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Infectious Bursal Disease Virus Variants: A Challenge for Commercial Vaccines?
Gumboro disease, also known as Infectious Bursal Disease (IBD) or Avian Infectious Bursitis, was first reported in Delaware, USA, in 1962. It is an immunosuppressive viral disease that primarily affects chickens between 3 to 6 weeks of age and has a global distribution.
The virus responsible for this disease belongs to Avibirnavirus genus, Birnaviridae family, and has two serotypes: I and II.
Serotype I has been detected in chickens, hens, pigeons, and guinea fowl (Kasanga et al., 2008) but is only pathogenic in chickens and hens.
Serotype I is further divided into two antigenic subtypes: classical and variants, while serotype II remains asymptomatic in turkeys, crows, ostriches, and ducks (Ogawa et al., 1998; Yilmaz et al., 2019).
Since its first report, numerous variants of the virus have been identified, complicating efforts to control the disease. Until the 1980s, vaccination was effective in control the disease, with mortality rates in broilers below 2%.
However, with continued mutation and reassortment of the virus, new antigenic variants emerged, leading to higher mortality rates, even in the presence of strict vaccination protocols.
These variants can appear subclinically, reducing growth and increasing susceptibility to secondary infections, which result in substantial economic losses for the poultry industry.
ZOOMING INTO THE VIRUS
The virus has an icosahedral shape, no envelope, and consists of two linear double-stranded RNA segments, designated as A and B.
Segment B encodes VP1, a viral polymerase RNA, while segment A produces the capsid proteins pVP2 and VP3, as well as the protease VP4 and VP5, a non-structural protein involved in regulatory functions and membrane disruption in infected cells (Mundt, 1999) (Figure 1).
Among the components mentioned above, the VP2 protein is particularly important as it determines the virus’s antigenicity, virulence, and pathogenicity. It contains regions that antibodies can bind to, and when exposed to the immune response, it tends to undergo greater mutation, making it a highly variable region (Letzel et al., 2007).
Figure 1. Structure and components of the Infectious Bursal Disease Virus (IBDV) genome
The capsid protein VP2 contains three distinct domains: base (B), envelope (S), and projection (P).
The P domain is made up of four loop struct...
