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Insights into the Molecular Epidemiology and Evolutionary Characteristics of Respiratory Syncytial Virus B in China from 2020 to 2025 | 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 Search Search ADVANCED SEARCH SCROLL This is a preprint and has not been peer reviewed.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. 15 December 2025 V1 Latest version Share on Insights into the Molecular Epidemiology and Evolutionary Characteristics of Respiratory Syncytial Virus B in China from 2020 to 2025 Authors : Kangsheng Zhou , Mingchun Luan , Xiaoman Cui , Huan Wang , Yuhui Wang , Teng Ge , Xisheng Yin , and Xingying Lang 0009-0003-3353-1932 [email protected] Authors Info & Affiliations https://doi.org/10.22541/au.176583254.45462026/v1 306 views 103 downloads Contents Abstract Supplementary Material Information & Authors Metrics & Citations View Options References Figures Tables Media Share Abstract Respiratory syncytial virus (RSV) is a major pediatric respiratory pathogen. The imported RSV-B lineage B.D.E.1 recently became dominant in Beijing. To study RSV-B evolution in China, we performed whole-genome sequencing of Dalian strains and integrated them with genomic data of Asian strains from public databases. This integrated dataset enabled a comprehensive analysis of RSV-B genetic evolution and amino acid variations in China from 2020 onward. Before B.D.E.1, lineages B.D.4.1.1 and the unique Chinese B.D.E.2 were prevalent. Since its introduction, B.D.E.1 has persisted as the dominant lineage. Protein analysis showed high mutation rates in the G protein’s mucin-like domain, while its conserved drug-targeted domain was stable. F protein variations were in the F1 subunit, with no critical mutations at key antigenic sites (Site Ø, II, IV), suggesting sustained efficacy of related therapeutics. Two coordinated mutation events occurred (2021, 2023), the latter persisting into 2025. Other proteins also had high-frequency mutations, including a unique premature termination codon (Q59*) in the SH protein, which was identified in Dalian sequences (5/29, 17.24%). Continuous monitoring of B.D.E.1 and evolution across all proteins is essential, highlighting the importance of whole-genome surveillance. Introduction Respiratory syncytial virus (RSV) is a major cause of pediatric acute lower respiratory tract infections (ALRTIs), infecting most children by age two [1,2] . Globally, RSV caused an estimated 33 million ALRTI cases, 3.6 million hospitalizations, and 26,300 in-hospital deaths in 2019 [3] . Understanding the molecular mechanisms of RSV is therefore crucial for evaluating its epidemiological impact and the efficacy of preventive and therapeutic interventions. Respiratory syncytial virus (RSV) is an enveloped, non-segmented virus with a negative-sense, single-stranded RNA genome of approximately 15.2 kilobases, which encodes eleven proteins: NS1, NS2, N, P, M, SH, G, F, M2-1, M2-2, and L. Among these, the surface glycoproteins G and F are essential for host cell attachment and entry, serving as primary targets for vaccine and therapeutic development. The G protein exhibits high variability, and its central conserved domain harbors a ”CX3C” motif that constitutes a key neutralizing epitope [4-6] . The F protein is synthesized as an inactive precursor (F0) that is cleaved to form the mature F1/F2 trimer, adopting a stable post-fusion conformation. Critical antigenic sites exist in both its pre-fusion (Pre-F) and post-fusion (Post-F) states, including Site II (shared by both conformations) and the Pre-F-specific, potent neutralizing sites Ø and V [7-9] . Palivizumab, the first FDA-approved monoclonal antibody for preventing RSV-associated lower respiratory tract infections in infants, binds to Site II on Pre-F. This interaction inhibits the conformational change to Post-F, thereby blocking membrane fusion [10-12] . More recently, nirsevimab has been approved; it targets the conserved Site Ø on Pre-F, locking the protein in its pre-fusion state and providing prolonged protection due to its extended half-life [13,14] . The imported RSV-B lineage B.D.E.1 has recently become dominant in Beijing, driving a surge in local positivity rates and posing immune-evasion risks [15] . Against this background, we observed a significant rise in RSV prevalence in Dalian in 2025, prompting whole-genome sequencing of local strains to investigate the epidemiological impact of viral molecular evolution. Despite global gaps in large-scale RSV-B genomic surveillance, such data are crucial for understanding evolutionary dynamics and immune-escape mechanisms. This study therefore systematically