Genomic Epidemiology and Evolution of Duck Hepatitis A Virus.

Enikő Fehér,Krisztián Bányai,Ádám Bálint,Krisztina Bali,Vilmos Palya,Szilvia Jakab,Borbála Nagy,Katalin Ihász,Eszter Kaszab

doi:10.3390/v13081592

Abstract

Duck hepatitis A virus (DHAV), an avian picornavirus, causes high-mortality acute disease in ducklings. Among the three serotypes, DHAV-1 is globally distributed, whereas DHAV-2 and DHAV-3 serotypes are chiefly restricted to Southeast Asia. In this study, we analyzed the genomic evolution of DHAV-1 strains using extant GenBank records and genomic sequences of 10 DHAV-1 strains originating from a large disease outbreak in 2004–2005, in Hungary. Recombination analysis revealed intragenotype recombination within DHAV-1 as well as intergenotype recombination events involving DHAV-1 and DHAV-3 strains. The intergenotype recombination occurred in the VP0 region. Diversifying selection seems to act at sites of certain genomic regions. Calculations estimated slightly lower rates of evolution of DHAV-1 (mean rates for individual protein coding regions, 5.6286 × 10−4 to 1.1147 × 10−3 substitutions per site per year) compared to other picornaviruses. The observed evolutionary mechanisms indicate that whole-genome-based analysis of DHAV strains is needed to better understand the emergence of novel strains and their geographical dispersal.

Highlights

Infection caused by duck hepatitis virus 1 (DHV-1 or DHV type I), recently renamed as duck hepatitis A virus (DHAV), may be fatal in up to 95% of ducklings, typically under three weeks of age [1,2,3]
Our analyses indicated that recombination events affected the viral genomes of DHAV-1 and DHAV-3 strains, and some recombinants seemed to have acquired RNA fragments from parental strains belonging to different DHAV genotypes (Table 2, Figure 2)
Evolutionary mechanisms of DHAV are similar to other picornaviruses; the main features shared by these viruses include high evolutionary rates and the potential for viral RNA recombination, even among heterotypic strains [32,33,35]

Summary

Introduction

Infection caused by duck hepatitis virus 1 (DHV-1 or DHV type I), recently renamed as duck hepatitis A virus (DHAV), may be fatal in up to 95% of ducklings, typically under three weeks of age [1,2,3]. The disease is characterized by hepatic failures (enlargement, hemorrhages and necrosis), neurological signs (ataxia, opisthotonus) and the sudden death of affected birds [1,2,3,4]. The duck industry has been heavily affected by this virus; the disease can be efficiently prevented by vaccination [5]. The viral genome is a ~7.7-kilobaselong positive-sense single stranded RNA and consists of a single large open reading frame (ORF) flanked by the 5 and 3 non-coding regions. The polyprotein encoded by the single ORF is predicted to code for the VP0, VP3, and VP1 structural proteins and the 2A1, 2A2, 2B, 2C, 3A, 3B, 3C, and 3D non-structural proteins [6,7]

Methods

Results

Conclusion