Kang-Seuk Choi

Infectious bronchitis virus (IBV) remains a major pathogen in global poultry production due to its extensive genetic diversity and rapid evolutionary capacity. Antigenic diversification driven by mutation, homologous recombination, and sustained immune selection pressure complicates long-term control and reduces vaccine effectiveness. Increasing evidence suggests that IBV evolution is largely driven by the selective expansion of pre-existing variants under changing ecological and immunological conditions, rather than by the de novo emergence of novel lineages. South Korea provides a valuable model for understanding these processes within intensive poultry systems characterized by high host density, extensive farm connectivity, widespread vaccination, and long-term molecular surveillance. Since its first isolation in 1986, IBV in Korea has undergone repeated cycles of lineage emergence, diversification, and replacement, culminating in the predominance of nephropathogenic GI-19 viruses, including KM91 and QX-like variants. Persistent co-circulation of multiple lineages, together with frequent recombination and regional viral introduction, has shaped a highly dynamic viral population. Within this environment, vaccination plays a central yet paradoxical role. While essential for disease control, widespread vaccination imposes continuous immune selection pressure and may contribute to co-circulation of vaccine-derived and field strains, facilitating recombination and the emergence of immune escape variants. These processes drive lineage turnover and antigenic mismatch between circulating viruses and vaccine strains, forming a vaccination-driven evolutionary cycle. This review integrates global IBV diversity with insights from the Korean system to propose an evolution-centered framework in which viral genetic plasticity, host population dynamics, and vaccination practices interact. These findings have important implications for optimizing vaccination strategies and provide broader insights into the evolutionary dynamics of rapidly evolving RNA viruses under sustained immune pressure.

Background: Although the influenza A virus (IAV) matrix protein 1 (M1) and nucleoprotein (NP) are attractive targets for cross-protective vaccines, their independent effects on host cell transcriptomes and subsequent immunogenicity in histocompatible hosts remain largely unexplored. Here, we utilized a previously established histocompatible DF-1 cell and a cognate B21 chicken (DF-1/B21) platform to characterize these interactions. Stable DF-1 cell lines expressing M1 or NP were analyzed via transcriptomic profiling and subsequently used as single-antigen vaccines. Results: Transcriptional analysis revealed distinct host signatures: M1 expression was primarily associated with alterations in membrane-associated and cytoskeletal pathways. In contrast, NP expression was linked to the broad downregulation of DNA replication and cell cycle regulators, actin network reorganization, and the modulation of early innate signaling without inducing a full interferon response. Functional assays corroborated these findings, showing that despite higher viral susceptibility in M1-expressing cells, NP expression established a potent antiviral state characterized by reduced viral replication and an increase in pro-inflammatory (TNF-α, IL-6) and immune-recruiting (IL-15, IL-12p40) cytokines in vitro. NP, but not M1, was also spontaneously released into culture supernatants. In vivo, both vaccines elicited measurable humoral responses and reduced viral shedding upon H9N2 challenge. Furthermore, distinct shifts in peripheral CD8⁺/CD4⁺ ratios post-challenge indicated that both antigens effectively modulated cellular immunity. Conclusions: Collectively, these findings validate the DF-1/B21 system as a versatile platform for dissecting host–pathogen interactions. By effectively bridging cellular transcriptomics with systemic immunity, this histocompatible model offers a valuable framework for the broad evaluation of avian immunogens and the rational design of future poultry vaccines.

Fetal bovine serum (FBS) is the standard supplement for cell culture, yet we previously demonstrated that it drives hyper-proliferation and phenotypic drift in Madin–Darby canine kidney (MDCK) cells, compromising their epithelial identity and ciliogenesis. In contrast, a modified chicken embryo extract (CEE) preserved these intrinsic properties, maintaining a stable and physiologically relevant phenotype. To elucidate the metabolic mechanisms driving these distinct cellular fates, we performed a comparative analysis of redox status and metabolomic profiles. We found that FBS forces a metabolic shift toward oxidative phosphorylation, resulting in mitochondrial stress characterized by elevated mitochondrial reactive oxygen species (mtROS), calcium overload, and the accumulation of uremic toxins like hippuric acid. Conversely, CEE established a balanced redox environment. Although CEE induced higher intracellular signaling ROS via NADPH oxidase 1/2, it prevented oxidative damage by upregulating antioxidant transcription factors, such as nuclear factor erythroid 2-related factor 2, and enzymes such as Mn superoxide dismutase. Additionally, metabolomic analysis revealed that CEE is enriched with antioxidants (ascorbic acid, proline) and signaling molecules (5-hydroxyindole-3-acetic acid). These findings indicate that while FBS imposes a metabolic burden leading to cellular stress, CEE provides a favorable metabolic microenvironment that supports homeostasis and epithelial integrity, validating its superiority as a culture supplement.

Kim NH, et al. Clin Exp Vaccine Res. 2026 Oct;15(4):353-361. https://doi.org/10.7774/cevr.2026.15.e34

Choi KS. Clin Exp Vaccine Res. 2026 ;15:e30. https://doi.org/10.7774/cevr.2026.15.e30

Lee JK, et al. J Vet Sci. 2026 Jan;27:e8. https://doi.org/10.4142/jvs.25249

Seung-Eun Son, Jin-Ha Song, Se-Hee An, Chung-Young Lee, Il-Hwan Kim, Ho-Won Kim, Kang-Seuk Choi, and Hyuk-Joon Kwon. J. Microbiol. Biotechnol. 2025;35:1-9. https://doi.org/10.4014/jmb.2510.10027

Efficient replication of influenza A viruses (IAVs) requires balanced activities of hemagglutinin (HA), neuraminidase (NA), and the RNA polymerase complex, whose functions are strongly influenced by PB2 mutations. We previously revealed three distinct evolutionary pathways for PB2 mutations, with two pathways leading to the emergence of viral strains responsible for human seasonal infections and the 2009 pandemic, and a third pathway giving rise to H5Nx highly pathogenic avian influenza viruses (HPAIVs) defined by a triad of mutations (I147T, K339T, and A588T) that occasionally spill over to humans. Here, we investigated the zoonotic risk posed by this triad and elucidated its evolutionary relationship with HA, NA, and vaccination. Recombinant PR8 and clade 2.3.2.1c H5N1 viruses carrying the triad replicated efficiently in embryonated chicken eggs and had moderate replication efficiency in mammalian cells; moreover, mice infected with these viral strains exhibited milder weight loss and lower lung titers than those infected with the E627K-carrying strain. Sequence analysis of H5Nx viruses revealed early emergence and long-term persistence of the triad across diverse genotypes, which was closely linked to HA glycosylation and NA-stalk truncation. However, the prevalence of these viral strains declined significantly after successive H5 poultry-vaccination campaigns. These data indicate that the triad provides a replication advantage compatible with both poultry and mammalian hosts but confers only moderate mammalian pathogenicity and that sustained vaccination can restrain the spread of viral strains with these mutations. Continuous molecular surveillance of PB2 alongside HA and NA remains essential for preventing H5Nx zoonotic threats.Please check and confirm that the authors and their respective affiliations have been correctly identified and amend if necessary.I have checked and modifed the email addresses of the corresponding authors. I confirm the information of other authors are correct.