Genetic mutations of avian leukosis virus subgroup J strains extended their host range
Shen, Yanwei and Cai, Liming and Wang, Yanming and Wei, Rongrong and He, Menglian and Wang, Shanhui and Wang, Guihua and Cheng, Ziqiang,, 95, 691-699 (2014),
doi = https://doi.org/10.1099/vir.0.059915-0,
publicationName = Microbiology Society,
issn = 0022-1317,
abstract= The genetic diversity of avian leukosis virus subgroup J (ALV-J) is determined not only by the env gene, but also by its 3′ UTR and 3′ LTR. They all play important roles in extending the host range and tumour development. In the present study, one ALV-J strain (ZB110604-6) from Black-Bone Silky Fowl (BSF) and three ALV-J strains (ZB110604-3/4/5) from grey partridge (GP), which bore multiple tumours and breed in one house of Farm A, were demonstrated extending their host to GP, while two other ALV-J strains (LC110515-3/4) from BSF of Farm B could not infect the embryo fibroblast of GP. The BSF is a unique species of chicken in China, while the GP is a close relative of the pheasant that previously demonstrated resistance to ALV-J. Histopathology showed that various tumours were induced by ALV-J in the two species. Phylogenetic tree analysis showed that the isolates from Farms A and B, rather than species, belong to two different clusters of ALV-J. Genetic mutations analysis revealed that the isolates obtained from Farm A showed a higher frequency of mutation in the hypervariable region 2 domain than in other variable regions of the gp85 gene. From the nucleotide alignment of the 3′ UTR and 3′ LTR gene, and the spectrum of tumours observed in this study, we speculate that the deletions or mutations in the redundant transmembrane region, E element and U3 (CAAT boxes, CArG box and Y box) might associate with tumour formation and development. The extension of the host range of ALV-J to the GP suggested that housing different species together provides more opportunities for ALV-J to evolve rapidly.,
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