ORIGINAL RESEARCH article
Front. Immunol.
Sec. Viral Immunology
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1600371
This article is part of the Research TopicViral Surface Spikes: Host Cell Entry, Immune Responses and Evasion, and Implications for Viral Infection, Inhibition and ReboundView all 4 articles
Q221K mutation in VP2 drives antigenic shift of infectious bursal disease virus
Provisionally accepted
- Yangzhou University, Yangzhou, Jiangsu Province, China
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Infectious bursal disease (IBD) is a severe immunosuppressive disease caused by the infection of infectious bursal disease virus (IBDV) in chicken. Recently, an emerging mutant named novel variant IBDV (nVarIBDV) has rapidly spread in China and become a prevalent strain. However, little is known about the unique antigenic sites of nVarIBDV escaped from current IBDV vaccines. Here, the expressed hypervariable region (HVR) of VP2 (VP2-HVR) of nVarIBDV was used as an immunogen and a novel monoclonal antibody (mAb) against VP2 (mAb 5B5) was generated. immunofluorescence assay (IFA) and ELISA demonstrated that mAb 5B5 specifically reacted with nVarIBDV and its VP2 protein, but not with classical IBDV (cIBDV), very virulent IBDV (vvIBDV), or attenuated IBDV (attIBDV) strains. Epitope mapping and site mutagenesis assay revealed that mAb 5B5 recognized the conformational epitope in peak A (212-224 aa) and heptapeptide (326-332 aa) regions, and identified residue 221K in VP2 as the key antigenic site, which is conserved exclusively in nVarIBDV strains. Notably, K221Q mutation in VP2 of nVarIBDV significantly altered the reaction profile for sera against vvIBDV or cIBDV. Neutralization assays revealed that mAb 5B5 could inhibit replication of an engineered attIBDV with carrying 221K in Leghorn male hepatoma (LMH) cells. Structural analysis further found that 221K is surface-exposed and alters local electrostatic potential, possibly facilitating immune evasion. All these demonstrated that 221K is a unique antigenic site in VP2 of nVarIBDV associated with immune escapeing, providing novel insights into the antigenicity of nVarIBDV and novel targets for efficient diagnostics, vaccine design, and molecular surveillance of IBDV.
Keywords: nVarIBDV, VP2, mAb, 221K, Antigenicity, differentiation
Received: 26 Mar 2025; Accepted: 23 Jun 2025.
Copyright: © 2025 Xiong, Wu, Xie, Li, Wan, Qin, Ye and Shao. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Jianqiang Ye, Yangzhou University, Yangzhou, 225009, Jiangsu Province, China
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