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Avian leukosis virus subgroup J (ALV-J) infection can cause tumors and immunosuppression. Endogenous viruses integrate into host genomes and can recombine with exogenous avian leukosis virus (ALV). In this study, we analyzed the interaction of endogenous retrovirus 21 ( ev21 ) with the ALV-J in late-feathering Chinese yellow chicken. Two ALV-J strains M180 and K243 were isolated from late-feathering and fast-feathering Chinese yellow chicken flocks, respectively. The  env  gene of the two strains showed 94.2–94.8% nucleotide identity with reference ALV-J strains. Compared with the  env  gene and the LTR of  ev21  and M180, the nucleotide identity of LTR was 69.7% and  env  gene was 58.4%, respectively, especially the amino acid identity of  env  gene as low as 14.2%. Phylogenetic analysis of the nucleotide sequence of the env gene and the 3′LTR showed that M180 was closely related to ALV-J, and was located in a distinct group with  ev21  in the phylogenetic tree. Using co-immunoprecipitation (co-IP), we next demonstrate that the envelope protein of  ev21  does not interact with the M180 envelope protein. We further show that the envelope protein of  ev21  cannot activate ALV-J LTR promoter activity using luciferase-reporter assays. qPCR and western blot analysis revealed that envelope protein of endogenous  ev21  can facilitate the expression of  PKR  at 6h post ALV-J infection (hpi) and facilitate the expression of  ISG12  and  CH25H  at 24 hpi. However, the expression of the  env  gene of M180 strain was not significantly at 6 and 24 hpi. We conclude that there is no evidence of recombination between endogenous retrovirus ev21 and ALV-J strain M180 in late-feathering Chinese yellow chicken, and envelope protein of ev21 can affect the expression of host ISGs, but appears not to influence the replication of ALV-J strain M180. This is the first report of interaction among the endogenous retrovirus ev21, ALV-J and the late-feathering chicken.

Endogenous Retrovirus ev21 Dose Not Recombine with ALV-J and Induces the Expression of ISGs in the Host