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Infectious bursal disease virus (IBDV) causes infectious bursal disease (IBD), an immunosuppressive disease of poultry. The current classification scheme of IBDV is confusing because it is based on antigenic types (variant and classical) as well as pathotypes. Many of the amino acid changes differentiating these various classifications are found in a hypervariable region of the capsid protein VP2 (hvVP2), the major host protective antigen. Data from this study were used to propose a new classification scheme for IBDV based solely on genogroups identified from phylogenetic analysis of the hvVP2 of strains worldwide. Seven major genogroups were identified, some of which are geographically restricted and others that have global dispersion, such as genogroup 1. Genogroup 2 viruses are predominately distributed in North America, while genogroup 3 viruses are most often identified on other continents. Additionally, we have identified a population of genogroup 3 vvIBDV isolates that have an amino acid change from alanine to threonine at position 222 while maintaining other residues conserved in this genogroup (I242, I256 and I294). A222T is an important mutation because amino acid 222 is located in the first of four surface loops of hvVP2. A similar shift from proline to threonine at 222 is believed to play a role in the significant antigenic change of the genogroup 2 IBDV strains, suggesting that antigenic drift may be occurring in genogroup 3, possibly in response to antigenic pressure from vaccination.

Infectious bursal disease virus (IBDV) induces severe immunosuppression in chickens, leading to significant economic losses in the global poultry industry. This study investigated 52 chicken flocks, including commercial broilers, layers, and baladi, from various Egyptian governorates in 2023. These flocks exhibited symptoms of depression, along with kidney and bursa lesions, indicative of IBDV infection. Pooled Bursal homogenates were tested using RT-PCR with VP2-specific primers, revealing that 20 flocks tested positive for IBDV. Six representative samples were selected from 20 positive flocks for isolation in embryonated chicken eggs. The embryonic lesions observed included haemorrhage, skull swelling, and liver necrosis with a pale-yellow appearance, in addition to congestion and thickening in the chorioallantoic membrane (CAM). Partial amplification of the VP2 gene from the harvested embryo suspensions of the six IBDV isolates was performed for sequencing. Phylogenetic analysis of the sequences revealed that five IBDV isolates (VV4, VV5, VV6, VV10, and VV16) belonged to the very virulent strain group A3 cluster, whereas one isolate (VV2) clustered with Chinese Variant strains in the A2d group. Sequence analysis of the hypervariable region (HVR) of VP2 compared to that of Egypt-USC-IBD-1-2019 and vvIBDV/Beh21/Egypt/18 highly virulent IBDV strains revealed several amino acid mutations. The VP2 HVR of all isolates maintained the serine-rich heptapeptide sequence SWSASGS, which is adjacent to the major hydrophilic peak B and serves as a virulence marker. Histopathological examination revealed that bursae from chickens infected with vvIBDV exhibited marked interlobular oedema and lymphoid depletion. In contrast, bursae from chickens infected with Variant IBDV showed massive lymphoid depletion, with hyperplasia of the bursal capsule. These findings highlight the circulation of both virulent and Variant IBDV strains in Egyptian chicken flocks, complicating disease control. Consequently, there is a need to update vaccination programs and vaccine strains for IBDV in Egypt.

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.

Infectious bursal disease (IBD), caused by the infectious bursal disease virus (IBDV), significantly threatens global poultry health by inducing immunosuppression and causing economic losses. To enhance vaccination efficacy, we engineered a transgenic strain of Eimeria acervulina (Ea-2C3d) expressing a fusion protein composed of IBDV VP2 and three tandem C3d segments (3C3d), utilizing C3d's adjuvant properties to boost immune responses. The transgene was generated by integrating codon-optimized VP2 and 3C3d sequences into the E. acervulina genome using restriction enzyme-mediated transfection. PCR, protein, and genome sequencing confirmed the successful integration and expression of VP2 fusion C3d, but only two copies of C3d were successfully expressed, due to a partial deletion of one C3d copy during the transfection process. In vivo studies demonstrated that Ea-2C3d elicited significantly higher anti-VP2 antibody titers than the parental Ea-VP2 strain (P < 0.05), especially following second immunization. Upon challenge with virulent IBDV, chickens immunized with Ea-2C3d displayed reduced bursal lesions (histopathological score ≤ 1) and maintained bursal integrity (bursal index >0.7), comparable to those receiving a commercial subunit vaccine. Despite reduced reproductive capacity in the transgenic parasites, Ea-2C3d maintained its immunogenicity and safety. These findings highlight that C3d adjuvant enhances VP2-mediated protection in a coccidial vector, presenting a novel dual-protection strategy against IBD and coccidiosis.