analyzes RSV infections in children with ILI/SARI at a Dalian hospital from 2023 to 2025 by integrating Dalian sequences with other Asian RSV-B full-genome sequences available since 2020 (including those from China). Our goal is to characterize the complete genomic and amino acid variation landscape of RSV-B in China, supporting ongoing surveillance and informing clinical and public health responses. Materials and Methods Sample Source This study defined the epidemic year as October–September for analysis. Over two epidemic years (October 2023–September 2025), 1,560 pharyngeal swabs were collected from children with respiratory infections at a sentinel hospital. Cases were classified per WHO criteria: ILI (n = 980; outpatients with fever ≥38°C plus cough/sore throat) and SARI (n = 490; hospitalized patients with fever ≥38°C, cough, and illness ≤10 days). For genetic analysis, reference strain NC_001781.1 was obtained from NCBI, along with 1,384 RSV-B full-genome sequences from Asia via GISAID and NCBI, including reference EPI_ISL_1653999. Redundancy was reduced using VSEARCH (Ubuntu), clustering sequences with 100% similarity from the same region and time. After deduplication, 974 sequences were retained, including 202 Chinese sequences from 2020 to September 2025. Nucleic Acid Extraction and Amplification Nucleic acid extraction and amplification were performed using the following commercial kits and instruments: nucleic acid extraction kits (Jiangsu Shuoshi Biotechnology Co., Ltd.) on a fully automated nucleic acid extraction system (Jiangsu Shuoshi Biotechnology Co., Ltd.); a 14-plex real-time fluorescent PCR kit for respiratory pathogens (Beijing Zhuocheng Huisheng Biotechnology Co., Ltd.); and 42-plex and 36-plex respiratory pathogen microfluidic chips (Thermo Fisher Scientific, USA) on QuantStudio 5/QuantStudio 7 real-time PCR systems (Thermo Fisher Scientific, USA). Whole-Genome Sequencing of RSV-B (1)Whole-genome sequencing of RSV-B via the Ion AmpliSeq DNA technology Based on the extracted RNA as template, cDNA was first synthesized by reverse transcription. Using the Ion AmpliSeq™ Kit for Chef DL8 and the Ion AmpliSeq™ RSV B Research Panel (number of amplicons: 84; amplicon length range: 125–275 bp; genome coverage: 100% of the RSV-B genome), the RSV-B library was constructed on the Ion Chef System (Thermo Fisher Scientific, USA). The Ion 510™ & Ion 520™ & Ion 530™ Kit-Chef and Ion 530™ Chip Kit were used to prepare high-throughput sequencing templates on the Ion Chef System, and sequencing was performed on the Ion GeneStudio S5 Plus (Thermo Fisher Scientific). (2)Whole-genome sequence assembly and mutation profiling Raw sequencing data from the Ion GeneStudio S5 Plus system were processed using its built-in plugins. With EPI_ISL_1653999 as the reference, the generateConsensus and variantCaller RSV B plugins performed base calling, alignment, variant analysis, and whole-genome assembly, yielding consensus FASTA files and quality metrics (e.g., depth, alignment rate). Sequences with >96% coverage and Viral genotyping and genomic characterization Consensus sequences were analyzed for genotyping and mutation profiling using the online Nextclade tool (https://clades.nextstrain.org/). Phylogenetic reconstruction Multiple sequence alignment was performed using MAFFT, incorporating the prototype strain, reference strain, Dalian sequences, and other Asian sequences. The optimal substitution model for phylogenetic reconstruction was determined with IQ-TREE 2.4.0, which identified the GTR+F+I+R5 model as the best fit. A maximum likelihood (ML) phylogenetic tree was subsequently constructed using this model with 1000 bootstrap replicates. Amino acid substitution profiling Amino acid mutations in the Chinese RSV-B full-genome sequences from the database (2020 onward) and the sequenced Dalian samples were analyzed, using EPI_ISL_1653999 (2019) as the reference sequence. Statistical Analysis and Visualization All statistical analyses and data visualizations were performed using RStudio 2024.12.1. The built-in stats package was used to perform chi-square tests, with a P-value < 0.05 considered statistically significant. The tibble, dplyr, and ggplot2 packages were employed to generate and refine lollipop plots illustrating the amino acid mutation sites. Data Availability Statement The viral genome sequences and associated metadata analyzed in this study were obtained from two publicly accessible databases: GISAID and the National Center for Biotechnology Information (NCBI) of the United States. All data are publicly available through their respective platforms. The accession numbers for the GISAID sequences used are listed in