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Gene expression and alternative splicing reveal the co-regulation of host response mechanisms to avian leukosis virus subgroup J-infected in laying hens

文献类型： 外文期刊

作者： Zhang, Yalan 1 ; Gao, Yahui 2 ; Miao, Xiaomeng 1 ; Qu, Lujiang 1 ; Ning, Zhonghua 1 ;

作者机构： 1.China Agr Univ, Coll Anim Sci & Technol, Natl Engn Lab Anim Breeding, Beijing 100193, Peoples R China

2.Hebei Univ Engn, Sch Life Sci & Food Engn, Handan 056021, Peoples R China

3.Guizhou Acad Agr Sci, Inst Anim Husb & Vet Med, Guiyang 550005, Peoples R China

关键词： Avian leukosis virus subgroup J; Laying hen; Gene expression; Alternative splicing

期刊名称：POULTRY SCIENCE （ 影响因子：4.2； 五年影响因子：4.5 ）

ISSN： 0032-5791

年卷期： 2025 年 104 卷 10 期

页码：

收录情况： SCI

摘要： Avian leukosis in China has spread from broiler chickens to the local breeds and commercial laying hens. Studying resistance to avian leukosis is important for disease-resistant breeding programs. Gene expression and different transcripts may affect immune function. In this study, we compared five naturally infected Rhode Island Red (RIR) hens carrying tumor with five uninfected individuals to explore avian leukosis virus subgroup J (ALVJ) induced differences in gene expression and alternative splicing (AS) in the liver, spleen caused. Analyses revealed 847, 80 differentially expressed genes (DEGs), along with 207, 167 differential alternative splicing genes (DASGs) in the liver, spleen respectively. Most differential splicing events involved exon skipping. Although most genes showed no significant expression changes, their protein spatial structures were altered by AS. In the liver, microtubule cytoskeleton-related functions were co-regulated by both gene expression and splicing, with CCSER2 and MAPT exhibiting the highest splicing frequency. In the spleen, splicing predominantly affected RNA-processing genes, where PKLR and SRSF7 functioned as key regulators. Notably, PKLR-interacting genes (THRSP, ADH1C, AQP3) were significantly downregulated in infected groups, potentially promoting viral replication and tumor proliferation. These findings demonstrate that AS contributes to the host response to ALV-J infection through multiple mechanisms, including protein structural remodeling and dysregulation of coordinated interaction networks. This study provides new insights into the genetic basis of ALV-J resistance in laying hens.

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