Predominance of influenza B/Yamagata lineage viruses in Bulgaria during the 2017/2018 season

Abstract

In this study, we investigated the antigenic and genetic characteristics of influenza viruses circulating in Bulgaria during the 2017/2018 season. The detection and typing/subtyping of influenza viruses were performed using real-time RT-PCR. Results of antigenic characterisation, phylogenetic and amino acid sequence analyses of representative influenza strains are presented. The season was characterised by the predominance of B/Yamagata viruses, accounting for 77% of detected influenza viruses, followed by A(H1N1)pdm09 (17%), B/Victoria (3.7%) and A(H3N2) (2.4%). The sequenced B/Yamagata, B/Victoria, A(H1N1)pdm09 and A(H3N2) viruses belonged to the genetic groups 3, 1A, 6B.1 and 3C.2a1, respectively. Amino acid analysis of B/Yamagata isolates revealed the presence of three changes in haemagglutinin (HA), eight changes in neuraminidase (NA) and a number of substitutions in internal proteins compared with the B/Phucket/3073/2013 vaccine virus. Despite the amino acid changes, B/Yamagata viruses remained antigenically related to the vaccine strain. B/Victoria isolates fell into a group of viruses with double deletion (Δ162–163) in HA1. Substitutions in HA and NA sequences of B/Victoria, A(H1N1)pdm09 and A(H3N2) viruses were also identified compared with the vaccine strains, including in antigenic sites. The results of this study confirm the genetic variability of circulating influenza viruses and the need for continual antigenic and molecular surveillance.

Divergent evolutionary trajectories of influenza B viruses underlie their contemporaneous epidemic activity

“…We also observed a marked change in population dynamics of Yamagata viruses that, from 2002 to 2013, were previously subject to weaker natural selection pressure with relatively low and constant levels of genetic diversity (10). However, from 2015 onwards, we observed more frequent seasonal oscillations in genetic diversity that coincide with global epidemics of Yamagata viruses (16)(17)(18)(19). The influenza vaccine strain for the Yamagata lineage (B/Phuket/ 3073/2013-like) has remain unchanged since 2015, and antigenic characterization of recent clade 3 viruses shows good crossreactivity with the vaccine strain (25), consistent with the lack of amino acid substitutions in the HA of these viruses.…”

“…Historically, influenza B virus epidemics have been characteristically low to sporadic in most countries during a year, with influenza A viruses predominant in most countries. Since the first reports of high influenza B virus activity in Europe in 2015, substantial epidemics have been reported globally, indicating major changes in the evolutionary and epidemiological dynamics of influenza B viruses (12,(15)(16)(17)(18)(19).…”

“…Here, we analyzed all available influenza B genomic data (>12,000) in combination with 158 genomes sequenced from Singapore to investigate the processes enabling the recent resurgence of epidemics due to influenza B virus (see global epidemic activity in SI Appendix, Fig. S1) (12,(16)(17)(18)(19). Our results show that both lineages have undergone selective sweeps prior to resurgence that follow long periods of HA divergence; however, Victoria and Yamagata viruses showed significantly different strategies for epidemiological success.…”

“…2B (Table 2 and SI Appendix, Figs. S15-S23), suggesting these mutations may have contributed to the severe epidemics observed in 2018 (16)(17)(18)(19).…”

High performance of rapid influenza diagnostic test and variable effectiveness of influenza vaccines in Mexico

“…Some study limitations include that we did not characterize the prevalence of B/Victoria/2/87-like and B/Yamagata/16/88-like lineages in our population to estimate influenza VE against these lineages. However, except for some Asian countries, epidemiological studies performed in different regions around the same period showed that the dominant influenza B virus lineage was the B/Yamagata/16/88-like lineage ( 2019; Korsun et al 2019). These data may explain our higher VE of the 2016-2017 IIV4 against influenza B, as the predominant lineage was absent in the IIV3.…”