ipnv
Molecular epidemiological study on Infectious Pancreatic Necrosis Virus isolates from aquafarms in Scotland over three decades
In order to obtain an insight into genomic changes and associated evolution and adaptation of Infectious Pancreatic Necrosis Virus (IPNV) the complete coding genomes of 57 IPNV isolates collected from Scottish aquafarms from 1982-2014 were sequenced and analysed. Phylogenetic analysis of the sequenced IPNV strains showed separate clustering of genogroups I, II, III and V. IPNV isolates with genetic reassortment of segment A/B of genogroup III/II were determined. About 59% of the IPNV isolates belonged to the persistent type and 32% to the low virulent type and only one highly pathogenic strain (1.79%) was identified. Codon adaptation index calculations indicated that the IPNV major capsid protein VP2 has adapted to its salmonid host. Underrepresentation of CpG dinucleotides in the IPNV genome to minimise detection by the innate immunity receptors, and observed positive selection in the virulence determination sites of VP2 embedded in the variable region of the main antigenic region, suggest an immune escape mechanism driving virulence evolution. The prevalence of mostly persistent genotypes together with the assumption of adaptation and immune escape indicates that IPNV is evolving with the host.
In order to obtain an insight into genomic changes and associated evolution and adaptation of Infectious Pancreatic Necrosis Virus (IPNV) the complete coding genomes of 57 IPNV isolates collected from Scottish aquafarms from 1982-2014 were sequenced and analysed. Phylogenetic analysis of the sequenced IPNV strains showed separate clustering of genogroups I, II, III and V. IPNV isolates with genetic reassortment of segment A/B of genogroup III/II were determined. About 59% of the IPNV isolates belonged to the persistent type and 32% to the low virulent type and only one highly pathogenic strain (1.79%) was identified. Codon adaptation index calculations indicated that the IPNV major capsid protein VP2 has adapted to its salmonid host. Underrepresentation of CpG dinucleotides in the IPNV genome to minimise detection by the innate immunity receptors, and observed positive selection in the virulence determination sites of VP2 embedded in the variable region of the main antigenic region, suggest an immune escape mechanism driving virulence evolution. The prevalence of mostly persistent genotypes together with the assumption of adaptation and immune escape indicates that IPNV is evolving with the host.