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. 2026 Feb 19;105(5):106669. doi: 10.1016/j.psj.2026.106669

Divergent tissue tropism and pathogenicity of novel recombinant GI-19 and GI-22 infectious bronchitis virus strains

Yuqing Li a, Xiaolin Zhang a, Ting Zhou a, Qingcheng Yang a, Qian Chen a, Ting Xu a, Chunlin Yu b, Chaowu Yang b, Hongning Wang a, Changwei Lei a, Anyun Zhang a, Xin Yang a,⁎
PMCID: PMC12964293  PMID: 41764964

Abstract

Infectious bronchitis virus (IBV) is a highly contagious pathogen in poultry that causes significant economic losses worldwide. In this study, two novel IBV isolates, CK/CH/MY/24053 of the GI-19 lineage and CK/CH/SC/25605 of the GI-22 lineage, were isolated and analyzed through whole-genome sequencing, recombination mapping, pathogenicity assessment in SPF chickens, and S1 protein structural comparison. Whole-genome analysis revealed that CK/CH/SC/25605 underwent recombination across different genotypes involving multiple parental lineages, whereas CK/CH/MY/24053 exhibited recombination within the same genotype. Pathogenicity assessment in specific-pathogen-free chickens showed that CK/CH/MY/24053 primarily exhibited kidney tropism, resulting in pronounced renal lesions and high viral loads in the kidneys, whereas CK/CH/SC/25605 predominantly targeted the respiratory tract, causing severe tracheal and pulmonary lesions and a higher mortality rate compared with typical QX strains. Viral shedding occurred in both the trachea and intestines, indicating active replication. Structural analysis of the S1 protein revealed only subtle differences within the hypervariable regions between the two isolates. Notably, both strains were isolated from flocks vaccinated with the QXL87 vaccine, and recombination analysis identified QX-derived genomic segments in each isolate. Although these structural differences alone do not provide direct evidence of antigenic variation or vaccine escape, they may reflect potential alterations in antigenicity under vaccine-induced immune pressure and therefore warrant further investigation. Overall, these findings demonstrate cross-genotype recombination, distinct tissue tropism, and subtle S1 structural variations, underscoring the importance of continued surveillance of recombination events in circulating IBV strains and their possible implications for vaccine effectiveness.

Keywords: IBV, Genome recombination, Pathogenicity, GI-19, GI-22

Introduction

Infectious bronchitis virus (IBV), belongs to the order Nidovirales, genus Gammacoronavirus of the family Coronaviridae, is one of the most economically significant pathogens in the global poultry industry (Cavanagh, 2007). The virus causes a highly contagious disease in chickens, characterized by respiratory distress, nephritis, and reduced egg production (Falchieri, et al., 2024), leading to significant economic losses. Despite decades of vaccine use, infectious bronchitis (IB) remains endemic in many regions, largely due to the extensive genetic and antigenic variability of IBV.(Jackwood, 2012).

The IBV genome consists of a single-stranded, positive-sense RNA of approximately 27.6 kb, encoding both structural and non-structural proteins (Quinteros, et al., 2022). Among these proteins, the spike (S) glycoprotein plays a critical role in receptor binding and membrane fusion, thereby determining viral infectivity and host specificity. The S1 subunit of the spike protein is the major determinant of serotype specificity and a key inducer of neutralizing antibodies (Valastro, et al., 2016; Xiao, et al., 2025), making it the principal target for molecular classification and vaccine development (Tan, et al., 2016; Wickramasinghe, et al., 2011).

Genetic variation within the S1 gene is frequently associated with antigenic drift, immune escape, and poor cross-protection among IBV strains (Wickramasinghe, et al., 2014).Currently, multiple genotypes, including QX and GI-22, are co-circulating in poultry populations worldwide, each exhibiting distinct tissue tropism, pathogenicity, and vaccine response (Abozeid, 2023; Rafique, et al., 2024). Among these, the QX genotype is one of the most prevalent lineages in Asia and Europe (Abro, et al., 2012; Lee, et al., 2021; Nakanishi, et al., 2023). First identified in China in the late 1990s (Wang YuDong, et al., 1998), QX-type strains have become dominant in commercial poultry farms due to their strong tissue tropism for both respiratory and renal systems, as well as limited cross-protection with classical vaccine such as H120 or 4/91 (Yan, et al., 2017). Despite the introduction of QX-based vaccines like QXL87 (Wang, et al., 2024), field outbreaks continue to occur, suggesting continuous viral evolution driven by immune pressure (Lu, et al., 2024).

