Q in Sa, S203T in Ca1, and S185T/P in Sb . Particularly, S185T/P located in antigenic site Sb was also residing within the 190‐helix domain of the receptor‐binding site, and the amino acid changes in or near the RBS domain of HA had previously been shown to influence the antigenic properties of influenza A(H1N1)pdm09 viruses .…”

“…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 …”

“…18 19 Korsun et al, 20 Clark et al, 21 Puig-Barberà et al, 22 Mohebbi et al 23 Cocirculation of 6B.1 and 6B.2 isolates was also observed in some other studies. [24][25][26][27][28] In the 2009-2010 and 2010-2011 seasons, the HA nucleotide sequence similarity rates between Turkish isolates and the A/ California/07/2009 virus were >98.9% and >98.7%, respectively, 11,12 but the similarity ranging 96.6% to 97.2% we observed in the 2015-2016 season was pointing out a rising divergence from the progenitor virus compared to the previous seasons. 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 12 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).…”

“…The common HA mutations detected in Turkish isolates of the 2015‐2016 season have previously been identified by other groups, and the accessibility of residues associated with antigenic sites and their possible impact in the antigenicity of the protein has already been discussed in detail . Despite carrying a higher number of HA mutations compared to the progenitor virus, the new subclades 6B.1 and 6B.2 of the 2015‐2016 season were closely related to the vaccine virus A/California/7/2009 and found to be antigenically indistinguishable by postinfection ferret antisera.…”