Insertion/deletion mutations within tva receptor gene confer chicken resistance to infection by avian leukosis virus subgroups A and K

Authors: XU, HUIJUAN - South China Agricultural Univerisity; ZUO, KEJING - Guangzhou Zoo & Wildlife Research Center; KUANG, ZHIXIANG - Guangdong Love-Health Agriculture Group Limited; CHEN, SHENG - South China Agricultural Univerisity; ZHU, XUEFENG - South China Agricultural Univerisity; Zhang, Huanmin; XIE, QINGMEI - South China Agricultural Univerisity; CHEN, WEIGUO - South China Agricultural Univerisity

Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/25/2025
Publication Date: 2/26/2025
Citation: Xu, H., Zuo, K., Kuang, Z., Chen, S., Zhu, X., Zhang, H., Xie, Q., Chen, W. 2025. Insertion/deletion mutations within tva receptor gene confer chicken resistance to infection by avian leukosis virus subgroups A and K. Poultry Science. 2025:104949. https://doi.org/10.1016/j.psj.2025.104949.
DOI: https://doi.org/10.1016/j.psj.2025.104949

Interpretive Summary: Avian leukosis virus (ALV) is a class of retroviruses that causes avian lymphoma tumors in susceptible chickens, causing serious economic loss to the poultry industry, particularly in Asia. ALV are subdivided into subgroups. This study reports identification of two genetic mutants of a host gene, known as tva in the chicken, both of which block the infection process of ALV subgroup A and subgroup K. These findings provide a path for breeding genetic resistant chickens against the subgroup ALV-A and ALV-K infection, which should benefit the poultry industry against ALV-caused economic loss and the public for quality poultry products.

Technical Abstract: Avian leukosis virus of the classic subgroup A (ALV-A) and newly emerging subgroup K (ALV-K) are primary pathogens causing avian leukemia in susceptible chickens and have become a significant threat to the poultry industry in Asia. Both viruses share a Tva protein encoded by the tva gene as a receptor to gain the entry into the host cells. In this study, we described the identifications of two alleles of the tva receptor gene in Qingyuan partridge chicken, which possesses an 11-nucleotide (GCTGCCCACCC) insertion, and a 6-nucleotide (ACCTCC) deletion independently located in exon 1 of the tab gene. The natural 11-nucleotide insertion causes a frameshift in the reading frame of the tva cDNA, which presumably blocks the expression of the normal tva allele and results resistance in chickens against infection by ALV-A and ALV-K. The natural 6-nucleotide deletion leads to a Tva receptor protein missing the amino acids residues T21 and S22, which appeared dysfunctional to mediate the viral entry. As a result, we observed that the deletion mutation in tva receptor gene significantly reduced the susceptibility to infection by ALV-A and ALV-K in vitro and in vivo, and significantly reduced the binding capacity of the Tva receptor protein to the envelope glycoproteins of ALV-A and ALV-K in our subsequent analysis. Taken together, these findings not only provide evidence that the insertion and deletion mutations within the tva receptor gene confer chicken resistance to infection by ALV-A and ALV-K but also provide ideal targets for selective breeding of ALV-A and ALV-K resistance in chicken.