In contrast, the GI-22 lineage has been reported mainly in China and neighboring regions (Guo, et al., 2025b). Although less prevalent than QX, GI-22 strains have drawn increasing attention in recent years due to their genetic relatedness to certain vaccine-derived viruses and frequent recombination with QX-like or Mass-type strains (Wang, et al., 2025a; Xie, et al., 2025c). Some GI-22 isolates have shown moderate pathogenicity and distinct antigenic characteristics, resulting in limited cross-protection when chickens vaccinated with heterologous serotypes are challenged (Meng, et al., 2024).

As a member of RNA viruses, recombination serves as a major evolutionary mechanism driving the genetic diversity of IBV (Bali, et al., 2021; Rohaim, et al., 2020; Zhao, et al., 2016). Natural recombination events have been frequently observed between vaccine and field strains (Guzmán, et al., 2025). These recombinant viruses may exhibit altered pathogenicity, tissue tropism, or immunogenicity compared with their parental strains (Zeng, et al., 2025a). Recombinant strains carrying a spike gene from one lineage and a genomic backbone from another are of particular concern, as such mismatches may alter replication properties or escape immune protection.

In this study, we isolated two IBV field isolates representing the GI-19 and GI-22 lineages. CK/CH/MY/24053 (GI-19) contained recombination signals derived from multiple QX-related fragments, whereas CK/CH/SC/25605 (GI-22) exhibited cross-genotype recombination, including QX-derived segments. These isolates, obtained from commercial poultry flocks in Sichuan, were selected to investigate how different recombination patterns influence viral phenotype. Although GI-22 strains have been increasingly reported in the field, it remains unclear whether cross-genotype recombination confers distinct pathogenic characteristics compared with within-genotype recombination, particularly under vaccine-induced immune pressure. To address this gap, we compared the pathogenicity, tissue tropism, viral shedding, and S1 structural features of the two isolates in vivo, providing insights into the impact of recombination on IBV phenotypic divergence and potential immune escape.

Material and methods

Sample collection and virus isolation

Tissue samples were collected from diseased layer chickens aged 10–90 days on an intensive chicken farm in Sichuan Province, China, between 2024 and 2025. All chickens had previously been vaccinated with H120, 4/91, or QXL87. Collected tissues were homogenized and centrifuged at 5000 x g for 10 min. The resulting supernatants were inoculated into 9-day-old specific pathogen-free (SPF) embryonated chicken eggs for virus amplification. After 48 h of incubation, allantoic fluid was harvested and subjected to three consecutive rounds of amplification. The final allantoic fluid was collected for RNA extraction using TRIzol regent (Invitrogen, USA). Complementary DNA (cDNA) was synthesized with the PrimeScrip RT reagent Kit (Takara, Japan) to confirm IBV infection. In addition, to exclude potential co-infections that might confound the recombination analysis, samples were tested for Newcastle disease virus (NDV), fowl adenovirus (FAdV), avian influenza virus (AIV), and avian leukosis virus (ALV) by RT-PC, and all results were negative. The primer sequences used for each virus are listed in Supplementary Table 1. The 50% of egg infection dose (EID50) was determined using the Reed-Muench method and used for subsequent virulence assessment (Matumoto, 1949).

Viral genome sequencing

Using cDNAs as the template, the complete viral genome was amplified with seven pairs of specificically designed primers. Adjacent genomic fragments were designed with overlapping regions of at least 200 bp to ensure accurate sequence assembly. Polymerase chain reaction (PCR) products were purified and cloned into the pMD18-T vector (Takara, Japan) for sequencing (Youkang Biological Technology, Zhejiang, China). The 5′ and 3′ terminal regions of each isolate were obtained using the SMARTer RACE 5′/3′ kit (634858, TaKaRa, China). Sequencing reads were assembled using the SeqMan program within the Lasergene 7.1 software package (DNASTAR Inc., Madison, WI, USA) to generate the full-length IBV genome sequences.

