Classification of infectious bursal disease virus into genogroups

Linda O Michel,Daral J Jackwood

doi:10.1007/s00705-017-3500-4

Abstract

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.

Highlights

Outbreaks of infectious bursal disease (IBD), a significant contagious immunosuppressive disease of poultry, are still reported throughout the world despite efforts to control the disease through vaccination
Control efforts are complicated by the fact that the causative agent, infectious bursal disease virus (IBDV), an avibirnavirus consisting of two segments of double-stranded RNA [1], is subject to frequent genetic mutations, reassortment of genome segments, and genomic recombination events that can potentially increase virulence and alter antigenicity, rendering vaccines less effective [2, 3]
Pathogenicity is important with regard to severity of the disease and degree of immune suppression, we focused our study on mutations located in the hypervariable region of the capsid protein VP2 (hvVP2)

Summary

Introduction

Outbreaks of infectious bursal disease (IBD), a significant contagious immunosuppressive disease of poultry, are still reported throughout the world despite efforts to control the disease through vaccination. Control efforts are complicated by the fact that the causative agent, infectious bursal disease virus (IBDV), an avibirnavirus consisting of two segments of double-stranded RNA [1], is subject to frequent genetic mutations, reassortment of genome segments, and genomic recombination events that can potentially increase virulence and alter antigenicity, rendering vaccines less effective [2, 3]. Young birds that survive the disease can be permanently immune suppressed; affected flocks typically have poor growth rates, poor feed conversion, decreases in egg production and egg quality, and impaired efficacy of

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