Global Circulation of RSV-A ON1 Genotype Strains without Characteristic 72-Nucleotide Duplication in the G Gene, 2010-2023

Global Circulation of RSV-A ON1 Genotype Strains without Characteristic 72-Nucleotide Duplication in the G Gene, 2010-2023 | Authorea try { document.documentElement.classList.add('js'); } catch (e) { } var _gaq = _gaq || []; _gaq.push(['_setAccount', 'G-8VDV14Y67G']); _gaq.push(['_trackPageview']); (function() { var ga = document.createElement('script'); ga.type = 'text/javascript'; ga.async = true; ga.src = ('https:' == document.location.protocol ? 'https://ssl' : 'http://www') + '.google-analytics.com/ga.js'; var s = document.getElementsByTagName('script')[0]; s.parentNode.insertBefore(ga, s); })(); Skip to main content Preprints Collections Wiley Open Research IET Open Research Ecological Society of Japan All Collections About About Authorea FAQs Contact Us Quick Search anywhere Search for preprint articles, keywords, etc. Search Search ADVANCED SEARCH SCROLL This is a preprint and has not been peer reviewed. Data may be preliminary. 25 June 2025 V1 Latest version Share on Global Circulation of RSV-A ON1 Genotype Strains without Characteristic 72-Nucleotide Duplication in the G Gene, 2010-2023 Authors : Kuganya Nirmalarajah 0000-0002-8226-7969 , Thomas Braukmann 0000-0002-2452-3776 , Shawn T. Clark , Alex Marchand-Austin , AliReza Eshaghi , Jonathan B. Gubbay , Maan Hasso , Samir N. Patel , Samira Mubareka 0000-0001-5012-2311 , and Venkata R. Duvvuri 0000-0001-7356-338X [email protected] Authors Info & Affiliations https://doi.org/10.22541/au.175087636.61539783/v1 442 views 172 downloads Contents Abstract Information & Authors Metrics & Citations View Options References Figures Tables Media Share Abstract Background: Human respiratory syncytial virus (RSV) is a primary etiological agent responsible for lower respiratory tract infections in children and older adults. The ON1 genotype replaced all previous strains of RSV-A and is characterized by a 72 base pair duplication in the G gene. Recent studies have reported the absence of this distinct feature. We examine publicly available RSV-A sequences to investigate the loss of this duplication. Methods: RSV-A G-gene and whole genome sequences from human samples collected between January 2010 and December 2023 were downloaded from the (GISAID) EpiRSV database. A total of 15,757 sequences classified as ON1 (alias A.D) were investigated. Sequence metadata including sample collection date, country of submission, and sequencing methods were recorded for RSV ON1 sequences missing the 72 base pair duplication. MAFFT and IQTREE2 were used to generate a maximum likelihood phylogenetic tree. Results: 417 sequences from 27 countries with sampling between 2010 to 2023 were identified without the characteristic 72 base pair duplication. All RSV-A sequences available from Cambodia and Pakistan from 2010-2023 lack the duplication while the remaining 25 countries report RSV-A sequences with and without the duplication. A phylogenetic tree was constructed, revealing that all global sequences with and without the duplication cluster together. Amino acid sequences of ON1 with and without the duplication were examined, showing shared mutations surrounding the duplication site. Conclusions: RSV-A ON1 sequences without the duplication are rare. The absence of the duplication does not interfere with phylogenetic relatedness among sequences with the duplication. The biological and clinical relevance of RSV-A ON1 viruses lacking the G gene duplication require further research. Global Circulation of RSV-A ON1 Genotype Strains without Characteristic 72-Nucleotide Duplication in the G Gene, 2010-2023 Short title: Loss of RSV-A ON1 G gene duplication Kuganya Nirmalarajah, 1,2,3 Thomas Braukmann, 1,3 Shawn T. Clark, 1 Alex Marchand-Austin, 1 Alireza Eshaghi 1 , Jonathan B. Gubbay 4 , Maan Hasso 1 , Samir N. Patel, 1,3 Samira Mubareka, 2,3 * and Venkata R. Duvvuri, 1,3,5 * 1 Public Health Ontario, Toronto, Ontario, Canada 2 Sunnybrook Research Institute, Toronto, Ontario, Canada 3 Department of Laboratory Medicine and Pathobiology, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada 4 Division of Microbiology, Department of Pathology and Laboratory Medicine, BC Children’s Hospital and BC Women’s Hospital Health Centre 5 Laboratory for Industrial and Applied Mathematics, Department of Mathematics and Statistics, York University, Toronto, Ontario, Canada *Co-corresponding author: Samira Mubareka, Division of Infectious Diseases, Department of Laboratory Medicine and Molecular Diagnostics, Microbiology, Sunnybrook Health Sciences Centre, Sunnybrook Research Institute and Shared Hospital Laboratory, 2075 Bayview Avenue, Toronto, Ontario, Canada, M4N 3M5. [email protected] *Corresponding