Alignments and phylogenetic analysis

Sequence similarity analyses were performed using nucleotide BLAST in the National Center for Biotechnology Information (NCBI) database. 173 representative S1 gene sequences of IBV strains, including multiple genotypes and commonly used vaccine strains, were retrieved from the GenBank database according to previously described criteria (Valastro, Holmes, Britton, Fusaro, Jackwood, Cattoli and Monne, 2016). Phylogenetic trees were conducted using MEGA version11 with the neighbor-joining method (Tamura, et al., 2021). Bootstrap analysis was performed with 1000 replicates to assess the robustness of the branching pattern. The resulting pathogenetic trees were visualized and annotated using the online tool iTOL (https://itol.embl.de/).

Putative recombination analysis

Potential recombination events were screened using seven algorithms in RDP4, including RDP, GENECONV, BootScan, MaxChi, Chimera, SiScan, and 3Seq. Only events supported by at least four of the methods with p-values below 10-5 were considered credible. To further validate the putative recombination signals, similarity plot analysis was performed using SimPlot version 3.5.1 with a window size of 200 bp, a step size of 20 bp, and a transition-to-transversion ratio of 2.0. Details of the recombination breakpoints and the corresponding statistical support values calculated by each method are provided in Supplementary Table 2.

Structural modeling and comparison of the S1 protein

Three-dimensional structural models of the S1 subunit of the IBV spike protein were generated using the SWISS-MODEL server (https://swissmodel.expasy.org). Amino acid sequences corresponding to the S1 region of the studied IBV strain, as well as the vaccine reference strains H120 (FJ888351.1), QXL87 (PP100176) and 4/91 (MH021175.1), were submitted for homology modeling. For all models, the cryo-electron microscopy structure of the IBV spike protein (PDB ID: 6CV0, chain A) was automatically selected by SWISS-MODEL as the template based on sequence similarity. Model quality was evaluated using the Global Model Quality Estimation (GMQE) and QMEAN scores provided by SWISS-MODEL. All models were generated using the same template and modeling pipeline to ensure structural comparability among strains. The predicted S1 structures were visualized and analyzed using PyMOL. Structural alignments were performed by Cα superposition, and root mean square deviation (RMSD) values were calculated to quantify structural differences between the S1 models. In addition, surface-exposed regions of the S1 protein were inspected to assess potential conformational variations relevant to antigenicity.

Pathogenicity of IBV isolates in 1-Day-Old SPF chickens

To evaluate the virulence of IBV different genotypes, QX and GI-22 were selected for pathogenicity assessment in 1-day-old SPF chickens. The chickens were randomly divided into 3 groups, with 20 chickens in each group. Each experimental group was inoculated intranasally with 105 EID50 of the corresponding strain via eye drops and intranasal routes, in a total volume of 0.2 mL, while the mock group received an equal volume of PBS. Chickens were observed daily for 14 days after infection to record clinical signs, morbidity and mortality. The clinical severity was scored as follows: 0 = normal; 1 = mild signs (slight tearing or tracheal rales); 2 = moderate to severe signs (excessive tearing, watery nasal discharge, frequent sneezing, or coughing); and 3 = death. At 3, 5, 7, 11 and 14 days post-infection (dpi), oropharyngeal and cloacal swabs were collected from all surviving chickens for quantitative detection of viral shedding using RT-qPCR. At 3, 5, 9, 12 and 14 dpi, the chicken flock was euthanized humanely to obtain tissue samples. Each group had 2 to 6 chickens at each time point, and the exact number depended on the previous death situation. Tissue samples, including the trachea, lungs, kidneys, bursa of Fabricius, cecum, ileum, and jejunum were collected for virus load determination. In addition, tissues showing evident lesions were fixed with 10% neutral buffered formalin for histopathological examination.

Histopathological examination

At 7 dpi, tissue samples from the trachea, lungs and kidneys were collected for histopathological examination. The tissues were fixed in 10% neutral buffered formalin, dehydrated through a graded ethanol series, embedded in paraffin, sectioned, and stained with hematoxylin and eosin (H&E) for observation under a light microscope.

