“The History of Avian Reovirus – From Early Control Success by Vaccination to Rapid Evolution of Field Isolates and Current Challenges in Control”  

By: Dr. Holly Sellers

The first isolation of reovirus was made by Fahey and Crawley in 1954 from chickens experiencing chronic respiratory disease. Several years later, an agent producing tenosynovitis in broilers that lacked sensitivity to several antibiotics was reported and appeared to only affect young chickens. At this time, several reovirus isolates demonstrated the ability to induce tenosynovitis and arthritis, including the original Fahey-Crawley isolate. Reoviruses were also isolated from cases of tenosynovitis and enteritis in several countries. While reovirus isolates from the US were serologically related, serologic variants were isolated in Europe and Israel. The ability of reoviruses to transmit vertically was soon revealed and the role of maternal antibodies to protect progeny determined to be important as early as 1975. The first reovirus vaccine was inactivated and contained isolate S1133 (Dr. Louis Van der Heide). This vaccine was used in broiler breeders to provide protection against infection and intended to provide progeny with maternal antibodies. However, insufficient levels of antibodies developed following vaccination and this led to efforts to develop a live vaccine. Isolate S1133 was passaged for attenuation in chicken embryos and the first licensed live vaccine was produced by Sterwin in 1978 for use in older birds. A more attenuated S1133 was produced by an additional combined 300 passages in embryos followed by cell culture and resulted in a fully attenuated reovirus safe for use in young chickens. In the 1980s, a second attenuated live reovirus vaccine, Enterovax, was licensed for use in young chickens. Over the next two decades, the combination of live attenuated and inactivated reovirus vaccines were used successfully in the US to protect against disease. In 2011, a significant increase in the incidence of tenosynovitis/viral arthritis was observed across the US. Variant reoviruses were isolated in US broilers from reovirus vaccinated breeders. Evidence that commercial vaccines did not provide sufficient protection and use of field isolates in autogenous vaccines became widespread in the industry. Genetic characterization of the reovirus Sigma C protein revealed seven genetic clusters (GC). Five of the seven GCs were identified in a retrospective study characterizing European reoviruses from the 1980s. Around the same time as tenosynovitis/viral arthritis (VA) appeared in chickens, it also appeared in turkeys. To date, companies continue to include field isolates from one or several of the seven GCs in their autogenous vaccines; they also continue use the modified live of S1133 origin or Enterovax. Incidence of disease fluctuates throughout the year and generally is not restricted to one GC. In fact, high levels of genetic diversity exist in reovirus populations from clinical cases of tenosynovitis/VA. Development of new vaccines is currently in progress and will be necessary to contribute to the control of reoviral disease in poultry.