Abstract

This study focuses on virus isolation of avian reoviruses from a tenosynovitis outbreak between September 2015 and June 2018, the molecular characterization of selected isolates based on partial S1 gene sequences, and the full genome characterization of seven isolates. A total of 265 reoviruses were detected and isolated, 83.3% from tendons and joints, 12.3% from the heart and 3.7% from intestines. Eighty five out of the 150 (56.6%) selected viruses for sequencing and characterization were successfully detected, amplified and sequenced. The characterized reoviruses grouped in six distinct genotypic clusters (GC1 to GC6). The most represented clusters were GC1 (51.8%) and GC6 (24.7%), followed by GC2 (12.9%) and GC4 (7.2%), and less frequent GC5 (2.4%) and GC3 (1.2%). A shift on cluster representation throughout time occurred. A reduction of GC1 and an increase of GC6 classified strains was noticed. The highest homologies to S1133 reovirus strain were detected in GC1 (~77%) while GC2 to GC6 homologies ranged between 58.5 and 54.1%. Over time these homologies have been maintained. Seven selected isolates were full genome sequenced. Results indicated that the L3, S1 and M2 genes, coding for proteins located in the virus capsid accounted for most of the variability of these viruses. The information generated in the present study helps the understanding of the epidemiology of reoviruses in California. In addition, provides insights on how other genes that are not commonly studied add variability to the reovirus genome.

Highlights

  • Extreme variability is an inherent characteristic of ARV

  • This study focused on virus isolation of avian reoviruses between September 2015 and June 2018, the molecular characterization of selected reoviruses based on partial S1 gene sequences, and the full genome characterization of seven selected isolates

  • Was detected by Reverse transcriptase polymerase chain reaction (RT-PCR) followed by virus isolation and tenosynovitis was confirmed by histopathological findings

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Summary

Introduction

Extreme variability is an inherent characteristic of ARV. This is based on their RNA nature and their segmented genome favouring mutations, recombination and reassortment events[8,9]. Despite the better understanding of the biology of the virus, their variability and the efforts of several groups across the U.S.5,6,16,17, Europe[14,18], Canada[19,20] and China[10] in detecting and typing ARV variants, classical vaccine strains used for immunization of commercial flocks, namely S1133, 1733 and 2408, have not changed since the 1970’s These strains have proven to be inefficient in controlling the infection, partly due to the RNA virus nature being prone to mutation and recombination events and generating variants that are partially or incompletely protected by antibodies generated by classical vaccine strains.

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