Tissue viral load and viral shedding determination

Total RNA was extracted from collected tissues, throat swabs, and cloacal swabs with TRIzol reagent (Invitrogen, USA) following the manufacturer’s protocol. First-strand cDNA synthesis was performed with the PrimeScript RT Reagent Kit (Takara, Japan) according to the supplier’s instructions. A pair of specific primers targeting the IBV nucleocapsid (N) gene (forward: 5′-TGCCGTAGGTTCAATACTCCT-3′; reverse: 5′-TCACCAGTGTATTTCTGCACC-3′) was designed using SnapGene software (version 6.1.1) and synthesized by Youkang Biological Technology (Zhejiang, China). The viral genome load was quantified by absolute real-time RT-qPCR using the standard curve method, and results were expressed as RNA copy numbers per microgram of total RNA.

Statistical analysis

Statistical analyses were performed using GraphPad Prism version 9 (GraphPad, USA). Survival curves were generated using the Kaplan–Meier method, and statistical differences between groups were assessed using the Log-rank (Mantel-Cox) test. Viral load and virus shedding data collected at multiple time points were analyzed using two-way analysis of variance (ANOVA) with repeated measures to assess the effects of time, group, and their interaction. Data are presented as mean ± standard error of the mean (SEM). A P value < 0.05 was considered statistically significant.

Animals and ethics statement

All procedures involving animals were reviewed and approved by the Animal Ethics Committee of the College of Life Sciences, Sichuan University (SCU250305001). Animal care and experimental protocols complied with the university’s regulations on animal management and welfare.

Results

Virus isolation and identification

The supernatant of homogenized IBV-positive tissues was inoculated into the allantoic cavities of 9-day-old SPF chicken embryos. After 48 hours of incubation, the allantoic fluid was collected and subsequently passaged for a total of three consecutive passages through embryos to enrich viral replication. The resulting third-passage (E3) IBV isolates were used for subsequent experiments, including pathogenicity and virulence assessment. Embryos in the experimental groups displayed classical IBV-associated lesions, including growth retardation, stunting, and spinal curvature (Fig. 1A). PCR assays confirmed the presence of IBV and excluded potential contaminants, including Newcastle disease virus (NDV), fowl adenovirus (FAdV), avian influenza virus (AIV), and avian leukosis virus (ALV), indicating successful isolation of pure IBV strains. The two isolates were designated CK/CH/MY/24053 and CK/CH/SC/25605 (Fig. 1B). Viral titers were determined by tenfold serial dilution of allantoic fluid in PBS, followed by inoculation into the allantoic cavities of 9-day-old SPF embryos. Embryo lesions were examined after 6 days, and the 50% embryo infectious dose (EID50) was calculated using the Reed-Muench method, yielding titers of 107.54 EID50/mL for CK/CH/MY/24053 and 106.72 EID50/mL for CK/CH/SC/25605.

Fig. 1.

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Detection of IBV and evaluation of embryo infection. (A) PCR detection of IBV in the two recombinant strains with a 2000-bp DNA marker. IBV-specific amplification is shown, and the absence of contamination by ALV, NDV, AIV, and FAV was confirmed. (B) Representative chicken embryos after inoculation with the recombinant strains. Left panel shows negative control and CK/CH/SC/25605 (GenBank ID: PX694006); right panel shows negative control and CK/CH/MY/24053 (GenBank ID: PX694005).

Genotypes of the IBV isolates in Sichuan Province

Phylogenetic analysis based on the S1 gene was performed for the two newly isolated strains together with 173 representative IBV strains covering all major lineages using MEGA11. CK/CH/MY/24053 clustered within the GI-19 genotype and CK/CH/SC/25605 belonged to GI-22 (Fig. 2). BLAST analysis showed that CK/CH/MY/24053 shared 99.82% nucleotide identity with QX strain L1148 (UK, 2017; GenBank:KY933090.1), while CK/CH/SC/25605 was 93.22% identical to CKCHSDWF2021-09 (Shandong, China, 2024; GenBank: PQ058543.1). These results indicate that both isolates represent distinct IBV genotypes currently circulating in poultry populations.

Fig. 2.

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Phylogenetic analysis of the S1 gene sequences of IBV isolates. The tree was constructed using the S1 gene sequences of the two isolates along with 173 reference strains representing 32 major genotypes (GI-GVI-1) using MEGA11 software. The newly isolated strains are highlighted with a yellow background.