author: Venkata R. Duvvuri, Public Health Ontario, 661 University Avenue, Toronto, Ontario, Canada, M5G 1M1. [email protected] Abstract: Background: Human respiratory syncytial virus (RSV) is a primary etiological agent responsible for lower respiratory tract infections in children and older adults. The ON1 genotype replaced all previous strains of RSV-A and is characterized by a 72 base pair duplication in the G gene. Recent studies have reported the absence of this distinct feature. We examine publicly available RSV-A sequences to investigate the loss of this duplication. Methods: RSV-A G-gene and whole genome sequences from human samples collected between January 2010 and December 2023 were downloaded from the (GISAID) EpiRSV database. A total of 15,757 sequences classified as ON1 (alias A.D) were investigated. Sequence metadata including sample collection date, country of submission, and sequencing methods were recorded for RSV ON1 sequences missing the 72 base pair duplication. MAFFT and IQTREE2 were used to generate a maximum likelihood phylogenetic tree. Results: 417 sequences from 27 countries with sampling between 2010 to 2023 were identified without the characteristic 72 base pair duplication. All RSV-A sequences available from Cambodia and Pakistan from 2010-2023 lack the duplication while the remaining 25 countries report RSV-A sequences with and without the duplication. A phylogenetic tree was constructed, revealing that all global sequences with and without the duplication cluster together. Amino acid sequences of ON1 with and without the duplication were examined, showing shared mutations surrounding the duplication site. Conclusions: RSV-A ON1 sequences without the duplication are rare. The absence of the duplication does not interfere with phylogenetic relatedness among sequences with the duplication. The biological and clinical relevance of RSV-A ON1 viruses lacking the G gene duplication require further research. Key words: Respiratory syncytial virus; RSV; genome sequences; nucleotide duplication; phylogenetics Main Text Introduction Human respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract infections in children and a major contributor to respiratory illness in older adults [1]. It is estimated to cause 3.2 million hospitalizations and upwards of 149,400 deaths worldwide annually in children under the age of 5 [2]. In the United States, annual RSV burden estimates indicate that children under 5 years of age account for approximately 2.1 million outpatient cases and 58,000-80,000 hospitalizations, while about 60,000-160,000 hospitalizations and 6,000-10,000 deaths are reported every year in older adults [3]. After decades of challenges in RSV vaccine development, two RSV vaccines were approved in 2023 for adults aged 60 and older [4]. Furthermore, in addition to palivizumab, advancements in next generation monoclonal antibody therapies resulted in the approval of nirsevimab for newborns and infants in 2023[4]. As a member of the Pneumoviridae family, RSV is a single stranded, negative-sense RNA virus with an approximate 15.2 kb genome size. Among its two surface glycoproteins, G and F, the genetically diverse G protein is responsible for differentiating the two common subgroups, RSV-A and RSV-B. RSV-A is typically more prevalent and thought to be associated with more severe disease than RSV-B [5]. Further classification of RSV subgroups into genotypes is accomplished via sequence analysis of the second highly variable region (HVR2) of the gene encoding the G protein. In the canonical RSV A2 strain, the HVR2 corresponds to codon positions 210 to 298 [6]. Conventionally, 14 genotypes of RSV-A have been described based on genetic difference in the G gene HVR2, which include GA1-7, SAA1, NA1-4, and ON1-2 [7]. However, efforts to unify RSV genotype definition and nomenclature have been proposed separately based on the G gene and the RSV whole genome [8, 9]. Proposed nomenclature to classify RSV-A genotypes based on G ectodomain sequences reduce the number of genotypes from 14 to 3 [8] whereas genotype definitions based on whole genome sequences distinguish 24 RSV-A genotypes [10]. Since its first detection and classification in Ontario, Canada, the ON1 genotype has become the most predominant RSV-A genotype worldwide [6, 8]. ON1 emerged from the NA1 genotype, with which it shares approximately 75.4% nucleotide (nt) and 72.7% amino acid homology in the G gene [6]. Many of the currently circulating lineages are either descendants of ON1 or are considered ON1-like [11]. RSV-A ON1 has been characterized by a 72 nucleotide (nt) base pair (bp) duplication in the HVR2 region of the G gene which spans amino acid positions 284 to 307 (approximate nt positions 5501-5572) [6]. Recent RSV