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Published on: July 29, 2012
Genetic mutations within tva receptor gene confer resistance to ALV-A and ALV-K infection in chickens
Huijuan Xu1, Huanqiang Chen2, Meifeng Yang1
1State Key Laboratory of Swine and Poultry Breeding Industry & Guangdong Laboratory for Lingnan Modern Agriculture, College of Animal Science, South China Agricultural University, Guangzhou, 510642, China; Guangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding, Guangzhou, 510642, China; Key Laboratory of Animal Health Aquaculture and Environmental Control, Guangdong, Guangzhou, 510642, China.
Abstract:
Avian leukosis virus subgroup A (ALV-A) and the newly emerging subgroup K (ALV-K) are primary causative pathogens of avian leukosis in chickens and continue to pose a persistent threat to poultry industry worldwide. Susceptibility or resistance of chicken cells to ALV-A and ALV-K is determined by the tva receptor gene. Indeed, six ALV-A resistant alleles (tvar1-tvar6) have been identified within the tva gene. However, whether these tva alleles confer resistance to ALV-K infection remains unclear. In this study, we identified five tva resistant alleles, namely tvar2, tvar3, tvar4, tvar5, and tvar6, in Qingyuan partridge chickens (QYPC). In vitro analyses, including flow cytometry and quantitative real-time PCR, we demonstrated that the tvar2 allele confers complete resistance to both ALV-A and ALV-K infection. In contrast, the tvar3, tvar4, tvar5, and tvar6 alleles each significantly reduced susceptibility to ALV-K. Furthermore, these in vitro observations were corroborated by in vivo infection experiments, which confirmed that the tvar2 allele consistently conferred complete resistance to both ALV-A and ALV-K, while tvar3, tvar4, tvar5, and tvar6 alleles each resulted in a significant reduction in ALV-K susceptibility. Additionally, the tvar2-tvar6 alleles were broadly distributed across QYPC lines, with notably high frequencies of resistant genotypes observed in specific QYPC populations. Collectively, these findings not only expand our understanding of tva-mediated resistance to both ALV-A and ALV-K but also provide valuable genetic targets for selective breeding programs aimed at enhancing resistance to ALV-A and ALV-K in chickens.
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