Recombination analysis

In order to investigate the genomic evolution of both IBV isolates, we conducted a systematic analysis of their complete genomes using RDP4 in combination with seven recombination detection methods. The RDP4 analysis revealed that CK/CH/MY/24053 originated from a homologous recombination event between two GI-19-related parental strains, whereas CK/CH/SC/25605 resulted from a cross-genotype recombination involving a GI-19 major parent and a GI-7 minor parent. All recombination events were supported by six independent detection methods in RDP4, indicating strong statistical confidence in the inferred recombination patterns. SimPlot analysis further confirmed the presence of clear recombination signals in both genomes (Fig. 3A-B).

Fig. 3.

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Recombination analysis and phylogenetic validation of CK/CH/MY/24053 and CK/CH/SC/25605. (A-B) SimPlot similarity plots showing recombination signals and breakpoint regions of CK/CH/MY/24053 (A) and CK/CH/SC/25605 (B). (C-E), Phylogenetic trees of breakpoint-defined fragments of CK/CH/MY/24053. (F-H), Phylogenetic trees of breakpoint-defined fragments of CK/CH/SC/25605. All phylogenies were generated using the Neighbor-Joining method with 1,000 bootstrap replicates.

For CK/CH/MY/24053, the 1–7987 nt and 25992–27662 nt regions shared 91.26% sequence identity with the major parental strain D2002/2/2012, while the 7988–25991 nt region exhibited 97.66% identity with the minor parental strain ZJJX211028-2. All recombination regions of CK/CH/MY/24053 are located within ORF1a, and the genome structure illustrates the correspondence between the breakpoints and functional domains. Phylogenetic analyses of these breakpoint-defined fragments showed overall concordant clustering with the inferred parental strains. Notably, the 25992–27662 nt region clustered with LDT3-A rather than GI-19 (Fig. 3C-E).

For CK/CH/SC/25605, the 1–21336 nt and 23004–27698 nt regions shared 96.6% sequence identity with the major parental strain CK/CH/SX/2106, while the 21337–23003 nt fragment exhibited 96.96% identity with the minor parental strain TW2575/98. The recombination region of CK/CH/SC/25605 is located within the S gene, and the viral genome structure clearly shows the breakpoints corresponding to the functional domain. All breakpoint-defined phylogenies demonstrated strict parental-specific clustering, fully consistent with RDP4 predictions (Fig. 3F-H).

Taken together, the congruence between topology switching, breakpoint distribution, and parental assignment strongly supports that CK/CH/MY/24053 originated from a homologous recombination within the GI-19 genotype, with all breakpoints located in ORF1a, whereas CK/CH/SC/25605 was formed through a recombination event between GI-19 and GI-7 genotypes, with the breakpoint occurring within the S gene. The genome structure and recombination analysis together provide a clear illustration of how these breakpoints correspond to specific ORFs and functional domains.

Structural comparison of the S1 protein

Structural comparison of the two field isolates GI-22 and GI-19 with the vaccine strains H120, 4/91 and QXL87 showed that both field strains share a high degree of overall similarity with the vaccine S1 proteins (Fig. 4A). Analysis of S1 domain organization showed the positions of HVR I, HVR II and HVR III in the two field isolates, with slight differences observed in the boundaries of these regions between CK/CH/SC/25605 and CK/CH/MY/24053 (Fig. 4B). Homology models for all S1 proteins were generated using SWISS-MODEL (https://swissmodel.expasy.org), with the cryo-electron microscopy structure of IBV spike protein (PDB ID: 6CV0, chain A) as the template. Model quality was assessed using GMQE (0.74) and QMEAN (0.74) scores, and sequence identity to the template was 81.07%. RMSD values for the HVR I, HVR II and HVR III regions were low, ranging from 0.015 to 0.115 angstroms, indicating that the core fold is largely conserved without noticeable global rearrangements (Fig. 4C). Minor structural differences were mainly observed in surface-exposed loop regions, including parts corresponding to the hypervariable regions (Fig. 4D). These local variations, although limited, are positioned on antigen-exposed surfaces. The isolation of these field strains from vaccinated flocks suggests that such structural features may influence antibody recognition, but their precise impact requires further experimental investigation.

Fig. 4.

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Comparison of S1 protein sequences, hypervariable regions, RMSD, and structures of field isolates and vaccine strains. (A) Amino acid sequence alignment of the S1 proteins from the two field isolates CK/CH/SC/25605 and CK/CH/MY/24053 and three vaccine strains H120, 4/91, and QXL87, highlighting sequence variation among strains. (B) Schematic representation of hypervariable regions in the S1 proteins of the two field isolates, with red indicating HVR I, HVR II, and HVR III. (C) RMSD comparison of different S1 regions between the field isolates and vaccine strains. (D) PyMOL superimposition of S1 protein trimers from the field isolates and vaccine strains, with colors representing distinct structural regions as shown.

