Avian Reovirus: From Molecular Biology to Pathogenesis and Control

Abstract

Avian reoviruses (ARVs) represent a significant economic burden on the poultry industry due to their widespread prevalence and potential pathogenicity. These viruses, capable of infecting a diverse range of avian species, can lead to a variety of clinical manifestations, most notably tenosynovitis/arthritis. While many ARV strains are asymptomatic, pathogenic variants can cause severe inflammation and tissue damage in organs such as the tendons, heart, and liver. In broilers and turkeys, ARVs can induce severe arthritis/tenosynovitis, characterized by swollen hock joints and lesions in the gastrocnemius tendons. Additionally, ARVs have been implicated in other diseases, although their precise role in these conditions remains to be fully elucidated. In recent years, ARV cases have surged in the United States, emphasizing the need for effective control measures. Routine vaccination with commercial or autogenous vaccines is currently the primary strategy for mitigating ARV's impact. Future research efforts should focus on enhancing our understanding of ARV-induced pathogenesis, identifying host factors that influence disease severity, and developing novel vaccines based on ongoing surveillance of circulating ARV strains. This review aims to explore the molecular aspects of ARV, including virus structure, replication, molecular epidemiology, the roles of its encoded proteins in host pathogenesis, and the immune response to ARV infection. Furthermore, we discuss the diagnostic approaches of avian reovirus and the potential biosecurity measures and vaccination trials in combating ARV and developing effective antiviral strategies.

Keywords: avian reovirus; epidemiology; immune response; pathogenesis; replication; vaccine.

Figure 1

Estimated impact of reovirus on breeders, broilers, and pullets in the US for 2022.

Figure 2

Electrophoretic mobility of genomic segments of avian reoviruses. (A) 2177 strain, (B) the vaccine strain S1133.

Figure 3

Diagrammatic structure of avian reovirus.

Figure 4

Posttranslational modification of the avian reovirus major capsid protein μB.

Figure 5

Two-dimensional secondary structure of avian reoviruses P10 fusogenic protein showing the three domains: the ectodomain, with potential extracellular exposure, and the endodomain, within the cytosol, intervened by the transmembrane domain. The color coding of the secondary structures is as follows: yellow arrows are β-strand, blue curved arrows are turns, white spirals are coil structure, and pink barrels are α-helix.

Figure 6

A diagrammatic representation of the avian reovirus replication cycle. Virus morphogenesis and release.

Figure 7

Avian reovirus assembly inside the viroplasm (cytoplasmic viral inclusions). Initially the M3-encoded protein (μNS) induces the viroplasm formation via the recruitment of the major core protein (λA) and the single-stranded RNA binding protein (σNS). Thereafter, the remaining core proteins are localized to the viroplasm, including λB, μA, and σA, within 30 min post-translation to form the core virus particle (step 2). Over 30 min later, the outer shell proteins are recruited to the viroplasm, with the primary assembly of the turret protein (λC), followed by the assembly of the minor capsid protein (σB) with the major capsid protein (μB) and its cleaved forms (μBC and μBN) forming a stable ternary heterocomplex prior to incorporation onto the core particle, as depicted in step 3, and eventually the introduction of viral attachment protein (σC) in step 4. Less is known about genome recruitment. However, the positive-stranded RNA strands of the virus genome are thought to be recruited prior to or during the encapsidation and are transcribed to produce the negative strands for the generation of the 10 genomic double-stranded RNA segments using the poly-C-dependent polymerase (σNS), as shown in step 2, followed by dissociation of σNS under high ionic strength once the dsRNA is generated in step 3. The color coding of the viral proteins is described in Figure 6.

Figure 8

Global geographical distribution of genotypic clusters of avian reovirus. The seven σC-based genetic clusters (GCs) of ARV is referred as I–VII.

Figure 9

Abnormal development of primary feathers due to avian reovirus infection referred as helicopter wing feathers.

Figure 10

Hemorrhage and tendon rupture in the pelvic limb of broiler breeder chickens. (a) Severe hemorrhage surrounding the femorotibiotarsal joint (circled), with subcuticular edema (arrow). (b) Rupture of the flexor tendons at the level of the intertarsal joint (circled), with hemorrhage and edema extending into the surrounding muscle (arrow), which has been removed for visualization of tendon pathology.

Figure 11

Histopathology in tendons of ARV-infected broilers. Tendon tissues showed mild to moderate multifocal thickening of the synovium with mononuclear inflammatory cell infiltrates and synovial hyperplasia (a,b). (c,d) are higher magnifications of the boxed areas in (a,b), respectively.

Figure 12

Histopathology of the heart of ARV-infected broilers. Heart tissue demonstrated moderate diffuse thickening of the pericardium ((a), pericardium delineated by a double-headed arrow) characterized by accumulations of fibrin, edema, vascular congestion (starred), and lymphoplasmacytic infiltration (asterisks) with multifocal extension into the myocardium (b) and epicardium (d). (c) is a higher magnification of the squared area of subfigure (a).