unified classification and naming conventions have been proposed, denoting RSV-A ON1 as the alias “RSV A.D” [10]. The clinical severity of the ON1 genotype remains unclear as some studies have demonstrated that ON1 is less virulent than genotypes preceding [5] while others have shown that infection with ON1 is more severe than the NA1 genotype [12]. Historically, the 72 bp HVR2 duplication has been recognized as a distinct feature of the ON1 genotype. Recent studies have reported the absence of this characteristic duplication in the sequences of some ON1 strains [12-15]. Although ON1-like strains without the duplication have been observed sporadically, the prevalence, outbreak potential, transmission dynamics, and underlying mechanisms remain unclear. In this study, we examine publicly available global RSV-A sequences from 2010 to 2023 to evaluate the frequency of the presence and absence of the 72 bp duplication in sequences classified as ON1. We seek to gather and report the methodological details associated with the loss of the G gene duplication, which could represent genetic reversion, a low-frequency or intra-host variant, or an artifact of sequencing and bioinformatic assembly. Collection of Sequence Data RSV-A whole genome sequences (WGS) and G gene sequences (greater than 300 nt) from specimens collected between January 2010 and December 2023 were retrieved from the Global Initiative on Sharing All Influenza Data (GISAID) EpiRSV database. Search criteria included filtering for only complete WGS and complete G gene sequences, which resulted in a total of 15,757 RSV-A sequences that were analyzed. Nextclade v3.2.0 was used to align sequences to the RSV-A-ON1 reference sequence (GISAID accession # EPI_ISL_412866), followed by mutation calling, and quality assessment. For detailed investigation on sequences without the G gene 72 bp duplication, sequences with the 72 bp duplication were excluded for the initial multiple sequence alignment. Associated metadata including sample collection date, submission country, and sequencing methodology were compiled for sequences lacking the 72 bp duplication. Sequence and Phylogenetic analysis G gene HVR2 sequences from specimens lacking the 72 bp duplication were screened for 97% similarity. These sequences along with available ON1 isolates with the G gene 72 bp duplication originating from the same geographical areas and seasons, and reference sequences of other RSV-A genotypes were aligned using the Multiple Alignment using Fast Fourier Transform (MAFFT) [16]. Amino acid (AA) sequence alignments were compared using BioEdit Alignment Software v.7.7 [17]. A maximum likelihood (ML) phylogenetic tree was inferred using IQ-TREE2 [18]. The Model Finder Plus option was employed to automatically select the best-fit nucleotide substitution model, which identified TN+F+R2 based on Bayesian Information Criterion (BIC). Branch support was evaluated using 1000 ultrafast bootstrap replicates [18] and 1000 Shimodaira–Hasegawa-like approximate likelihood ratio tests [19, 20] providing robust statistical confidence in the resulting tree topology. The phylogenetic tree was then visualized and annotated in R version 4.3.2 using ggtree v3.10.1 package [21]. Results Temporal and Global Distribution of RSV-A ON1-like strains without 72 base pair duplication in G-gene HVR2 A search in the GISAID EpiRSV database identified a total of 417 sequences from 27 different countries spanning from 2010 to 2023 that lacked the characteristic 72 bp duplication in the G gene HVR2. These sequences constituted 2.6% of all RSV-A sequences reported during this period ( Table 1 ). Notably, all RSV-A isolates sequenced in Cambodia and Pakistan throughout various seasons from 2010 to 2023 were found to lack the HVR2 duplication ( Table 1 ). Conversely, in China, Italy, Germany, Lebanon, and Russia only isolated instances of RSV-A lacking this duplication were detected, while the remainder of the sequenced specimens from these countries exhibited intact duplications. The remaining 20 countries displayed a mix of sequences, some with the intact G gene duplication and others with more than one missing the duplication. The sequencing and analysis methods varied across the 27 countries during the 2010 to 2023 period, with Illumina technology being the most predominant application. Instances where sequences with and without the G gene duplication were found to be submitted from the same institution using identical sequencing technology and assembly pipelines. For example, an institution in Louisiana, USA used an Illumina instrument and bbmap, samtools, and ivar analysis tools to generate sequences with (EPIISL17402455) and without the duplication (EPIISL17402453, EPIISL17402456) from samples collected in the same 2022 