Clinical signs and mortality of IBV-infected chickens

To evaluate the pathogenicity of two IBV isolates, groups of 20 SPF 1-day-old chickens were inoculated with 105 EID50 of CK/CH/MY/24053 or CK/CH/SC/25605 via eye drops and intranasal routes, while the control group received PBS. Clinical signs were monitored until 14 dpi. The infected groups exhibited a similar onset of clinical symptoms around 4 dpi, including head shaking, sneezing, tracheal wheezing, and watery feces. Chickens infected with CK/CH/SC/25605 exhibited more severe clinical signs than those infected with CK/CH/MY/24053. Clinical scores peaked between 8 and 10 dpi for all isolated and gradually declined thereafter (Fig. 5B). The mortality rates of the two inoculated groups were 3/20 (15%) for CK/CH/MY/24053 and 7/20 (35%) for CK/CH/SC/25605, respectively, whereas no clinical signs or deaths were observed in the control group (Fig. 5A). Survival analysis revealed a significant difference between CK/CH/SC/25605-infected chickens and the PBS control group (Log-rank test), whereas no significant difference was observed between the CK/CH/MY/24053 and PBS groups.

Fig. 5.

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Survival and clinical assessment of chickens infected with recombinant IBV strains. (A) Survival curves of chickens following infection with CK/CH/MY/24053 or CK/CH/SC/25605. (B) Clinical scores of infected chickens over the observation period, showing the progression of disease symptoms.

Histopathological observation in trachea, lung and kidney

Histopathological examination showed that both isolates caused notable lesions in multiple organs, with distinct tissue tropism. In the trachea, CK/CH/SC/25605 induced ciliary loss, epithelial cell swelling, tissue disorganization, goblet cell hyperplasia, and inflammatory cell infiltration, and CK/CH/MY/24053 showed epithelial structure changes and inflammatory infiltration. In the lungs, CK/CH/SC/25605 showed tissue disruption and inflammatory cell infiltration, and CK/CH/MY/24053 displayed alveolar septal thickening, focal consolidation, and inflammatory infiltration. In the kidneys, CK/CH/MY/24053 showed tubular degeneration, structural disorganization, and inflammatory infiltration, and CK/CH/SC/25605 showed tubular epithelial swelling and interstitial inflammation. Overall, CK/CH/SC/25605 affected the respiratory tract, particularly the trachea and lungs, whereas CK/CH/MY/24053 affected the renal tissue (Fig. 6).

Fig. 6.

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Histopathological analysis of trachea, lung, and kidney at 7 days post-infection (dpi). Representative hematoxylin and eosin (HE) stained sections from chickens infected with CK/CH/MY/24053 or CK/CH/SC/25605 are shown, illustrating typical lesions induced by the recombinant IBV strains.

Viral load in tissues and viral shedding dynamics

To evaluate the tissue tropism and viral excretion characteristics of CK/CH/SC/25605 and CK/CH/MY/24053 in chickens, we collected oropharyngeal and cloacal swabs and quantified viral loads in the trachea, lung, kidney, jejunum, ileum, and cecum using RT-qPCR. Viral shedding in the trachea for both strains increased rapidly during the early phase of infection, peaking at 5 dpi before gradually declining. Cloacal viral shedding rise sharply from 3 to 7 dpi and then decreased gradually by 14 dpi. Both strains exhibited similar temporal patterns of viral shedding, with differences in viral loads observed among tissues. CK/CH/SC/25605 showed higher viral loads in the trachea and lung compared with CK/CH/MY/24053, whereas CK/CH/MY/24053 exhibited higher loads in the kidney. In the intestinal tract, including the jejunum, ileum, cecum, and colon, viral loads were generally comparable between the two strains, with CK/CH/MY/24053 slightly higher in some segments. Overall, the two strains exhibited distinct, yet partially overlapping, patterns of viral load distribution across respiratory, renal, and gastrointestinal tissues Fig. 7.

Fig. 7.

