Evidence of genetic drift and reassortment in infectious bursal disease virus and emergence of outbreaks in poultry farms in India.

Abstract

Recurrent outbreaks of infectious bursal disease (IBD) have become a burning problem to the poultry industry worldwide. Here, we performed genetic analysis of IBD virus (IBDV) field isolates from recent outbreaks in various poultry farms in India. The sequence analysis of IBDV VP2 hypervariable region revealed amino acid pattern similar to that of very virulent (222A, 242I, 253Q, 256I, 272I, 279D, 284A, 294I, 299S and 330S) and intermediate plus virulent (222A, 242I, 253Q, 256I, 272T, 279N, 284A, 294I, 299S and 330S) type whereas analysis of VP1 revealed presence of sequence similar to that of very virulent (61I, 145T) and unique (61I, 141I, 143D, 145S) type in field isolates. Among the eight field isolates, two isolates contained very virulent type VP2 and unique type VP1, three contained intermediate plus virulent type VP2 and unique type VP1 whereas five contained both VP2 and VP1 of very virulent type. The phylogenetic analysis based on VP2 nucleotide sequence showed clustering of all eight isolates close to known very virulent strains whereas based on VP1, five isolates formed unique cluster and three isolates were placed close to very virulent strains. The isolates forming unique VP1 cluster showed highest similarity with classical virulent IBDVs suggesting their possible evolution from segment B of non-very virulent IBDVs. Interestingly, these five isolates were responsible for outbreaks in four different farms located at three different geographic locations in India. These observations indicates genetic reassortment between segment A and segment B from co-infecting IBDV strains leading to emergence of very virulent strains and their widespread prevalence in Indian poultry farms. The presence of 272I and 279D in VP2 protein of five field isolates may explain possible cause of Gumboro intermediate plus vaccine failure in prevention of the outbreaks. However, mortality caused by other three strains which are antigenically similar to VP1 of intermediate plus vaccine strains could not be explained and the possible role of their unique VP1 in enhancing the pathogenesis needs to be investigated further.