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Infectious bursa disease (IBD) is an acute, highly contactable, lethal, immunosuppressive infectious disease caused by the Infectious bursa disease virus (IBDV). Currently, the emerged novel variant IBDV (nVarIBDV) and the sustainedly prevalent very virulent IBDV (vvIBDV) are the two most prevalent strains of IBDV in China. The antigenic properties of the two prevalent strains differed significantly, which led to the escape of nVarIBDV from the immune protection provided by the existing vvIBDV vaccine. However, the molecular basis of the nVarIBDV immune escape remains unclear. In this study, we demonstrated, for the first time, that residues 252, 254, and 256 in the P DE of VP2 are involved in the immune escape of the emerging nVarIBDV. Firstly, the IFA-mediated antigen-antibody affinity assay showed that P BC and P DE of VP2 could affect the affinity of vvIBDV antiserum to VP2, of which P DE was more significant. The key amino acids of P DE influencing the antigen-antibody affinity were also identified, with G254N being the most significant, followed by V252I and I256V. Then the mutated virus with point or combined mutations was rescued by reverse genetics. it was further demonstrated that mutations of V252I, G254N, and I256V in P DE could individually or collaboratively reduce antigen–antibody affinity and interfere with antiserum neutralization, with G254N being the most significant. This study revealed the reasons for the widespread prevalence of nVarIBDV in immunized chicken flocks and provided innovative ideas for designing novel vaccines that match the antigen of the epidemic strain. • P DE and P BC of IBDV VP2 affect the antiserum-VP2 affinity, with P DE being more significant. • Residues 252, 254, and 256 in P DE significantly affect the antiserum-VP2 affinity. • Residues 252, 254, and 256 play vital roles in nVarIBDV escaping antiserum neutralization, and G254N is the most significant. [ABSTRACT FROM AUTHOR]

The avian leukosis virus (ALV) strain DL00766 was isolated from a farm in China. The phylogenetic analysis showed that env had the highest homology with the E subgroup reference strain, ranging from 94.5% to 94.9%, whereas gp85 had the highest homology with the B and E subgroups, which were 89.0% to 91.3% and 91.3% to 91.8%. In addition, point mutation analysis of gp85 showed that a 400 bp long fragment in gp85 of DL00766 had the highest homology with subgroup B, ranging from 90.1% to 97.5%, and only 82.7% to 83.1% with E subgroup. These results indicate, DL00766 may be an AVL subgroup E isolate with a subgroup B-like gp85 region. This is also the first finding that the E subgroup is used as a recombinant subject, and the subgroup B provides a recombinant virus of an exogenous gene. [ABSTRACT FROM AUTHOR]

• A mutated IBDV belonging to genotype A8B1 was identified and designated as IBDV-HeN20-7103. > IBDV-HeN20-7103 showed unique mutation H253Q compared to attenuated IBDV. > IBDV-HeN20-7103 could induce severe bursal lesions. Infectious bursal disease virus (IBDV), the causative agent of infectious bursal disease (IBD), mainly damages the bursa of Fabricius, which is a central immune organ of birds. As an RNA virus, IBDV is prone to mutation owing to a combination of factors including natural selection pressure. In this study, a naturally occurring mutated IBDV associated with bursa damage was identified, IBDV-HeN20-7103 strain, in an infected chicken flock in central China. Its full-length genome was cloned, and sequence analysis showed that the IBDV-HeN20-7103 strain was located along with the attenuated IBDV, which corresponds to genotype A8B1 of the recently proposed classification scheme, on the branch of the phylogenetic tree. The amino acid sequence comparisons further highlighted the specific characteristics of IBDV-HeN20-7103 with mutation H253Q compared to the attenuated strain. Animal experiments showed that IBDV-HeN20-7103 could induce serious bursal lesions without mortality, which revealed a unique cause of disease in this flock. The identification of such a strain reaffirms the complexity of IBDV evolution and prevalence. [ABSTRACT FROM AUTHOR]