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Viral shedding and tissue viral loads in chickens infected with recombinant IBV strains. Data are presented as mean ± SEM. (A–B) Viral shedding measured in cloacal swabs (A) and tracheal swabs (B). (C–I) Viral loads in various tissues, including trachea (C), lung (D), kidney (E), jejunum (F), ileum (G), cecum (H), and Bursa of Fabricius (I), as determined by quantitative RT-PCR.

Discussion

Coronaviruses are a type of pathogen that can infect various hosts and cause respiratory, gastrointestinal or systemic diseases in both humans and animals (Lin, et al., 2021; Weiss and Leibowitz, 2011; Zhai, et al., 2022). Infectious bronchitis virus (IBV) is one of the most economically significant pathogens in poultry (Cavanagh, 2007), and it evolves rapidly through mutations and recombination, leading to the emergence of diverse antigenic and genetic variants worldwide (Xie, et al., 2025a; Xiong, et al., 2024b). In this study, two newly isolated IBV strains, CK/CH/MY/24053 and CK/CH/SC/25605, were classified into the GI-19 and GI-22 lineages, respectively, both of which have been increasingly implicated in recent IB outbreaks in China, particularly in regions with long-term vaccination programs (Meng, Zhang, Wan, Li, Xie, Qin, Shao, Zhang and Ye, 2024). Consistent with previous nationwide surveillance studies (Hou, et al., 2020; Xie, et al., 2025b), GI-19 currently represents one of the predominant genotypes circulating in multiple regions of China and continues to act as an important genetic reservoir for the generation of novel variants through mutation and recombination (Guo, et al., 2025a; Wang, Yan, Liu, Shu, Yang and Xu, 2025a). In contrast, GI-22 has been reported less frequently in earlier surveys but has shown a marked increase in detection in vaccinated chicken flocks in recent years (Zhao, et al., 2019), with an expanding geographic distribution across East and Southeast Asia (Xiong, et al., 2024a). The concurrent circulation of GI-19 and GI-22 in vaccinated farms, as observed in the present study, further support the notion that sustained immune pressure imposed by widespread vaccination may contribute to the maintenance and diversification of multiple IBV genotypes in the field (Fan, et al., 2019; Ren, et al., 2020).

Whole-genome analysis indicates that both CK/CH/MY/24053 and CK/CH/SC/25605 possess the typical IBV genomic organization, with multiple open reading frames consistent with classic IBV structure. Despite differences in evolutionary lineage, both strains show clear evidence of genetic recombination, a phenomenon that has been frequently reported in circulating IBV field strains (Shah, et al., 2025; Zhang, et al., 2025). CK/CH/MY/24053 is a recombinant GI-19 strain, with fragments derived from other members of the same genotype, suggesting that intragenic recombination contributes to genetic diversification within the QX lineage (Wang, et al., 2025b; Zeng, et al., 2025b). In contrast, CK/CH/SC/25605 exhibits a recombination pattern involving sequences from multiple genotypes, including GI-19 and GI-7. Bootscan and phylogenetic analyses identified at least three recombination breakpoints in the CK/CH/SC/25605 genome, involving fragments from GI-19 and a short fragment resembling GI-7, which is consistent with previous reports describing intergenotypic recombination in IBV (Marandino, et al., 2022).

When assessing the pathogenicity of CK/CH/MY/24053 and CK/CH/SC/25605 in SPF chickens, both viruses induced similar respiratory clinical signs around 4 days post-infection (Yan, et al., 2023), including sneezing, rapid breathing and depression, which is consistent with the early respiratory manifestations commonly reported for IBV infections regardless of genotype. However, pronounced differences in tissue tropism and pathological outcomes were observed between the two strains. CK/CH/SC/25605 primarily targeted the respiratory tract, causing severe lesions in the trachea and lungs, characterized by epithelial cell swelling, disorganized tissue architecture, goblet cell hyperplasia, and extensive inflammatory cell infiltration, accompanied by a mortality rate of 35%. Such predominant respiratory tropism has been reported for several GI-22 and related IBV strains in previous pathogenicity studies (Zhao, Xie, Zhang, Cheng, Xu and Zhang, 2019), supporting the classification of CK/CH/SC/25605 as a highly respiratory-pathogenic variant. In contrast, CK/CH/MY/24053 exhibited only mild lesions in the respiratory tract but caused pronounced renal pathology, characterized by tubular degeneration, structural disorganization, and dense inflammatory infiltration, accompanied by high viral loads in the kidneys. This renal tropism is consistent with previous studies reporting that QX-like (GI-19) IBV strains preferentially infect the kidneys (Chen, et al., 2024; Wu, et al., 2024), although the severity may vary among isolates. Viral load distribution further supported these observations, with CK/CH/SC/25605 replicating predominantly in the trachea and lungs, whereas CK/CH/MY/24053 showed preferential replication in renal tissues. Together, these findings reinforce the notion that genotype-associated differences contribute to distinct tissue tropism and pathogenic profiles among circulating IBV strains, while also highlighting the heterogeneity that exists within each genotype.

