Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2017 Feb;23(2):264-271.
doi: 10.3201/eid2302.161149.

Spread and Evolution of Respiratory Syncytial Virus A Genotype ON1, Coastal Kenya, 2010-2015

Free PMC article

Spread and Evolution of Respiratory Syncytial Virus A Genotype ON1, Coastal Kenya, 2010-2015

James R Otieno et al. Emerg Infect Dis. .
Free PMC article

Abstract

In February 2012, the novel respiratory syncytial virus (RSV) group A, genotype ON1, was detected in Kilifi County, coastal Kenya. ON1 is characterized by a 72-nt duplication within the highly variable G gene (encoding the immunogenic attachment surface protein). Cases were diagnosed through surveillance of pneumonia in children at the county hospital. Analysis of epidemiologic, clinical, and sequence data of RSV-A viruses detected over 5 RSV seasons (2010/2011 to 2014/2015) indicated the following: 1) replacement of previously circulating genotype GA2 ON1, 2) an abrupt expansion in the number of ON1 variants detected in the 2014/2015 epidemic, 3) recently accumulation of amino acid substitutions within the ON1 duplicated sequence, and 4) no clear evidence of altered pathogenicity relative to GA2. The study demonstrates the public health importance of molecular surveillance in defining the spread, clinical effects, and evolution of novel respiratory virus variants.

Keywords: G protein; RSV; evolutionary dynamics; genetic diversity; phylogenetic analysis; respiratory diseases; respiratory infections; respiratory syncytial virus; viruses.

Figures

Figure 1
Figure 1
Circulating patterns of respiratory syncytial virus (RSV) in Kilifi, Kenya, September 2010– August 2015. A) Total RSV-positive cases (gray continuous line) and typed RSV-A samples (dotted orange line) by month. B) The proportion of RSV-A genotypes ON1 (black) and GA2 (green) per epidemic season. An RSV epidemic season is designated to start in September of 1 year until August of the following year. Unusually, for the last 3 seasons, group A represents most of all RSV cases
Figure 2
Figure 2
Maximum-likelihood phylogenetic tree of unique respiratory syncytial virus (RSV) genotype ON1 G gene ectodomain sequences from Kilifi, Kenya, 2012–2015. The taxa are color coded by the epidemic season of detection (key), and the names represent KEN/Kilifi/serialnodate of collection. Note that although the study detected RSV ON1 in the epidemic season 2011/2012, the first ON1 cases were in 2012. Scale bar indicate nucleotide substitutions per site.
Figure 3
Figure 3
Amino acid substitutions in respiratory syncytial virus A (RSV-A) G protein for sequences isolated in Kilifi Kenya from season 2011/2012 to 2014/2015. All unique protein sequences per epidemic were collated, aligned and the amino acid differences from the earliest sequence determined and marked with vertical colored bars, with the substituted amino acid residue color coded as shown by the key between panels A and B. A) Full aligned aa sequence inferred from the G gene sequences (ON1 and GA2); B) (ON1 only) focuses on the region of the ON1 duplication. The positions shown at the bottom of panels A and B are relative to the first amino acid of the regions analyzed, i.e., from amino acid positions 94 and 260, respectively, of the reference strain A2 (Ref: M74568). Indicated at the top of these panels are the functional domains of the G protein (panel A) and the 72-nt duplication of genotype ON1 (panel B; duplicated sequence I in “orange” and duplicated sequence II in “purple”). Below this, the histogram indicates the total number of changes at each position. C) Concurrent aa positions within the duplicated sequences I and II, and the respective aa substitutions (numbering similar to positions in panel B).

Similar articles

See all similar articles

Cited by 13 articles

See all "Cited by" articles

References

    1. Nair H, Nokes DJ, Gessner BD, Dherani M, Madhi SA, Singleton RJ, et al. Global burden of acute lower respiratory infections due to respiratory syncytial virus in young children: a systematic review and meta-analysis. Lancet. 2010;375:1545–55. 10.1016/S0140-6736(10)60206-1 - DOI - PMC - PubMed
    1. Nokes DJ, Okiro EA, Ngama M, Ochola R, White LJ, Scott PD, et al. Respiratory syncytial virus infection and disease in infants and young children observed from birth in Kilifi District, Kenya. Clin Infect Dis. 2008;46:50–7. 10.1086/524019 - DOI - PMC - PubMed
    1. Agoti CN, Mwihuri AG, Sande CJ, Onyango CO, Medley GF, Cane PA, et al. Genetic relatedness of infecting and reinfecting respiratory syncytial virus strains identified in a birth cohort from rural Kenya. J Infect Dis. 2012;206:1532–41.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=22966119&dopt=Abstract 10.1093/infdis/jis570 - DOI - PMC - PubMed
    1. Cane PA, Pringle CR. Evolution of subgroup A respiratory syncytial virus: evidence for progressive accumulation of amino acid changes in the attachment protein. J Virol. 1995;69:2918–25. - PMC - PubMed
    1. Mufson MA, Orvell C, Rafnar B, Norrby E. Two distinct subtypes of human respiratory syncytial virus. J Gen Virol. 1985;66:2111–24. 10.1099/0022-1317-66-10-2111 - DOI - PubMed

Publication types

MeSH terms

Substances

LinkOut - more resources

Feedback