Abstract
Avian reoviruses (ARVs) are ubiquitous in domestic poultry with 80% of them being non-pathogenic and they are frequently found in clinically healthy birds. ARVs have also been known to be the etiological agents of viral arthritis (VA), tenosynovitis, myocarditis, runting-stunting syndrome (RSS), and respiratory and enteric disease in chickens. Significant economic losses during the process of poultry husbandry are due, in part, to unmitigated ARV infections throughout the poultry industry. Recently, many isolates shared genetic similarities between those recovered from wild birds and those recovered from poultry. One explanation may be that there is a degree of spillover and spillback of ARVs between the two groups. However, studies on the role of wild birds in the epidemiology and pathogenicity of ARVs are insufficient. Here, we describe the pathogenicity in specific pathogen-free (SPF) chickens of ARV originating from wild birds. The challenge experiment was conducted in six groups including a negative control group, a positive control group (reference strain of S1133), and four groups (A15-157, A18-13, A18-205, A19-106) infected with ARVs from wild birds. The 7-day-old SPF chickens were inoculated with 106TCID50 ARV to evaluate the clinical signs, changes in weight gain, gross lesions, histological changes, virus replication, and serum antibody levels. The peak of clinical signs was from 3 to 5 days post infection (dpi). In addition, the death of one chicken was found in the group infected with the A18-13 isolate. Reduced body weight was also found in chickens infected with ARVs from wild birds compared to the negative control group. All the ARVs infection groups showed noticeable swelling of the footpad. In addition, ARVs were detected in the bursa, tendon, and hock joint by reverse transcription-polymerase chain reaction (RT-PCR) in all infected groups at 5 and 15 dpi. Histopathological observations revealed acute inflammatory responses on the synovium covering the joint surfaces (arthritis) and tendon sheaths (tenosynovitis), as well as bursa atrophy and lymphocyte depletion. The analysis of the humoral response was performed by ELISA assay, and chickens infected with ARVs showed seroconverted. In conclusion, this study described the typical severe disease of acute VA and tenosynovitis in SPF chickens infected with ARVs derived from wild birds. This study confirmed the pathogenicity of ARVs infection in SPF chickens for the first time, and these results enrich our understanding of the pathogenicity of ARVs derived from wild birds.
Highlights
Avian reoviruses (ARVs) are part of the Reoviridae family in the genus Orthoreovirus
Given the limited information in the literature concerning the pathogenicity of ARV isolates recovered from wild birds, in this study, we evaluated the pathogenicity of ARVs from wild birds in specific-pathogen-free (SPF) 7-dayold chickens
Clinical signs were observed in chickens infected with ARVs at 1 dpi, which gradually increased to a peak at 3–5 dpi (Supplementary Table 1)
Summary
Avian reoviruses (ARVs) are part of the Reoviridae family in the genus Orthoreovirus. They are non-enveloped viruses composed of two concentric icosahedral capsids with an external diameter of 80–85 nm [1]. ARVs infection can cause viral arthritis (VA)/tenosynovitis, which is characterized by swelling of the hock joints and lesions in the gastrocnemius tendons [5,6,7,8]. ARVs are transmitted by the horizontal and vertical routes [16] They affect mostly young birds and are disseminated through the oral-fecal route [17] and vertically from breeders to progeny [18]. ARVs survive for at least 10 days on feathers, wood shavings, eggshells, feed, and in drinking water, the virus was detectable for at least 10 weeks [20]
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