Abstract

Simple SummaryThe accumulation of point mutations and/or recombination between different serotypes drives the evolution of the duck hepatitis A viruses (DHAVs). Duck viral hepatitis, caused by DHAV, is a highly infectious disease that has been detected in Egypt since 1970. Low performance, nervous signs and sudden deaths of young ducklings were the main characteristics of the disease. The aim of this study was to identify the causative agent through viral and molecular detection for the causative virus. The causative virus was isolated in embryonated duck eggs (EDEs), with complete genome sequencing that indicate the clustering of our isolates reported in this study with Chinese duck hepatitis virus 1 that may help in new vaccine manufacturing and the development of a more sensitive diagnostic assays. Future studies to evaluate the potential protection of available commercial vaccines against the newly detected isolates will be needed.Duck hepatitis virus (DHV) is one of the commercially important diseases of ducklings worldwide. It is an acute and highly infectious disease of ducklings caused by three different serotypes (1–3) of duck hepatitis A virus (DHAV), and serotype 1 is the most common in poultry. To date, little is known about the prevalence and genetic characterisation of DHAV-1 in Egypt. In the current study, isolation and complete genomic analyses of DHAVs circulating in commercial duck farms in different Egyptian governorates were conducted. A total of eighteen samples were collected from six Egyptian governorates of 3–11 days old ducklings (Pekin and Mullard) with a history of nervous signs and high mortality rates. Five out of eighteen (5/18) samples were screened positive for the DHAV-1 based on the VP1 gene. These samples were individually used for virus isolation in embryonated duck embryos (EDE), followed by complete genome sequencing. Phylogenomic analyses showed that DHAV serotype I; genotype I were diversified into four different groups (1–4). Most of the recent circulating Egyptian DHAV strains are clustered within group 4, while isolates characterised within this study were clustered within group 1. Recombination analyses revealed that the emergence of a new recombinant virus—DHAV-1 strain Egypt-10/2019—through recombination. Likewise, the selective pressure analyses showed the existence, inside or near areas of the viral attachment or related functions, of positive scores highlighting the importance of natural selection and viral evolution mechanism at different protein domains. The findings of this study provide updated information on the epidemiological and genetic features of DHAV-1 strains and underscore the importance of DHAV surveillance as well as re-evaluation for currently used vaccines.

Highlights

  • Duck viral hepatitis (DVH) is a highly contagious disease of ducks characterised by severe morbidity and mortality, in ducklings under the age of four weeks old [1]

  • All samples were collected from ducklings showing lethargic, nervous signs of ataxia and a high mortality rate (~60%)

  • The high mortality rate associated with the duck hepatitis A virus (DHAV)-1 outbreaks, which is often over 50% and can exceed up to 95% in field conditions, continues to be a threat to duck farms [12,25]

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Summary

Introduction

Duck viral hepatitis (DVH) is a highly contagious disease of ducks characterised by severe morbidity and mortality, in ducklings under the age of four weeks old [1]. Duck hepatitis A virus (DHAV), causative of DVH, is classified into three types I, II and III. The DHAV type I belongs to the genus Avihepatovirus, family Picornaviridae and has three distinguishable serotypes designated as serotypes 1–3. II and III were recently classified as duck astrovirus 1 and 2 (DAstV-I and DAstV-II) and belong to the family Astroviridae and are antigenically distinct from DHAV type I. DHAV serotype 1 is the most widespread serotype; serotype 2 was reported in Taiwan, and serotype 3 was first characterised in South Korea and China [2,3]. The evolution of the DHAV is driven by the accumulation of point mutations and/or recombination between different serotypes [4]

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