season. The majority of RSV-A sequences had the 72 bp G gene HVR2 duplication (15,340/15,757; 97%), indicating that sequences without this duplication represent minority populations globally from 2010 to 2023 ( Figure 1a ). The years 2018 and 2022 reported the highest numbers of RSV-A sequences where the G gene HVR2 duplication was notably absent. However, the count of sequences without the duplication did not increase proportionally to the count of sequences with the duplication over time. Kenya was the predominant source of sequences lacking the duplication, contributing approximately 60% of the 417 sequences identified globally ( Figure 1b ). Phylogenetic relatedness of ON1 with and without 72 bp duplication We constructed a ML phylogenetic tree to evaluate the evolutionary relationship between the RSV-A isolates with and without the G gene HVR2 duplication ( Figure 2a ). All global sequences lacking the G gene HVR2 duplication ( Supplementary Table 1) belong to the RSV-A ON1 genotype, despite the absence of the duplication. Sequences without the duplication cluster together with those that have the duplication, and in some instances, they cluster specifically with the sequences originating from the same RSV season, geographical region, and institution. Closer examination of the G gene HVR2 nucleotide sequences with and without the duplication reveal common AA mutations surrounding the duplication, even in instances where the geographic location and originating lab are not the same. This observation may suggest that these shared point mutations are likely responsible for the close relatedness of sequences ( Figure 2a ) regardless of the presence or absence of the duplication, rather than the absence of the duplication itself being the ON1 genotype defining characteristic. The AA alignments of residues 212 to 321 of the G gene HVR2 for a subset of the studied sequences along with A2, NA1, and ON1 references are shown in Figure 2b . The AA alignments reveal some sequences from 2010 onward lacking the characteristic duplication, appearing more like the prototype A2 or NA1 strains in the regions where the duplication would be. Nonetheless, these sequences still exhibit ON1-specific mutations in other parts of the alignment. This confirms that while the characteristic duplication might be absent in some sequences, they retain other distinctive mutations associated with the ON1 strains ( Figure 2b ). Most glycosylation sites are preserved among ON1 sequences with and without the duplication [6]. Discussion: The majority of RSV-A ON1 genotype like sequences from 2010 to 2023 maintained the characteristic 72 bp G gene duplication. Phylogenetic analysis comparing sequences with and without the G gene duplication that originate from the same geographical areas and seasons revealed that these sequences cluster together and are primarily classified as ON1 whether the duplication is present or not. This poses the question of whether the 72 bp duplication first identified in ON1 can continue to be coined as a distinct feature of this genotype. The absence of the characteristic ON1 72 bp duplication in RSV-A G-gene was first described in sequences from Germany obtained hematological patients with prolonged viral shedding. However, the deletion of the duplication was only identified using deep sequencing methods, suggesting it may represent minority of low frequency variants [12]. The loss of the duplication was also detected in ON1-classified sequences obtained from Vietnam from multiple seasons, 2017 to 2020 [13]. Furthermore, RSV sentinel surveillance in Senegal from 2022 revealed that sequences with and without the RSV-A G gene duplication cluster together and are classified as ON1 [15]. An observational cohort study from country found that RSV-A strains lacking the G gene duplication were more frequently detected in male infants while those bearing the duplication were observed in both males and females [14]. Given that the RSV-A G gene HVR2 72 bp duplication has been denoted as a characteristic feature of the ON1 genotype, the absence of this duplication may pose confusion and challenges around how these sequences would be classified. Sequences with and without the duplication originating from the same seasons and geographical areas were processed using the same sequencing platforms and analysis pipelines by one institution. This observation suggests that the absence of the G gene duplication is likely not due to sequencing or bioinformatics errors, but could represent genetic reversion back to a non-duplicated HVR2. A similar trend has been observed in the BA genotype of RSV-B which exhibits a 60bp duplication in the HVR2 region. For RSV-B, the loss of the 60bp duplication was coined as a “flip-flop” pattern with reversion