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Avian reovirus (ARV) is a double stranded RNA virus belonging to the genus Neoreovirus in the family Neoreoviridae. It has a segmented genome and high thermal stability. The virus mainly proliferates by infecting chicken embryo fluid or chicken embryo kidney cell culture. After 2-3 days of cultivation at 37 ℃, it can cause chicken embryo death and trigger syncytial cell pathology. The freeze-drying storage temperature is -70 ℃. Its host range covers poultry such as chickens, ducks, and geese, and can cause various clinical symptoms such as arthritis, tenosynovitis, and immune suppression syndrome. The virus has 11 serotypes and 6 σ C genotypes, with significant differences in nucleotide homology between genotypes. The survey showed that the positive rate of white feathered broiler chickens was 62.1%, with genotype 1 accounting for the highest proportion (38.85%). The detection techniques include RT-PCR, fluorescence quantitative PCR, and immunological methods. The existing vaccines have insufficient protection against mutant strains and require continuous monitoring of virus mutations.
Figure 1. Posttranslational modification of the avian reovirus major capsid protein μB. (Nour, Islam,et al, 2024)
Avian reoviruses (ARVs) are double-stranded RNA viruses of the family Reoviridae, genus Orthoreovirus, that can infect both domestic and wild birds. In crows, the ARV called corvid orthoreovirus causes a disease known as winter mortality of crows in which large numbers of crows become infected and die as they congregate in winter roosts. Winter mortality of crows was first identified in 2001 and has been seen over a broad range of North America and in parts of Europe. Crows infected with corvid orthoreovirus are typically found dead. On gross and histologic examination, birds show severe inflammation and necrosis of the intestines and colon, spleen, and sometimes the liver. Most die-offs due to corvid orthoreovirus occur in winter months when large numbers of crows congregate at winter roosts. Overcrowded conditions lead to increased fecal-oral transmission of the virus. Hundreds of crows may be infected and die.
A key feature of ARV infection is its strategic interference with the host's innate immune response, particularly the type I interferon (IFN) system, which is the first line of defense against viral infection. ARV encodes specific proteins that act as virulence factors by targeting key nodes in the host signaling pathway. The following table summarizes the key viral proteins involved in the pathogenesis of ARV and their interactions with host cell targets:
| Key Host Target / Pathway | Function & Role in Pathogenesis |
| dsRNA Sensors (PKR, MDA5/RIG-I) | Acts as a dsRNA-binding protein. It sequesters viral dsRNA intermediates, shielding them from detection by host cytoplasmic sensors like MDA5 and preventing the activation of the IRF3/7 pathway and subsequent IFN-β production. It also inhibits the dsRNA-activated protein kinase PKR, thereby preventing the shutdown of host protein synthesis. |
| Viral RNA, Host IFN Response | A non-structural RNA-binding protein. It plays a role in viral genome packaging and replication. Studies suggest it also contributes to IFN antagonism, possibly by further sequestering viral RNA from cellular sensors. |
| NF-κB, Apoptosis, Inflammatory Cytokines | ARV infection activates the NF-κB pathway, leading to the production of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α). This contributes to the inflammation seen in tenosynovitis and enteritis. The virus can also induce apoptosis in infected cells via both death receptor and mitochondrial pathways, contributing to tissue damage. |
ARVs have been isolated from a variety of wild bird species. ARVs related to corvid orthoreovirus have been linked to deaths of other corvid species: the hooded crow in Finland, magpie in England, and carrion crow in Belgium. Other ARVs have been isolated from wild birds, including storks, herons, buzzards, and pigeons, with no signs of disease. An ARV was isolated from woodcocks found dead in New Jersey and Virginia in the winters of the early 1990s. These birds were emaciated but had no obvious gross abnormalities, unlike crows with winter mortality. However, the infection appeared to be systemic, because the virus was isolated from several different tissues.
ARVs are transmitted primarily by the fecal-oral route, although respiratory transmission may also occur. In winter mortality of crows, high densities of birds in roosts allow for easy transmission of the virus via the fecal-oral route. It is possible that strains of ARV are transmissible between different bird species. However, it is unknown if wild birds act as reservoirs of infection for domestic poultry.
| Diagnosis, Control, and Prevention | Details |
| Diagnosis | Clinical signs are suggestive but not definitive. Laboratory confirmation is essential:
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| Control | No specific antiviral treatment exists. Management relies on an integrated approach:
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Avian reovirus is a multifaceted pathogen, and its economic impact stems from its ability to cause persistent infections and regulate host immunity. The molecular pathogenesis of this disease is centered around immune evasion, mainly through the action of σ A protein, which effectively neutralizes the host's dsRNA induction and PKR mediated defense system. This enables the virus to replicate effectively while triggering NF-κB mediated inflammation, which is the basis for key clinical symptoms such as arthritis and enteritis. Continuing to study specific host factors targeted by viral proteins such as σ A and σ C is crucial for developing more effective vaccines and control strategies to combat this economically significant avian virus.
Reference
| Target | Cat. No. | Product Name | Host | |
| ARV | DAGC536 | Avian Reovirus (S1133) Chorioallantoic Membrane Homogenate | N/A | Inquiry |
| DAGC537 | Avian Reovirus (S1133) Tissue Culture | N/A | Inquiry |
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