Abstract
Respiratory syncytial virus (RSV) is recognised as a leading cause of severe acute respiratory disease and deaths among infants and vulnerable adults. Clinical RSV isolates can be divided into several known genotypes. RSV genotype BA, characterised by a 60-nucleotide duplication in the G glycoprotein gene, emerged in 1999 and quickly disseminated globally replacing other RSV group B genotypes. Continual molecular epidemiology is critical to understand the evolutionary processes maintaining the success of the BA viruses. We analysed 735 G gene sequences from samples collected from paediatric patients in Kilifi, Kenya, between 2003 and 2017. The virus population comprised of several genetically distinct variants (n = 56) co-circulating within and between epidemics. In addition, there was consistent seasonal fluctuations in relative genetic diversity. Amino acid changes increasingly accumulated over the surveillance period including two residues (N178S and Q180R) that mapped to monoclonal antibody 2D10 epitopes, as well as addition of putative N-glycosylation sequons. Further, switching and toggling of amino acids within and between epidemics was observed. On a global phylogeny, the BA viruses from different countries form geographically isolated clusters suggesting substantial localized variants. This study offers insights into longitudinal population dynamics of a globally endemic RSV genotype within a discrete location.
Highlights
Respiratory syncytial virus (RSV) is a leading cause of severe lower respiratory tract infections, with an estimated 3.2 million annual hospitalizations and approximately 60,000 deaths globally, primarily in children younger than 1-year-old[1,2,3]
We analyzed the G glycoprotein of RSVB genotype BA strains collected over 15 successive RSV epidemics in Kilifi
Over 15 RSV epidemics (2002 to 2017), a total of 903/12203 (7.4%) respiratory samples tested positive for RSVB
Summary
Respiratory syncytial virus (RSV) is a leading cause of severe lower respiratory tract infections, with an estimated 3.2 million annual hospitalizations and approximately 60,000 deaths globally, primarily in children younger than 1-year-old[1,2,3]. In 1999, the RSVB genotype BA emerged with a 60-nucleotide duplication in the G gene and disseminated globally, replacing all other RSVB g enotypes[14,15] It is likely the additional residues of the 60-nucleotide duplication provide a selective advantage and modified the antigenic characteristics of the G protein, allowing escape from antibody neutralization, as well as enhancing fitness[15]. Studying the genetic and antigenic evolution of local strains is crucial for understanding how annual RSV epidemics are maintained locally. This may help with designing comprehensive infection reduction/control measures and rationalize respiratory virus epidemic response p olicies[24,25]. This work extends previous analyses[18,24] by a further six years of new data and augments our knowledge of the evolutionary trajectory and adaptation of a single RSV genotype in a single local setting when observed longitudinally
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