Molecular characterization of reassortant infectious bursal disease virus (IBDV) strains of genogroup A3B1 detected in some areas of Britain between 2020 and 2021
Vishwanatha R. A. P. Reddy, Carlo Bianco, Christopher J. Poulos, S. Egaña-Labrin, Andrew J. Brodrick, Salik Nazki, A. Schock, Andrew Broadbent
Abstract
Infectious bursal disease virus (IBDV) causes a major immunosuppressive disease of chickens. As part of ongoing epidemiological surveillance for IBDV, the hypervariable region (HVR) of the VP2 capsid gene encoded by segment A, and a region of the VP1 polymerase gene, encoded by segment B, were sequenced from 20 IBDV-positive bursal samples obtained in 2020 and 2021, from 16 commercial British broiler farms. Birds had received a live IBDV vaccine at 17–22 days of age, and samples were obtained at 25–55 days of age. Of the 16 farms, none contained very virulent (vv) strains, one contained a classical virulent strain, two contained vaccine strains, and five contained sequences of reassortant strains with a vv segment A and a non-vv segment B belonging to genogroup A3B1. In eight of the farms, we identified the sequences of both genogroup A3B1 reassortant strains and vaccine strains in the same samples. Therefore, the majority of the farms (13/16 (81%)) contained genogroup A3B1 reassortant viruses. Of the flocks containing reassortant strains, 5/13 (38%) had HVR mutations Q219L, G254D, D279N, and N280T, consistent with a recently described Western European clade, but the rest had other mutations or no mutations, demonstrating that multiple clades were present in the samples. Taken together, vv strains were not detected, but reassortant strains predominated in the farms, which belonged to different clades, and were frequently found together with vaccine strains. • True very virulent strains of genogroup A3B2 were not detected in the British broiler flocks. • Whereas reassortant IBDV strains belonging to genogroup A3B1 predominated. • Multiple clades of A3 reassortant viruses were found to be circulating, and co-amplification of A3 and A1 was common. • The consequences of reassortment, antigenic drift, and co-infection remains poorly understood.