Zhang Y, Guan X, Chen Z, Cao D, Kang Z, Shen Q, Lei Q, Li F, Li H, Leghari MF,Wang Y, Qi X, Wang X, Gao Y. The high conserved cellular receptors of avian leukosis virus subgroup J in Chinese local chickens contributes to its wide host range. Poult Sci. 2018 Aug 13.-最新论文-保定市金诺兽药研究所

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Zhang Y, Guan X, Chen Z, Cao D, Kang Z, Shen Q, Lei Q, Li F, Li H, Leghari MF,Wang Y, Qi X, Wang X, Gao Y. The high conserved cellular receptors of avian leukosis virus subgroup J in Chinese local chickens contributes to its wide host range. Poult Sci. 2018 Aug 13.

The high conserved cellular receptors of avian leukosis virus subgroup J in Chinese local chickens contributes to its wide host range.
Zhang Y , Guan X , Chen Z , Cao D , Kang Z , Shen Q , Lei Q , Li F , Li H , Leghari MF , Wang Y , Qi X , Wang X , Gao Y .
Poult Sci. 2018 Aug 13. doi: 10.3382/ps/pey331

Abstract
Avian leukosis virus (ALV) is a tumor-inducing virus that spreads among most chicken species, causing serious financial losses for the poultry industry. Subgroup J avian leukosis virus (ALV-J) is a recombinant exogenous ALV, which shows more extensive host range in comparison with other subgroups, especially in Chinese local chickens. To identify the relationship between ALV-J host range and the polymorphism of its cellular receptors, we performed a wide range epidemiological investigation of current ALV-J infection in Chinese local chickens, and discovered that all the 18 local chicken breeds being investigated from main local chicken breeding provinces were ALV-J positive. Furthermore, we cloned ALV-J cellular receptor genes of chNHE1 and chANXA2 of these 18 chicken breeds. Sequence alignment demonstrated that despite several regular mutations at the nucleotide level, there were no corresponding amino acid mutations for either chNHE1 gene or chANXA2 gene. Additionally, virus entry assay indicated that the level of viral enter into cells is stable among different chicken breeds. Results of this study indicated that the wide host range of ALV-J in Chinese local chickens was partially due to the high conservatism of its cellular receptors, and also provide target sites for drug design of resistance to ALV-J infection.
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