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Gao, H.; Wang, Y.; Gao, L.; Zheng, S.J. Epidemics and Pathogenesis of Different IBDV Strains. Encyclopedia. Available online: (accessed on 14 April 2024).
Gao H, Wang Y, Gao L, Zheng SJ. Epidemics and Pathogenesis of Different IBDV Strains. Encyclopedia. Available at: Accessed April 14, 2024.
Gao, Hui, Yongqiang Wang, Li Gao, Shijun J. Zheng. "Epidemics and Pathogenesis of Different IBDV Strains" Encyclopedia, (accessed April 14, 2024).
Gao, H., Wang, Y., Gao, L., & Zheng, S.J. (2023, May 19). Epidemics and Pathogenesis of Different IBDV Strains. In Encyclopedia.
Gao, Hui, et al. "Epidemics and Pathogenesis of Different IBDV Strains." Encyclopedia. Web. 19 May, 2023.
Epidemics and Pathogenesis of Different IBDV Strains

Infectious bursal disease virus (IBDV) is an immunosuppressive pathogen causing enormous economic losses to the poultry industry across the globe. As a double-stranded RNA virus, IBDV undergoes genetic mutation or recombination in replication during circulation among flocks, leading to the generation and spread of variant or recombinant strains. 

infectious bursal disease virus (IBDV) genetic evolutionary typing viral genome diversity

1. Classical IBDV (cIBDV)

In 1957, the original outbreak of IBD occurred in the area of Gumboro, Delaware, USA, where researchers observed a high rate of disease occurrence in chicks [1]. Early symptoms of IBD include diarrhea, loss of appetite, weakness, and even death [1]. The main target organ of the virus is the bursa of Fabricius (BF) of 3–6-week-old chicks, which is characterized by enlarged or hemorrhagic bursa during the first four days, followed by bursal atrophy later in the course of the disease [2][3][4]. The infection eventually leads to lymphocyte failure and destruction of the bursa, which is the main feature of IBD pathogenesis [5][6]. In classical epidemic situations, mortality in diseased chickens may range between 1% and 50%, with significant effects on both broilers and laying hens [2]. In addition to mortality, IBDV also has an immunosuppressive effect, which affects the host's immune response and the efficacy of other vaccinations [2][4][7]. The virus genome consists of two segments of RNAase-resistant, double-stranded RNAs [8]. The complete terminal sequences of IBDV genomic dsRNA have been identified, indicating that different RNA structures may have an impact on the ability of the virus to replicate [9]. As more complete genomic information on IBDV has become available, the correlation between genetic and pathogenic phenotypes among different strains of IBDV could be more precisely assessed [10][11][12][13][14][15].

2. Variant IBDV (varIBDV)

In the late 1980s, it was first reported that IBDV variants were identified by virus neutralization tests as serotypeI IBDV with significant antigenic differences from classical strains [16][17]. These antigenically altered strains were collectively referred to as variants IBDV to distinguish them from previous classical IBDV isolates [1][18]. Initially, the variant IBDV-infected chickens were characterized by little or no mortality and no obvious clinical signs, but their bursa and spleen were damaged [19][20][21]. Subsequent studies have shown that amino acid mutations in the hypervariable region (HVR, nt 616–1050, aa 206–350) of VP2 are the major cause of IBDV variants [22][23][24]. The VP2 hypervariable region includes many amino acid residues exposed on the protein surface, and mutations in these residues can lead to a variation in the antigenicity of VP2, allowing the variant to escape from the neutralizing antibodies produced by vaccination against the cIBDV [21][24]. This phenomenon is known as antigenic drift and is the primary reason for antigenic diversity [22][25]. Several mutations in the specific residues (222 T, 249 K, 254 S, 286 I, and 318 D) in the HVR may cause antigenic drift [26][27].

