TURKEY CORONAVIRUS: AN UPDATED REVIEW

Abstract

Turkey coronavirus (TCoV) causes acute atrophic enteritis and uneven flock growth in turkey farms leading to economic loss. Since 1990's, turkey flocks have kept experiencing coronaviral enteritis sporadically in the United States, Canada, Europe, and Brazil. Poult enteritis and mortality syndrome (PEMS) caused by the co-infection of TCoV, astrovirus, and other viruses or bacteria resulted in significantly high mortality. Diagnosis of TCoV depends on reverse transcription polymerase chain reaction (RT-PCR), quantitative real-time PCR, immunohistochemistry (IHC), immunofluorescent antibody assay and virus isolation (VI). Genomic organization of TCoV is as follows: 5′ UTR-1a-1b-S-3a-3b-E-M-5a-5b-N-UTR 3′. Genomic analysis suggests the emergence of TCoV from infectious bronchitis virus (IBV) through the recombination of spike (S) gene. Both TCoV and IBV belong to species Avian coronavirus in genus Gammacoronavirus and have a single stranded RNA genome with a size about 27 kb. High similarity of S genes has been found between TCoV isolates in contrast to low similarity between IBV strains. TCoV infection induced strong humoral and cellular immune responses, characterized by high levels of antibody and interferon gamma. The fragment containing neutralizing epitopes in the S protein has been identified. Vaccines conferring protection against TCoV have not been developed and used in the fields but live attenuated, killed, DNA, and fowlpox virus vectored vaccines have been generated and their efficacies were evaluated. Molecular epidemiology of TCoV in recent outbreaks sheds more information on the evolution and transmission of TCoV, which will aid in developing effective vaccines or treatment to prevent, control, or eliminate TCoV infection.