between the 2 duplicated/non-duplicated states [22] and its presence was found to increase viral attachment in vitro, thereby enhancing viral fitness [23]. Given that the ON1 genotype with the 72 bp duplication replaced the majority of previously circulating RSV-A genotypes, there is likely to be a fitness advantage associated with this duplication. However, the potential functional and clinical significance of a similar pattern among RSV-A strains is unclear. No current studies compare the phenotypic effects of the ON1 genotype with and without the 72 bp duplication in vitro, in vivo, or in clinical contexts. Intriguingly, the observation that both Cambodia and Pakistan reported 100% ON1 sequences without the 72 bp duplication could be attributed to: i) region-specific host population characteristics and the transmission dynamics of RSV-A strains, which may influence the virus genetic stability and evolution in these areas, and ii) the choice of sequencing technologies and bioinformatic pipelines used for genome assembly. The use of Illumina sequencing, a short-read technology that typically struggles with the accurate assembly of repetitive regions, may corroborate with the reported results of 100% ON1 sequences without the 72 bp duplication. Long-read-sequencing could address these issues by providing continuous reads that span repetitive regions more effectively. However, Belgium and Kenya’s use of Nanopore’s long-read technology also resulted in sequences without the duplication. This likely indicates that RSV-A ON1 sequences without the 72 bp duplication are true events. Studies involving deep sequencing and variant analyses could further explain whether sequences without the duplication reflect viral population-level diversity within a given host and to better understand if they are fixed, rare, or intermediate variants. Additionally, a thorough validation of existing RSV bioinformatic pipelines could be essential to improve the consistency and accuracy of genomic data representations across different platforms. In conclusion, our study indicates that RSV-A sequences classified as ON1 lacking the G gene HVR2 duplication were relatively rare between 2010 and 2023. Although the absence of the G gene duplication does not interfere with close relatedness among sequences with the duplication, updating existing RSV lineage naming schemes to distinguish the two should be considered. These findings highlight the importance of active RSV genomic surveillance programs. Further studies examining clinical implications, immunological effects, and fitness advantage of RSV lacking evolutionary recent duplications are warranted. Acknowledgements We acknowledge the authors, originating and submitting laboratories of the sequences from GISAID’s EpiRSV™ Database on which this research is based. Funding This work was supported by awards from the University of Toronto’s Department of Laboratory Medicine and Pathobiology, Institute for Pandemics, and Emerging and Pandemic Infections Consortium. This work was supported by Mitacs through the Mitacs Accelerate Program. Consent No patient information or factors necessitating patient consent were included in this study. Conflict of Interest JBG is a paid consultant scientific editor for GIDEON Informatics, Inc. (https://www.gideononline.com/), which is unrelated to the current work. Author contributions Conceptualization: K.N., and V.R.D., methodology: K.N., and V.R.D., formal analysis: K.N., funding acquisition: S.M., and V.R.D, investigation: K.N., supervision: S.M., and V.R.D, validation: T.B., V.R.D, visualization: K.N., writing - original draft preparation: K.N., writing – review & editing: K.N., T.B., S.T.C., A.M.A., A.E., M.H., J.B.G., S.N.P., S.M., and V.R.D. References 1. Falsey AR, Hennessey PA, Formica MA, Cox C, Walsh EE. Respiratory syncytial virus infection in elderly and high-risk adults. New England Journal of Medicine. 2005 Apr 28;352(17):1749–59. doi:10.1056/nejmoa043951 2. Shi T, McAllister DA, O’Brien KL, Simoes EA, Madhi SA, Gessner BD, et al. 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Table 1: Geographical and temporal detection of RSV-A lacking the ON1 G gene HVR2 duplication from 2010 to 2023 Argentina 2018-2019 2/748 0.3% Sanger Australia 2017-2019 14/296 4.7% Illumina Trinity Ion Torrent PGM Illumina Trinity v. 2.11.0 In-house pipeline Belgium 2022 2/94 2.1% Nanopore MinION INSaFLU Galaxy Brazil 2017, 2020-2023 8/122 6.6% Illumina Miniseq RVOP Cambodia 2023 1/1 100.0% Illumina Miniseq CZID Canada 2011 1/83 1.2% Sanger dideoxy sequencing Not available China 2017 1/753 0.1% Sanger dideoxy sequencing Not available Croatia 2013 2/43 4.7% Sanger dideoxy sequencing Not available England 2017-2018, 2022-2023 19/570 3.3% Illumina Nextseq, Illumina MiSeq UKHSA