Supplementary Table S1, and those for the NCBI sequences are listed in Supplementary Table S2. Ethics Statement This study utilized previously collected pathogen nucleic acid samples from routine surveillance for detection and analysis. All samples were de-identified to protect participant privacy, and the waiver of informed consent was granted as the research posed no foreseeable risk to participants’ rights or health. Furthermore, the study involves no personal privacy concerns or commercial interests. The protocol has been reviewed and approved by the Medical Ethics Committee of the Dalian Center for Disease Control and Prevention (see Supplementary Materials for details). RSV detection profile Between October 2023 and September 2025, a total of 1,560 pharyngeal swab samples were collected from children with respiratory infections at a sentinel hospital in Dalian. The overall RSV positivity rate was 6.09% (94/1560). The positivity rate was 5.49% (56/1040) among ILI cases and 7.69% (38/520) among SARI cases, with no statistically significant difference between the two groups (X² = 2.3553, P > 0.05). During the study period, two epidemic periods were identified: the first from November 2023 to March 2024 (winter-spring), which peaked in February 2024 (13.33%, 8/60), and the second from January to September 2025 (winter-spring-summer), which peaked in April 2025 (30.00%, 9/30)( Figure 1). Fig.1 Line graph showing monthly RSV positivity rates from October 2023 to September 2025 Whole-genome sequencing of RSV-B Among 77 RSV-positive Dalian samples, 38 were RSV A and 39 RSV B. Thirty-two RSV-B samples (6 from 2023, 3 from 2024, 23 from 2025) were sequenced, yielding genomes of 8,909–15,157 bp. Alignment to reference EPI_ISL_1653999 showed 58.5–99.6% coverage; 29 sequences with control for analysis. RSV-B molecular epidemiology and phylogenetic inference A phylogenetic tree was constructed using the prototype strain, the reference strain, 29 Dalian sequences, and 974 Asian sequences (which included 202 sequences from China). Phylogenetic analysis revealed that all Asian RSV-B strains belonged to the B.D lineage. The descendant B.D.4.1.1 became dominant in multiple Asian countries. In China, all sequences since 2020 fall within B.D.4.1 and its derivatives, with B.D.4.1.1 being locally dominant in 2020–2021. A unique local clade, B.D.E.2, evolved in China during this period, causing significant local circulation and forming a distinct monophyletic cluster; outside China, it was only reported in two cases from South Korea, and did not replace B.D.4.1.1. Chinese B.D.4.1.1 strains clustered with sequences from South Korea, Laos, and the Philippines, none of which evolved into B.D.E.2.B.D.E.1, first reported in South Korea in 2021, was introduced into China in late 2022 and rapidly displaced B.D.4.1.1 as the national dominant lineage. It remains the predominant RSV-B lineage in Asia. While B.D.E.1.2 has been detected in several countries (e.g., Philippines, Laos, India) in 2023–2024, and isolated cases of B.D.E.5 reported in Japan and the Philippines, neither has been identified in China to date. In Dalian, most sequences clustered with other Chinese strains, with B.D.E.1 accounting for 93.10% (27/29) of sequenced samples from 2023 onward (Figure 2). Fig.2 Phylogenetic tree of RSV-B including prototype, reference, Dalian, and Asian strains (with Chinese sequences). Tip label colors indicate sub-lineages; branch colors show geographic origin. The Dalian clade is enlarged in an inset. Amino Acid Mutations in the Full-Length Genomes of Respiratory Syncytial Virus B in China Analysis of the 202 Chinese sequences from 2020 to the present identified a total of 553 amino acid mutations, of which 36 occurred at a frequency greater than 10% (hereafter referred to as ”high-frequency mutations”). Consistent with previous studies, the NS2, M, SH, and M2-1 proteins exhibited relatively few amino acid substitutions, and no high-frequency mutation sites were identified in these four proteins in the present study. A limited number of high-frequency mutation sites were detected in the NS1, N, P, and M2-2 proteins. Specifically, one high-frequency mutation site was located in the α/β core domain of the NS1 protein. The N protein contained one high-frequency mutation site each in its N-terminal domain (NTD) and C-terminal domain. One high-frequency mutation site was identified in the oligomerization domain (PCO) of the P protein. In the M2-2 protein, amino acid mutations were primarily concentrated in the C-terminal regulatory extension (C-tre), where three high-frequency mutation sites were observed. In contrast, the N-terminal core functional region was