Infectious bursal disease virus (IBDV) is one of the most impactful pathogens of poultry, with disease manifestations ranging from acute forms to subclinical but immunosuppressive infections. This heterogeneity, accompanied by a significant antigenic variability, is sustained by high mutation rates and frequent reassortments between the two genome segments, along with less frequent recombination events. In recent years, the proposal of several classification systems relying on phylogeny contributed to the characterization of several new IBDV genotypes, shedding light on an increasingly diverse epidemiological scenario. One of the most notable examples is the discovery of novel variant IBDVs (nvIBDVs, genotype A2dB1b), which, after emerging in China around 2015, rapidly spread across East and Southeast Asia. More recently, nvIBDVs were also reported in Egypt and Argentina, prompting concern due to their well‐established immunosuppressive potential and divergent antigenic features. The detection of A2dB1b strains in Egypt elicited a molecular survey to track their spread within the Middle East. From November 2023 to November 2024, diagnostic samples were collected from 138 flocks in 7 Near East and Persian Gulf countries. The analyses revealed that 55 of them (39.9%) were positive for field strains belonging to 3 genotypes, suggesting a high infectious pressure. Two genotypes, A3B1c and A6B1a, were already reported in the region, although they were found in additional areas. On the other hand, A2dB1b was identified for the first time in Jordan, Lebanon, and the United Arab Emirates, representing a large share of the field viruses detected in these countries. Phylodynamic analyses revealed that this swift spread may have been caused by separate introduction events from Egypt, East Asia, and even South America, highlighting the complexity of IBDV epidemiology. The obtained results will be crucial to better tackle IBDV in the region, guiding monitoring activities and raising awareness toward its proper control.

Infectious bursal disease virus (IBDV) is an acute and highly infectious RNA virus known for its immunosuppressive capabilities, chiefly inflicting rapid damage to the bursa of Fabricius (BF) of chickens. Current clinical control of IBDV infection relies on vaccination. However, the emergence of novel variant IBDV (nVarIBDV) has posed a threat to the poultry industry across the globe, underscoring the great demand for innovative and effective vaccines. Our previous studies have highlighted the critical role of IBDV VP5 as an apoptosis-inducer in host cells. In this study, we engineered IBDV mutants via a reverse genetic system to introduce amino acid mutations in VP5. We found that the mutant IBDV-VP5/3m strain caused reduced host cell mortality, and that strategic mutations in VP5 reduced IBDV replication early after infection, thereby delaying cell death. Furthermore, inoculation of chickens with IBDV-VP5/3m effectively reduced damage to BF and induced neutralizing antibody production comparable to that of parental IBDV WT strain. Importantly, vaccination with IBDV-VP5/3m protected chickens against challenges with nVarIBDV, an emerging IBDV variant strain in China, reducing nVarIBDV loads in BF while alleviating bursal atrophy and splenomegaly, suggesting that IBDV-VP5/3m might serve as a novel vaccine candidate that could be further developed as an effective vaccine for clinical control of IBD. This study provides a new clue to the development of novel and effective vaccines.

Infectious bursal disease virus (IBDV) is one of the most important immunosuppressive viral agents in poultry production. Prophylactic vaccinations of chicken flocks are the primary tool for disease control. Widely used immunoprophylaxis can, however, provide high pressure which contributes to the genetic diversification of circulating viruses, e.g. through reassortment of genome segments. We report the genetic and phenotypic characterization of a field reassortant IBDV (designated as Bpop/03) that acquired segment A from very virulent IBDV and segment B from classical attenuated D78-like IBDV. Despite the mosaic genetic make-up, the virus caused high mortality (80%) in experimentally infected SPF chickens and induced lesions typical of the acute form of IBD. The in vivo study results are in contrast with the foregoing experimental investigations in which the natural reassortants exhibited an intermediate pathotype, and underline the complex nature of IBDV virulence.

RNA interference (RNAi) and autophagy are two pivotal biological processes that regulate virus replication. This study explored the complex relationship between autophagy and RNAi in controlling influenza virus replication. Initially, we reported that influenza virus (H9N2) infection increases the viral load and the expression of autophagy markers while inhibiting the RNAi pathway. Subsequent studies employing autophagy enhancer and inhibitor treatments confirmed that avian influenza virus (AIV, H9N2) promotes viral replication by enhancing autophagy pathways. Further analysis revealed that ATG7, an autophagy protein, can interact with dicer to affect its antiviral functions. Finally, we discovered that infection with other avian RNA viruses, including infectious bursal disease virus (IBDV) and infectious bronchitis virus (IBV), induced the upregulation of ATG7, which blocked the RNAi pathway to facilitate virus replication. Our findings suggested that virus infection might trigger the upregulation of autophagy and downregulation of the RNAi pathway, revealing a complex interaction between these two biological processes in the defence against viral replication.

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.

The re-emergence of virulent strains of the Infectious Bursal Disease Virus (IBDV) leads to significant economic losses of poultry industry in Pakistan during last few years. This disease causes the infection of bursa, which leads to major immune losses. A total number of 30 samples from five IBD outbreaks during the period of 2019–20 were collected from different areas of Faisalabad district, Pakistan and assayed by targeting the IBD virus VP2 region through RT-PCR. Among all the outbreaks, almost 80% of poultry birds were found positive for the IBDV. The bursa tissues were collected from the infected birds and histopathological examination of samples revealed severe lymphocytic depletion, infiltration of inflammatory cells, and necrosis of the bursa of Fabricius (BF). Positive samples were subjected to re-isolation and molecular characterization of IBDV. The Pakistan IBDV genes were subjected to DNA sequencing to determine the virus nucleotide sequences. The sequences of 100 Serotype-I IBDVs showing nearest homology were compared and identified with the study sequence. The construction of the phylogenetic tree for nucleotide sequences was accomplished by the neighbor-joining method in MEGA-6 with reference strains. The VP2 segment reassortment of IBDVs carrying segment A were identified as one important type of circulating strains in Pakistan. The findings indicated the molecular features of the Pakistan IBDV strains playing a role in the evolution of new strains of the virus, which will contribute to the vaccine selection and effective prevention of the disease.