3. Very Virulent IBDV (vvIBDV)

At the time the variant IBDV was identified in North America, very virulent IBDV (vvIBDV) emerged in Europe [28][29]. In contrast to the variant strains, vvIBDV typically causes high morbidity and mortality in SPF chickens, resulting in mortality of 50–100%, along with typical signs and lesions. Importantly, vvIBDV can establish infection in the presence of maternal antibodies to the classical strain and cause lesions in immune organs other than the bursa [3][30]. As a highly transmissible virus, vvIBDV has spread rapidly throughout the world, causing significant economic losses to the poultry industry [14][31][32][33][34][35]. However, the emergence of vvIBDV promoted scientific research on the pathogenicity of IBDV infection.
Genetic studies revealed that the emergence of the vvIBDV strains was due to the reassortment of genetic segments, specifically the reassortment of the mutated segment A with the segment B of unknown origin, resulting in a sudden increase in the pathogenicity of the virus [36]. Residues 222 A, 242 I, 256 I, 294 I, and 299 S of the vvIBDV segment A are conserved compared to other strains of IBDV and serve as markers of pathogenicity [30][37][38]. In addition, residues 253 and 284 of VP2 are proposed to be the determinants of cell tropism and major contributors to IBDV virulence [39][40][41]. Phylogenetic analysis has shown that segment B of vvIBDV is distinct and highly conserved [26][36][42]. Additional studies have confirmed that both genomic segments contribute to the high virulence of vvIBDV [43][44][45][46][47]. As the efforts in exploring vvIBDV continue, more critical residues that may be involved in the pathogenicity of the virus have been identified [48][49][50].

4. Novel Variant IBDV (nVarIBDV)

Since 2015, China has experienced an outbreak of the novel variant IBDV (nVarIBDV) [51]. These isolated strains have distinct subclusters, indicating genetic evolution in both segments A and B of the viral genome, which rarely occurred in China before [52][53][54][55]. While the vvIBDV strain has historically been the most prevalent with low variability in field transmission [11][31], the recent emergence of nVarIBDV outbreaks in other Asian countries such as Japan [56], South Korea [57], and Malaysia [58] are of concern. It was reported that nVarIBDV does not cause severe clinical signs but causes irreversible damage to the immune organs of chickens, including bursal lesions, spleen swelling and atrophy, and long-term immunosuppression, to a greater extent than the previous varIBDV [51][59][60]. In addition, the new strains can break through the immune protection provided by existing vvIBDV vaccines [57][61][62].
The novel variant spectrum of IBDV strains exhibits significant genetic differences from previously reported IBDV strains. The strains contain multiple amino acid substitutions, with VP2 having typical residues similar to varIBDV (222 T, 249 K, 286 I, and 318 D) [26], as well as other residues such as 221 K, 252 I, and 299 S, and VP1 containing 147 D and 508 K [51]. Although the same amino acid differences have been reported in other studies [63], the relationship between these amino acid substitutions and the antigenicity and pathogenicity of the strains has not been fully investigated. Therefore, further investigations into novel variant IBDV strains are needed to better understand the epidemics of currently circulating IBDV strains.

5. Other Strain Types of IBDV

There are several other strain types of IBDV, including attenuated, reassortant, and recombinant strains. Attenuated strains usually refer to those attenuated live vaccine strains made especially for the control of cIBDV or vvIBDV infection and are classified as mild, intermediate, or intermediate-plus based on their attenuation [3]. The immunization of chicks with attenuated vaccine strains has become the primary defense against IBD in young chickens. Although attenuated strains are generally not lethal to chickens, intermediate and intermediate plus attenuated strains can cause varying degrees of bursal damage in vaccinated chickens [64]. However, due to the widespread use of live vaccines, the spread of different strain types among flocks in recent years has led to the increasing emergence of reassortant and recombinant strains of IBDV, such as strains with segment A of vvIBDV and segment B of attenuated strains [47][65][66], segment A of vvIBDV and segment B of serotypeII [46], and segment A of vaccine strains and segment B of vvIBDV [67][68], etc. Homologous recombination between different strains of IBDV has also been reported [26][69][70][71]. Recombination and reassortment between different strains pose new challenges to the prevention and control of IBD and require continued efforts to investigate the genetics and epidemics of IBDV.


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