relatively conserved, with only one amino acid site mutated across the entire region, albeit at a 100% mutation frequency (Fig.3A–E, Table.S3). RSV-B G, F, and L proteins showed higher mutation diversity than other proteins. The G protein was most variable (144 mutation sites, 18 high-frequency), mainly in MLD-I/II (17 high-frequency sites), while the CCD was largely conserved (Fig.3G, Table.S3). The F protein exhibited lower overall mutation frequency than the G protein. All three high-frequency mutation sites in the F protein were located in the F1 subunit, which harbors multiple critical antigenic sites; sites II and IV remained stable without high-frequency mutations, whereas site Ø carried the high-frequency S211D/N substitution. HR1/HR2 exhibited more mutations than other regions of the F protein, though only one high-frequency site (S190N) was identified (Fig.3H, Table.S3). L protein mutations clustered in RdRp, MTase, and CTD domains, with high-frequency sites including K570R (RdRp) and others in MTase and CTD(Fig.3K, Table.S3). Fig.3 Amino acid mutation frequencies across 11 RSV-B proteins in 202 Chinese sequences (GISAID/NCBI). Panels A–K correspond to NS1, NS2, N, P, M, SH, G, F, M2-1, M2-2, and L. Sites with >10% mutation frequency are labeled. Clustering analysis was performed on mutation sites with frequencies between 10% and 90% in the 202 Chinese sequences from the database. Sites with 100% mutation frequency are conventionally termed ”fixed mutations” [16] , while those with frequencies between 90% and 99% were defined in this study as ”near-fixed mutations”; both categories were excluded from the clustering analysis. The analysis revealed two distinct events of multi-site coordinated mutation (defined as multiple sites co-occurring at a frequency the first event (55/202, 27.23%), characterized by the coordinated occurrence of three mutations in the G protein and one in the N protein. This coordinated mutation pattern initially emerged in 2020 and was predominantly observed in 2021 (38/55, 69.09%). Region B corresponds to the second event (25/202, 12.38%), which involved 18 amino acid sites across four proteins: G, F, M2-2, and L. This coordinated mutation pattern first appeared in 2022 and persisted through 2025, with the majority of sequences carrying this pattern detected in 2023 (12/25, 48%). Notably, all sequences exhibiting the Region B coordinated mutation pattern lacked the mutations defining the Region A event (Fig. 4). Fig.4 Clustered heatmap of amino acid mutations from 202 Chinese RSV-B sequences (GISAID/NCBI). Regions A and B mark two coordinated mutation events. The vertical axis displays mutation sites (10-90% frequency) with an adjacent color bar for protein segments; the horizontal axis shows sequence identifiers with an adjacent color bar for collection time. The 29 Dalian sequences contained mutations at 127 amino acid sites, including 44 high-frequency mutation sites. The G protein had the most high-frequency sites (15), followed by the L (9) and F (7) proteins. The M2-2 protein contained 5 high-frequency sites, the NS2 and N proteins each contained 2, while the NS1, P, SH, and M2-1 proteins each contained 1 high-frequency site. Nineteen mutation sites showed frequencies exceeding 50%, distributed as follows: 1 in the N protein, 8 in G, 4 in M2-2, and 3 in L. Further analysis showed that 15 of these 19 high-frequency mutation sites were included in the second coordinated mutation event identified in Chinese sequences. The other four high-frequency mutations—V97I (N), A74V (G), I2T (M2-2), and T1987I (L)—all showed mutation frequencies exceeding 95% in the Chinese sequences from the database (Fig. 5). Notably, the Dalian sequences contained a unique mutation in the SH protein: a glutamine-to-stop codon substitution at position 59 (Q59*), found in 5 of 29 sequences (17.24%). Although the frequency of this mutation was below 50% in the local dataset, it had been reported in only one of the 202 Chinese sequences from the database (Figs. 5 and 6). Fig.5 Lollipop plot of amino acid mutations in Dalian sequences relative to reference strain EPI_ISL_1653999. The horizontal colored bar represents the reference protein regions (NS1, NS2, N, P, M, SH, G, F, M2-1, M2-2, L). Lollipop markers denote mutation sites; their height corresponds to mutation frequency, with sites >10% highlighted in red. Fig.6 Three-dimensional structure of the SH protein amino acid residues. The blue ribbon represents amino acid residues 1–58. The glutamine-to-stop codon mutation at position 59 (Q59*) is highlighted in red. The gray ribbon represents residues 60–65. Discussion This study reports the epidemiological characteristics