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Infectious bursal disease (IBD) is an acute, highly contagious, immunosuppressive, and fatal infectious disease of young chickens caused by infectious bursal disease virus (IBDV). Since 2017, a new trend has been discovered in the IBDV epidemic, with very virulent IBDV (vvIBDV) and novel variant IBDV (nVarIBDV) becoming the two current dominant strains in East Asia including China. In this study, we compared the biological characteristics of the vvIBDV (HLJ0504 strain), nVarIBDV (SHG19 strain), and attenuated IBDV (attIBDV, Gt strain) using specific-pathogen-free (SPF) chicken infection model. The results showed that vvIBDV distributed in multiple tissues, replicated the fastest in lymphoid organs such as bursa of Fabricius, induced significant viremia and virus excretion, and is the most pathogenic virus with a mortality of more than 80%. The nVarIBDV had a weaker replication capability and did not kill the chickens but caused severe damage to the central immune organ bursa of Fabricius and B lymphocytes and induced significant viremia and virus excretion. The attIBDV strain was found not to be pathogenic. Further studies preliminarily suggested that the expression level of inflammatory factors triggered by HLJ0504 was the highest, followed by the SHG19 group. This study is the first to systematically compare the pathogenic characteristics of three IBDVs closely related to poultry industry from the perspectives of clinical signs, micro-pathology, virus replication, and distribution. It is of great importance to obtain an extensive knowledge of epidemiology, pathogenicity, and comprehensive prevention, and control of various IBDV strains. [ABSTRACT FROM AUTHOR]

Infectious bursal disease is an acute, immunosuppressive infectious disease in chickens caused by the infectious bursal disease virus (IBDV), which causes huge economic losses to the global poultry industry. Persistently circulating very virulent IBDV (vvIBDV) and newly emerging novel variant IBDV (nVarIBDV) are the two dominant epidemic strains of IBDV in East Asian countries such as China. Compared to lethal vvIBDV, nonlethal nVarIBDV has more insidious pathogenicity and can partially escape the immune protection of the existing vvIBDV vaccine, suggesting its potential adaptive survival strategy. However, the underlying molecular mechanism remains unknown. The viral capsid protein VP2 is closely related to cell tropism, virulence, and antigenic variation of IBDV. In this study, for the first time, we demonstrated that residue 279 of VP2 is responsible for the difference in pathogenicity between nVarIBDV and vvIBDV and that the D279N substitution reduces the lethality of vvIBDV from 70% to 0%. Moreover, a significant reduction in the viral load and inflammatory factor levels in the immune organs and blood of infected chickens may be important mechanisms for reducing the lethality of IBDV. Additionally, residue 279 was an important molecular basis for the antigenic differences between nVarIBDV and vvIBDV. D279N substitution reduced the neutralizing ability of vvIBDV antiserum against nVarIBDV by affecting the binding ability of antibodies and antigens. Our results indicate that nVarIBDV has an infection transmission strategy that facilitates its survival by hiding viral pathogenicity and escaping antiserum neutralization, which not only has significant implications for the systemic cognition of viral genetic evolution and pathogenesis but also provides new ideas for the comprehensive prevention and control of IBDV. [ABSTRACT FROM AUTHOR]

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]

Infectious bursal disease virus (IBDV) is a non-enveloped, bi-segmented double-stranded RNA virus and the causative agent of a poultry immunosuppressive disease known as infectious bursal disease (IBD). The novel variant IBDV (nVarIBDV) recently posed a great threat to the development of the poultry industry. In this study, we identified a novel segment-reassortant IBDV strain, IBDV-JS19-14701 (Genotype A2dB3). Phylogenic analysis showed that Segments A and B of IBDV-JS19-14701 were derived from emerging nVarIBDV (Genotype A2dB1) and long-prevalent HLJ0504-like strains (Genotype A3B3) in China, respectively. The pathogenicity of IBDV-JS19-14701 was further evaluated via animal experiments. IBDV-JS19-14701 exhibited a similar virulence to chickens with the nVarIBDV. The identification of this reassortment event is beneficial for understanding the epidemiology of nVarIBDV and will contribute to the efficient prevention and control of IBD. [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]