pipeline (BWA-SAMtools-Qausibam), PHE pipeline (BWA-SAMtools-Quasibam) Germany 2011 1/218 0.5% Sanger dideoxy sequencing Not available India 2012, 2015 2/144 1.4% Sanger dideoxy sequencing Not available Ireland 2022 58/128 45.3% Illumina, Sanger dideoxy sequencing Not available Italy 2021 1/153 0.7% Unknown Not available Japan 2014, 2018 19/479 4.0% Sanger Not available Kenya 2017-2018, 2021-2023 227/988 23.0% Nanopore Sequencing Assembly minimap2 v. v.2.2.4; bcftools v. 1.10.2; medaka v. 1.0.3 Lebanon 2014 1/22 4.5% Unknown Not available Myanmar 2014 2/116 1.7% Sanger dideoxy sequencing Not available Pakistan 2022-2023 4/4 100.0% Illumina Miniseq Not available Panama 2010 4/47 8.5% Sanger dideoxy sequencing Sequencher v.4.5 Russia 2020 1/86 1.2% Illumina CLC Genomics Workbench v. 5.5 Senegal 2022-2023 14/65 20.0% Illumina Not available Slovenia 2020 2/6 33.3% Sanger Not available Spain 2022 5/256 1.1% Illumina Not available Uganda 2021 4/112 3.6% Illumina Not available USA 2011, 2013, 2015, 2019, 2022 12/515 2.3% Illumina Bbmap, samtools, ivar, Iterative Refinement Meta-Assembler v.0.9.3 Vietnam 2012, 2017-2018, 2020 8/149 5.4% Illumina, Sanger dideoxy sequencing Miniseq CLC Genomics Workbench 11 Zambia 2013, 2018 3/86 3.5% Sanger Not available Figure 1. Temporal distribution of RSV-A ON1 Genotype Strains with and without 72 bp duplication in G-genes based on sequences submitted to GISAID from 2010 to 2023 (A). Global distribution of the 417 sequences without the 72 bp duplication detected in 20 countries (B). Approximately 64% of 417 sequences without the duplication are from Kenya, 15% from Ireland, 5% from England, 4% from Australia, and 2% from USA. Figure 2. Phylogenetic tree constructed with RSV-A nucleotide sequences obtained from the second hypervariable region of the G gene (A) . Reference strains representing known genotypes are indicated by solid black squares and circles. ON1-like sequences without the 72 bp duplication in G-gene are indicated by a solid red square. Multiple sequences alignment and phylogenetic trees were constructed using MAFTT and maximum likelihood algorithm running within IQ-TREE2. Tree topology was supported by bootstrap analysis with 1000 pseudo replicate datasets. Bootstrap values ≥ 70 are shown at the branch nodes. The tree was visualized using MEGA software, version 11.0.13. The scale bar represents the number of nucleotide substitutions per site between close relatives. Amino acid similarity between A2 and NA1 reference strains and ON1 classified representative sequences (B). Alignments are displayed relative to the canonical A2 reference strain. Residues that are identical to the A2 reference are denoted as dots. Undetermined residues are marked by X. N glycosylation sites are shown in black outlined boxes. Amino acid changes that deviate from the A2 and NA1 references are ON1-specific, as indicated by the shaded grey areas, with a few exceptions showing reversions. Information & Authors Information Version history V1 Version 1 25 June 2025 Copyright This work is licensed under a Non Exclusive No Reuse License. Keywords genome sequences nucleotide duplication phylogenetics respiratory syncytial virus rsv Authors Affiliations Kuganya Nirmalarajah 0000-0002-8226-7969 Public Health Ontario View all articles by this author Thomas Braukmann 0000-0002-2452-3776 Public Health Ontario View all articles by this author Shawn T. Clark Public Health Ontario View all articles by this author Alex Marchand-Austin Public Health Ontario View all articles by this author AliReza Eshaghi Public Health Ontario View all articles by this author Jonathan B. Gubbay BC Children's Hospital View all articles by this author Maan Hasso Public Health Ontario View all articles by this author Samir N. Patel Public Health Ontario View all articles by this author Samira Mubareka 0000-0001-5012-2311 Sunnybrook Research Institute View all articles by this author Venkata R. Duvvuri 0000-0001-7356-338X [email protected] Public Health Ontario View all articles by this author Metrics & Citations Metrics Article Usage 442 views 172 downloads .FvxKWukQNSOunydq8rnd { width: 100px; } Citations Download citation Kuganya Nirmalarajah, Thomas Braukmann, Shawn T. Clark, et al. Global Circulation of RSV-A ON1 Genotype Strains without Characteristic 72-Nucleotide Duplication in the G Gene, 2010-2023. Authorea . 25 June 2025. DOI: https://doi.org/10.22541/au.175087636.61539783/v1 If you have the appropriate software installed, you can download article citation data to the citation manager of your choice. Simply select your manager software from the list below and click Download. For more information or tips please see 'Downloading to a citation manager' in the Help menu . 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