of RSV in Dalian from October 2023 to September 2025. The RSV epidemic period in the 2024–2025 season was both delayed and prolonged compared to the previous year, with a marked increase in epidemic intensity. In contrast to most previous studies reporting the dominance of either subtype A or B [17,18] , subtyping results in this study revealed that both subtypes circulated at comparable intensities during the 2023–2025 surveillance period. Phylogenetic analysis indicated that B.D.4.1.1 was the dominant RSV-B lineage in China during 2020–2021. Although closely related to strains from other countries, large-scale local evolution toward B.D.E.2 occurred exclusively in China, suggesting region-specific constraints on viral evolution despite high cross-regional transmissibility. B.D.E.2 circulated notably but never replaced B.D.4.1.1, potentially due to non-pharmaceutical interventions (NPIs) during 2020–2021 that disrupted RSV transmission [19,20] . Globally dominant since 2021, B.D.E.1 entered China in late 2022, was reported in Beijing in 2023, and rapidly supplanted B.D.4.1.1 to become the nationally dominant lineage. Altered selection pressure in B.D.E.1 may contribute to its immune evasion potential [15] . In Dalian, B.D.E.1 comprised >90% of locally sequenced cases from 2023–2025, with some strains clustering in transboundary transmission chains. The sporadic detection of B.D.E.1.2 elsewhere underscores the need for sustained genomic surveillance of B.D.E.1 evolution, although this sublineage has not been observed in China to date. The F and G proteins of RSV-B carry antigenic determinants capable of eliciting neutralizing antibodies in the host. They play critical roles in viral infectivity and pathogenesis, making them key targets for the development of vaccines and antiviral therapeutics [21] . The F protein is the primary target for RSV antivirals and vaccines. Currently approved F protein-targeting strategies against RSV-B include two monoclonal antibodies—palivizumab [10] and nirsevimab [22] —and the vaccine Abrysvo [23] . Palivizumab binds to antigenic site II (residues 254–277), present in both Pre-F and Post-F conformations. Mutations in its core (K272, S275) or secondary (N268, T270, E271, S276) thermolabile residues can reduce neutralizing activity by respectively [24-26] , with N262D and K272E also linked to resistance [27] .In this study, site II was relatively conserved among the 202 Chinese sequences, with only a low-frequency S276N variant detected. The Dalian sequences remained highly conserved in this region, with no relevant mutations observed.Nirsevimab targets the Pre-F-specific site Ø (residues 62–69 & 196–212). Key residues affecting its efficacy include K65, K68, M206, N208, R209, and S211 [28-30] . Notably, K68E disrupts binding electrostatically, N208Y/S severely impairs it, and the K65Q+S211N combination reduces neutralization.In our dataset, S211N was prevalent in Chinese sequences but not accompanied by K65Q; low-frequency variants K68N, M206I, and R209Q were also detected. All Dalian sequences carried S211N alone. It is noteworthy that nirsevimab is currently the only RSV prophylactic agent approved for clinical use in China. Although our analysis suggests that its key binding sites in site Ø may not be substantially compromised, the ongoing accumulation of variations in this region underscores the need for continued vigilance against the emergence of vaccine-escape variants. The G protein is an increasingly important target for RSV countermeasures. In circulating Chinese RSV-B strains, high-frequency mutations are concentrated in the mucin-like domains (MLD-I/II), while the central conserved domain (CCD) remains relatively conserved and can induce cross-protective immunity. The CCD harbors the CX3C motif, a key immunological target that mimics host Fractalkine (CX3CL1) to bind CX3CR1, disrupting immune signaling and aiding viral evasion [31-33] . Although CCD-targeting antibodies offer protection, the G protein’s inherent low immunogenicity limits durable immunity [34-35] . To overcome this, a preclinical nanoparticle vaccine candidate incorporating a S177Q mutation within the CCD was developed, which enhanced immunogenicity and specifically blocked the CX3C–CX3CR1 interaction in mice without affecting endogenous CX3CL1 binding [36]. Our mutation analysis found the CCD to be largely stable; aside from N176S (which has not been detected since late 2023), few mutations occurred. This conservation suggests that vaccine candidates like the S177Q-modified version may retain immunogenicity against currently dominant strains in China. However, this hypothesis requires further validation