# Epidemiological characteristics and whole-genome analysis of respiratory syncytial virus in Jining city from February 2023 to December 2024

**Authors:** Julong Wu, Yongjian Jia, Yajuan Jiang, Feifei He, Xuezhen Shi, Xiaoyu Wang, Ying Yue, Wei Liu, Huixin Dou, Boyan Jiao

PMC · DOI: 10.3389/fmicb.2026.1702525 · Frontiers in Microbiology · 2026-02-11

## TL;DR

This study analyzed RSV in Jining city from 2023 to 2024, finding patterns in its spread and genetic changes, especially in children under 5.

## Contribution

The study provides new insights into RSV's genetic diversity and antigenic evolution in Jining, China.

## Key findings

- RSV positivity was 1.98%, with higher rates in children under 5 years of age.
- RSV-A and RSV-B strains showed alternating dominance during two peaks in 2023.
- Mutations in antigenic epitopes of G and F proteins suggest ongoing antigenic evolution.

## Abstract

Respiratory syncytial virus (RSV) is a major viral pathogen causing respiratory tract infections in children, often leading to bronchiolitis, pneumonia, and even death. This study aimed to investigate the epidemiological patterns and whole-genome characteristics of RSV circulating in Jining city between February 2023 and December 2024.

From February 2023 to December 2024, a total of 5,042 throat swab samples were collected from influenza-like illness (ILI) cases at two sentinel hospitals in Jining. RSV was detected using reverse transcription quantitative real-time PCR (RT-qPCR). RSV-positive samples were subjected to whole-genome sequencing. Phylogenetic trees were constructed based on the whole genome and G gene sequences, and antigenic variation in viral proteins was analyzed.

RSV positivity was 1.98% (100/5042), with higher rates in children under 5 years of age. RSV activity peaked in April–May 2023 and December 2023–January 2024. A total of 29 RSV genomes were sequenced, including 18 RSV-A and 11 RSV-B. RSV-A was dominant during the first peak, and RSV-B during the second. Most RSV-A strains belonged to clade AD.3 and genotype ON1; RSV-B strains clustered into clades B.D.E.1, B.D.4.1.1, and B.D.E.2, all within genotype BA9. Mutations were identified in antigenic epitopes of the G and F proteins, including amino acid substitutions and changes in glycosylation and phosphorylation sites.

RSV-A and RSV-B circulated in Jining in an alternating pattern, with evidence of ongoing antigenic evolution. Continued RSV surveillance and accelerated vaccine development are essential.

## Linked entities

- **Proteins:** g (garnet), f (forked)
- **Diseases:** bronchiolitis (MONDO:0002465), pneumonia (MONDO:0005249)

## Full-text entities

- **Genes:** NS2 [NCBI Gene 57762], OCA2 (OCA2 melanosomal transmembrane protein) [NCBI Gene 4948] {aka BEY, BEY1, BEY2, BOCA, D15S12, EYCL}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, IVNS1ABP (influenza virus NS1A binding protein) [NCBI Gene 10625] {aka ARA3, FLARA3, HSPC068, IMD70, KLHL39, ND1}, CX3CR1 (C-X3-C motif chemokine receptor 1) [NCBI Gene 1524] {aka CCRL1, CMKBRL1, CMKDR1, GPR13, GPRV28, V28}, IFNA1 (interferon alpha 1) [NCBI Gene 3439] {aka IFL, IFN, IFN-ALPHA, IFN-alphaD, IFNA13, IFNA@}, IFNB1 (interferon beta 1) [NCBI Gene 3456] {aka IFB, IFF, IFN-beta, IFNB}, IFI27 (interferon alpha inducible protein 27) [NCBI Gene 3429] {aka FAM14D, ISG12, ISG12A, P27}
- **Diseases:** cough (MESH:D003371), infection (MESH:D007239), dyspnea (MESH:D004417), RSV infection (MESH:D018357), Viral infections (MESH:D014777), death (MESH:D003643), respiratory illness (MESH:D012140), sore throat (MESH:D010612), ILI (MESH:D007251), rhinorrhea (MESH:D012818), inflammatory (MESH:D007249), respiratory tract infections (MESH:D012141), infectious disease (MESH:D003141), illness (MESH:D002908), bronchiolitis (MESH:D001988), fever (MESH:D005334), pneumonia (MESH:D011014), wheezing (MESH:D012135)
- **Chemicals:** P (MESH:D010758), BK-RSVAB024 (-), BA9 (MESH:C518022)
- **Species:** Influenza B virus (no rank) [taxon 11520], Homo sapiens (human, species) [taxon 9606], H3N2 subtype (serotype) [taxon 119210], Respiratory syncytial virus (no rank) [taxon 12814], H1N1 subtype (serotype) [taxon 114727], Orthopneumovirus (genus) [taxon 1868215], Human adenovirus sp. (species) [taxon 1907210], Severe acute respiratory syndrome coronavirus 2 (no rank) [taxon 2697049], Morganella morganii (species) [taxon 582]
- **Mutations:** P95S, A42V, S276N, T1969, S265, L15F, I118T, T310, T1942I, I1780V, S299, T241P, A1943T, N27, V1646I, K2065N, I114T, S283P, V269A, L248I, M73L, D35N, Y177, T1381I, S1745T, S143, I227T, G1550S, N299, T118, T300I, C49F, T12I, T126P, S137, F300, N121S, I1741M, V225I, T241, H1707N, V151I, Y61H, E49D, T300, S291L, L289I, N126, H258L, T105, C49R, N1773I, T219I, N380H, S265P, H2135Y, I32V, I63T, T28, I40L
- **Cell lines:** ON1 — Mus musculus (Mouse), Hybridoma (CVCL_C7RB), BA9 — Homo sapiens (Human), Melanoma, Cancer cell line (CVCL_U803), SKY-8237 — Homo sapiens (Human), Transformed cell line (CVCL_5B65)

## Full text

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## Figures

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## References

82 references — full list in the complete paper: https://tomesphere.com/paper/PMC12932593/full.md

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Source: https://tomesphere.com/paper/PMC12932593