Structural comparison indicates that the S1 proteins of CK/CH/MY/24053 and CK/CH/SC/25605 are closely aligned with vaccine strains, showing low RMSD values even within the HVR I–III regions. Nevertheless, subtle yet reproducible differences were observed in several surface-exposed loop regions corresponding to HVR I–III, which are known to harbor major neutralizing epitopes and are frequently involved in antigenic variation (Shan, et al., 2018; Sives, et al., 2023). Given that both isolates were obtained from vaccinated flocks experiencing IB outbreaks, these localized conformational differences may contribute to reduced antibody recognition or incomplete vaccine protection, although direct functional evidence remains to be established.

This study isolated and characterized two novel IBV strains from central China, CK/CH/MY/24053 of the GI-19 type and CK/CH/SC/25605 of the GI-22 type, and systematically evaluated their genomic features and pathogenicity. By integrating whole-genome sequencing with in vivo pathogenicity assessment, our results demonstrate that both strains have undergone recombination and originate from distinct evolutionary backgrounds, underscoring the dynamic and ongoing evolution of IBV driven by mutation and recombination in the field. In animal experiments, CK/CH/MY/24053 primarily exhibited renal tropism, whereas CK/CH/SC/25605 predominantly targeted the respiratory tract, causing more severe respiratory lesions and higher mortality, highlighting genotype-associated differences in tissue tropism and disease outcome. Subtle structural variations in the S1 protein’s hypervariable regions were observed, suggesting potential antigenic divergence at a local level; however, these observations remain correlative, and the present study does not establish a direct causal link between specific structural changes and immune escape or tissue specificity. Future studies incorporating functional assays, such as cross-neutralization or reverse genetics approaches, will be required to clarify these relationships.

In conclusion, this study highlights the complex recombination patterns of these two newly isolated IBV strains and their potential links to differences in tissue tropism and pathogenicity. These findings reinforce the importance of sustained molecular surveillance combined with pathogenic characterization to track the emergence of biologically distinct IBV variants, providing practical reference points for risk assessment and the optimization of prevention and control strategies.

Data availability statement

The nucleotide sequences generated in this study have been deposited in GenBank under accession numbers PX694005 and PX694006. All other data supporting the findings of this study are available from the corresponding author upon reasonable request.

CRediT authorship contribution statement

Yuqing Li: Writing – original draft, Conceptualization. Xiaolin Zhang: Data curation. Ting Zhou: Software. Qingcheng Yang: Investigation, Conceptualization. Qian Chen: Formal analysis. Ting Xu: Validation. Chunlin Yu: Resources. Chaowu Yang: Methodology. Hongning Wang: Writing – review & editing. Changwei Lei: Project administration. Anyun Zhang: Validation. Xin Yang: Writing – review & editing.

Disclosures

The authors declare that they have no conflict of interest.

Acknowledgements

This work was supported by the Earmarked Fund for Modern Agroindustry Technology Research System (CARS-40-K14); Sichuan Innovation Team Construction Project (SCCXTD-2026-24); Sichuan Academy of Agricultural Sciences Special Project for Breakthroughs in Agricultural Frontier Technologies (5+1QYGG003).

Footnotes

Supplementary material associated with this article can be found, in the online version, at doi:10.1016/j.psj.2026.106669.

Appendix. Supplementary materials

mmc1.docx (17.9KB, docx)

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

mmc1.docx (17.9KB, docx)

Data Availability Statement

The nucleotide sequences generated in this study have been deposited in GenBank under accession numbers PX694005 and PX694006. All other data supporting the findings of this study are available from the corresponding author upon reasonable request.

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