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PMAIP1 promotes J subgroup avian leukosis virus replication by regulating mitochondrial function

文献类型： 外文期刊

作者： Zhao, Yongxia 1 ; Zhao, Changbin 1 ; Deng, Yuelin 2 ; Pan, Ming 1 ; Mo, Guodong 1 ; Liao, Zhiying 1 ; Zhang, Xiquan 1 ; Zhang, Dexiang 1 ; Li, Hongmei 1 ;

作者机构： 1.South China Agr Univ, Coll Anim Sci, Dept Anim Genet Breeding & Reprod, Guangzhou 510642, Peoples R China

2.Minist Agr, Guangdong Prov Key Lab Agroanim Genom & Mol Breedi, Guangzhou 510642, Peoples R China

3.Minist Agr, Key Lab Chicken Genet Breeding & Reprod, Guangzhou 510642, Peoples R China

4.South China Agr Univ, State Key Lab Conservat & Utilizat Subtrop Agrobio, Guangzhou 510642, Guangdong, Peoples R China

5.South China Agr Univ, Coll Anim Sci, Dept Anim Nutr Syst, Guangzhou 510642, Peoples R China

关键词： ALV-J; PMAIP1; mitochondrial function; immune; DF-1

期刊名称：POULTRY SCIENCE （ 影响因子：4.4； 五年影响因子：4.4 ）

ISSN： 0032-5791

年卷期： 2024 年 103 卷 6 期

页码：

收录情况： SCI

摘要： Avian leukosis virus Subgroup J (ALVJ) exhibits high morbidity and pathogenicity, affecting approximately 20% of poultry farms. It induces neoplastic diseases and immunosuppression. Phorbol-12-myristate-13-acetate-induced protein 1 ( PMAIP1 ), a proapoptotic mitochondrial protein in the B-cell lymphoma-2 (Bcl-2) family, plays a role in apoptosis in cancer cells. However, the connection between the PMAIP1 gene and ALV -J pathogenicity remains unexplored. This study investigates the potential impact of the PMAIP1 gene on ALV -J replication and its regulatory mechanisms. Initially, we examined PMAIP1 expression using quantitative real -time PCR (qRT-PCR) in vitro and in vivo. Furthermore, we manipulated PMAIP1 expression in chicken fibroblast cells (DF-1) and assessed its effects on ALV -J infection through qRTPCR, immunofluorescence assay (IFA), and western blotting (WB). Our findings reveal a significant downregulation of PMAIP1 in the spleen, lung, and kidney, coupled with an up-regulation in the bursa and liver of ALV -J infected chickens compared to uninfected ones. Additionally, DF-1 cells infected with ALV -J displayed a notable up-regulation of PMAIP1 at 6, 12, 24, 48, 74, and 108 h. Over-expression of PMAIP1 enhanced ALVJ replication, interferon expression, and proinflammatory factors. Conversely, interference led to contrasting results. Furthermore, we observed that PMAIP1 promotes virus replication by modulating mitochondrial function. In conclusion, the PMAIP1 gene facilitates virus replication by regulating mitochondrial function, thereby enriching our understanding of mitochondriarelated genes and their involvement in ALV -J infection, offering valuable insights for avian leukosis disease resistance strategies.

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