细胞凋亡在宿主抗病毒防御中起着至关重要的作用。禽白血病病毒 J 亚群 (ALV-J) 是一种禽致癌逆转录病毒，已被证明可以抑制细胞凋亡，同时促进其自身复制。 ALV-J 会诱发鸡的骨髓瘤和血管瘤，给商业蛋鸡和肉用鸡生产造成重大经济损失。 B 细胞淋巴瘤/白血病 11B (Bcl11b) 编码 C2H2 型锌指蛋白 - BCL11B，在细胞增殖、分化中发挥关键功能，并在免疫系统中发挥重要作用。先前的研究已表明Bcl11b与ALV-J感染有关。在本研究中，我们进一步研究了ALV-J感染细胞的病理变化，并检测了鸡Bcl11b的作用和表达调控。我们的结果表明，Bcl11b 作为干扰素刺激基因 (ISG)，编码 C2H2 型锌指蛋白 BCL11B，可促进细胞凋亡，从而抑制 ALV-J 感染。此外，gga-miR-1612和gga-miR-6701-3p调节细胞凋亡，并通过靶向Bcl11b参与ALV-J感染，从而揭示宿主和ALV-J之间的免疫应答策略。尽管潜在的机制需要进一步验证，但 Bcl11b 及其调节 miRNA 是第一个证明通过细胞凋亡抑制 ALV-J 复制的。 BCL11B 可以成为治疗 ALV-J 感染引发的疾病的重要靶点。版权所有 © 2024。由 Elsevier B.V. 出版。

Apoptosis plays a crucial role in host antiviral defense. The avian leukosis virus subgroup J (ALV-J), an avian oncogenic retrovirus, has been shown to suppress apoptosis while promoting its own replication. ALV-J induces myeloid tumors and hemangiomas in chickens resulting in significant economic losses for commercial layer and meat-type chicken production. B-cell lymphoma/leukemia 11B (Bcl11b) encodes a C2H2-type zinc finger protein-BCL11B, that exerts critical functions in cell proliferation, differentiation, and plays an essential role in the immune system. Previous study has been shown that Bcl11b is associated with ALV-J infection. In this study, we further investigated the pathological changes in ALV-J infected cells and examined the role and expression regulation of chicken Bcl11b. Our results demonstrate that Bcl11b, as an interferon-stimulated gene (ISG), encodes C2H2-type zinc finger protein BCL11B that promotes apoptosis to inhibit ALV-J infection. Additionally, gga-miR-1612 and gga-miR-6701-3p regulate apoptosis and are involved in ALV-J infection by targeting Bcl11b, thus revealing immune response strategies between the host and ALV-J. Although the underlying mechanisms require further validation, Bcl11b and its regulatory miRNAs are the first to demonstrate inhibition of ALV-J replication via apoptosis. BCL11B can a valuable target for treating diseases triggered by ALV-J infection.Copyright © 2024. Published by Elsevier B.V.