They can be confirmed using virus isolation, complement fixation, ELISA, immunodiffusion or histopathology (following postmortem exam).

Common areas where this virus can survive include galvanized metal, glass, rubber, feathers, and wood shavings.

There are several primary chicken cell cultures/areas that are susceptible to avian reoviruses, which include the lungs, liver, kidney, and fibroblasts of the chick embryo.

Of the following susceptible areas, liver cells from the chick embryo have been found to be the most sensitive for primary isolation from clinical material.

CPE, or cytopathic effects are the visible changes in a host cell that takes place because of viral infection.

[5] Alpha and beta interferons belong to a family of multifunctional cytokines, which are expressed and activated/distributed by fibroblasts and leukocytes in response to infections.

In an experiment where primary cultures of chicken embryo fibroblasts were treated with alpha/beta interferon, results indicated that this interaction induced an antiviral state that strongly inhibited vaccinia and vesicular stomatitis virus (VSV) replication, but didn't have an effect on avian reovirus, specifically the replication of the S1133 strain.

Research has shown that this core protein may possibly disrupt the IFN-induced cellular response against avian reovirus through the blockage of enzyme pathways that are dependent on dsRNA.

[6] In addition to the possible disruption of IFN-induced cellular responses, chicken embryo fibroblasts that are infected with strain S1133 have displayed significant cytopathic effects.

Disregarding infectivity, the number of inoculated virus particles is the significant factor that leads to apoptosis from avian reovirus.

Blue wing disease affects young broiler chickens and has an average mortality rate of 10%.

[9] Chickens that have contracted runting-stunting syndrome cause a number of individuals in a flock to appear noticeably small due to its delayed growth.

[12] In an experiment, avian reovirus was recovered from mononuclear, plasma, and erythrocyte cell fractions of blood within 30 hours of infection in young chicks.

The tibiotarsal-tarsometatarsal (hock joint) was the site where virus replication caused the most severe damage and in some extreme cases, tendon rupture.

[14] The sera of birds infected with avian reovirus display circulating antibodies through the validation of ELISA, agar gel immunodiffusion, indirect immunofluorescence (IIF), and virus neutralization (VN).

[15] Maternal antibodies have displayed protection against the development of microscopic lesions of tenosynovitis in chicks that have been infected one day after birth.

[16] An experiment that used monoclonal antibodies that were specific for chick Ia (a chicken class II major histocompatibility complex antigen), and T and B-lymphocytes were observed to determine its effects on cellular infiltrates during the development of reovirus arthritis.

Confirming infection of avian reovirus can be detected through an ELISA test by using and observing the expression of σC and σB proteins.

Isolation is most successfully attained through inoculation of material into chick embryo cultures or fertile chicken eggs.

Currently, efforts toward administering inactivated or live vaccines to breeding stock to allow passive immunity to the offspring via the yolk are being taken.

Infection may also enter through the exposure of broken skin of the feet or legs of the chickens, where it then can become established in the hock joints.