Abstract: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 se… Show more
“…Based on a recent study, it is proposed that, worldwide, about 60–76% of IBDV isolates are of vvIBDV genotype 15. Rampant vaccination without genotype matching resulted in genetic diversification of circulating viruses through reassortment that acquired segment A from very virulent IBDV and segment B from classical atIBDV D78 strain in Poland 16. The chimeric virus caused 80% mortality in Specific Pathogen Free chickens along with acute form of bursal lesions.…”
Infectious bursal disease (IBD), also known as Gumboro disease, is a highly contagious, immunosuppressive disease of young chickens. Although first observed about 60 years ago, to date, the disease is responsible for major economic losses in the poultry industry worldwide. IBD virus (IBDV), a double-stranded RNA virus, exists as two serotypes with only serotype 1 causing the disease in young chickens. The virus infects the bursa of Fabricius of particularly the actively dividing and differentiating lymphocytes of the B-cells lineage of immature chickens, resulting in morbidity, mortality, and immunosuppression. Immunosuppression enhances the susceptibility of chickens to other infections and interferes with vaccination against other diseases. Immunization is the most important measure to control IBD; however, rampant usage of live vaccines has resulted in the evolution of new strains. Although the immunosuppression caused by IBDV is more directed toward the B lymphocytes, the protective immunity in birds depends on inducement of both humoral and cell-mediated immune responses. The interference with the inactivated vaccine induced maternally derived antibodies in young chicks has become a hurdle in controlling the disease, thus necessitating the development of newer vaccines with improved efficacy. The present review illustrates the overall dynamics of the virus and the disease, and the recent developments in the field of virus diagnosis and vaccine research.
“…Based on a recent study, it is proposed that, worldwide, about 60–76% of IBDV isolates are of vvIBDV genotype 15. Rampant vaccination without genotype matching resulted in genetic diversification of circulating viruses through reassortment that acquired segment A from very virulent IBDV and segment B from classical atIBDV D78 strain in Poland 16. The chimeric virus caused 80% mortality in Specific Pathogen Free chickens along with acute form of bursal lesions.…”
Infectious bursal disease (IBD), also known as Gumboro disease, is a highly contagious, immunosuppressive disease of young chickens. Although first observed about 60 years ago, to date, the disease is responsible for major economic losses in the poultry industry worldwide. IBD virus (IBDV), a double-stranded RNA virus, exists as two serotypes with only serotype 1 causing the disease in young chickens. The virus infects the bursa of Fabricius of particularly the actively dividing and differentiating lymphocytes of the B-cells lineage of immature chickens, resulting in morbidity, mortality, and immunosuppression. Immunosuppression enhances the susceptibility of chickens to other infections and interferes with vaccination against other diseases. Immunization is the most important measure to control IBD; however, rampant usage of live vaccines has resulted in the evolution of new strains. Although the immunosuppression caused by IBDV is more directed toward the B lymphocytes, the protective immunity in birds depends on inducement of both humoral and cell-mediated immune responses. The interference with the inactivated vaccine induced maternally derived antibodies in young chicks has become a hurdle in controlling the disease, thus necessitating the development of newer vaccines with improved efficacy. The present review illustrates the overall dynamics of the virus and the disease, and the recent developments in the field of virus diagnosis and vaccine research.
“…Segment B encodes VP1, an RNA-dependent RNA polymerase (RdRp) responsible for the replication of the viral genome and synthesis of mRNAs [ 16 ]. In recent years, more and more mosaic/novel variant IBDVs have been reported, which may have evolved by reassortment events of the two genome segments [ 17 , 18 , 19 ], by homologous recombination within segments [ 20 , 21 , 22 ], and by gene mutations in the hypervariable region of VP2 ( v VP2) [ 23 , 24 ]. Especially, since 2017, more and more novel variant strains with great immunosuppressive effects in chickens emerged in most parts of China [ 23 ].…”
Infectious Bursal Disease Virus (IBDV) has haunted the poultry industry with severe, prolonged immunosuppression of chickens when infected at an early age and can easily lead to other secondary infections. Understanding the pathogenic mechanisms could lead to effective prevention and control of Infectious Bursal Disease (IBD). Evidence suggests that the N-terminal domain of polymerase in segment B plays an important role, but it is not clear which part or residual is crucial for the pathogenicity. Using a reverse genetics technique, a molecular clone (rNN1172) of the parental vvIBDV strain NN1172 was generated, and its pathogenicity was found to be the same as the parental virus. Then, three recombinant chimeric viruses were rescued based on the rNN1172 and substituted with the counterparts in the N-terminal domain of the attenuated vaccine strain B87: the rNN1172-B87VP1a (substituting the full region of the 1–167 aa residuals), the rNN1172-B87VP1a∆4 (substituting the region of the 5–167 aa residuals), and the rNN1172-VP1∆4 (one single aa residual substitution V4I), to better explore the role of the N-terminal domain of polymerase on the viral pathogenicity. Interestingly, all these substitutions played different roles in the viral pathogenicity: the mortality of the rNN1172-B87VP1a-challenged chickens was significantly reduced from 30% to 0%. No obvious lesion was found in the histopathological examination, and the lowest viral genome copy number was also detected in the bursa when compared to the parental and two other recombinant viruses. The mortalities caused by rNN1172-B87VP1a∆4 and rNN1172-B87VP1∆4, respectively, were all reduced to 10% and had a delayed onset of death. Our results also revealed that the pathogenicity of the IBDV was consistent with the viral replication efficiency in vivo (bursae). This study demonstrated that the full region of the N-terminal of polymerase plays an important role in viral replication and pathogenicity, but the substitutions of its partial region or a single residual do not completely lead to the virus attenuation to Three-Yellow chickens, although that significantly reduces its pathogenicity.
“…The increased number of current reports concerning the emergence of new antigenic variants (Fan et al, ), or new mosaic IBDV strains (Abed et al, ; Pikula, Lisowska, Jasik, & Smietanka, ; Samy et al, ) indicates that the virus is undergoing intensive genetic changes representing a permanent concern to the current status quo . In the current study, the genetic characterization and phylogenetic analysis of IBDV field strains collected from acute Gumboro disease outbreaks in Poland during 1991–2015 was accomplished.…”
Infectious bursal disease virus (IBDV) is a non-enveloped, bisegmented double-stranded RNA virus included into the Birnaviridae family (Delmas et al., 2019). This virus was first described in the United States in 1962 and linked as aetiological agent of a highly contagious chicken immunodeficiency disorder known as Gumboro disease (Cosgrove, 1962). The initial classical IBDV strains were widely spread across the world, and the outbreaks caused by this type of strains were successfully controlled by application of vaccination policies. However, in the late 80s the epidemiological situation concerning IBDV suddenly changed and the scientific community was facing the emergence of very virulent IBDV (vvIBDV) strains, that caused severe economic losses in poultry, mainly due to an increase in the mortality of the infected animals up to 60% (Berg, Gonze, & Meulemans, 1991). Notoriously, the emergence of vvIBDV strains resulted from a reassortment event in which the new viral pathogenic fitness was initiated by the acquisition of a 'very virulent'
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.