through additional biological experiments. The L protein plays a critical role in multiple stages of viral mRNA synthesis, including RNA strand elongation, 5′-cap formation (via GpppN transfer), and subsequent methylation (cap-0/1), thereby ensuring mRNA integrity and aiding in the evasion of host innate immune responses [37] . Its diverse enzymatic activities and central role in regulating viral replication make the L protein one of the most promising targets for antiviral drugs aimed at inhibiting RSV replication [38] . Several therapeutic agents targeting the L protein have advanced into clinical trials, such as PC786, which inhibits RSV RNA-dependent RNA polymerase (RdRp) activity, and EDP-323, which binds to the capping domain of the L protein to suppress RSV replication. In this study, although multiple amino acid variations were observed in the RdRp and PRNTase regions of the L protein, none of them corresponded to previously reported resistance mutations associated with the aforementioned drugs [39-41] . Past RSV research has centered on the F, G, and L proteins. Advances in whole-genome sequencing now enable broader analysis. Here, we analyzed coordinated amino acid mutations across the RSV-B genome in Chinese sequences. The second coordinated mutation event (emerging mainly in 2023) involved significantly more sites than the first (2021) and spanned different proteins (F, G, L, M2-2 vs. G and N). Key mutations in this event lie in functionally important regions, such as S211N in F protein SiteØ, K570R in L protein RdRp, and R1759K in L protein MTase. Whether this coordinated pattern enhances immune escape requires further study. The impact of a unique SH protein mutation (Q59*) found in Dalian sequences on viral fitness and transmission also warrants investigation. While whole-genome sequence analysis of RSV-B in China has been limited in the past, this study presents the first whole-genome sequencing of RSV-B from pediatric pharyngeal swabs in Dalian. By integrating these data with Chinese sequences from public databases spanning 2020 to the present, we conducted a comprehensive genomic characterization, providing valuable information for global RSV surveillance. Our findings document the shift in the dominant RSV-B lineage in China from B.D.4.1.1 to B.D.E.1 in recent years, confirm the high variability of the G protein reported in earlier studies, and identify amino acid mutations in drug-target regions of the G and F proteins. Furthermore, this work supplements previously scarce data on proteins such as NS1, NS2, N, P, M2-1, M2-2, and SH, offering a more complete perspective on RSV and supporting the development of targeted preventive therapeutics. Conclusion The results of this study indicate that respiratory syncytial virus B (RSV-B) continues to be dominated by the B.D.E.1 genotype in China, and locally circulating strains have gradually evolved into geographically distinct sub-lineages during transmission. 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EDP-323, a small molecule L-protein inhibitor in development against respiratory syncytial virus. Enan. Pharmaceut. Available: https://www.enan ta.com/wp-content/uploads/2022/10/EDP-323-RSV22-Final-1.pdf. (Accessed 5 August 2024). Supplementary Material File (fig2.tif) Download 9.65 MB File (fig3-1.tif) Download 7.52 MB File (fig3-2.tif) Download 8.12 MB File (fig4.tif) Download 8.07 MB File (fig5.tif) Download 7.10 MB File (fig6.tif) Download 5.57 MB File (s1.xlsx) Download 160.80 KB File (s2.xlsx) Download 15.51 KB File (s3.xlsx) Download 887.58 KB Information & Authors Information Version history V1 Version 1 15 December 2025 Copyright This work is licensed under a Non Exclusive No Reuse License. Keywords epidemiology genetic variation genetics infection respiratory syncytial virus virus classification Authors Affiliations Kangsheng Zhou Dalian Medical University View all articles by this author Mingchun Luan Dalian Medical University View all articles by this author Xiaoman Cui Dalian Medical University View all articles by this author Huan Wang Dalian Medical University View all articles by this author Yuhui Wang Dalian Medical University View all articles by this author Teng Ge Dalian Medical University View all articles by this author Xisheng Yin Dalian Medical University View all articles by this author Xingying Lang 0009-0003-3353-1932 [email protected] Dalian Medical University View all articles by this author Metrics & Citations Metrics Article Usage 306 views 103 downloads .FvxKWukQNSOunydq8rnd { width: 100px; } Citations Download citation Kangsheng Zhou, Mingchun Luan, Xiaoman Cui, et al. 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