Research Center of Avian Disease, College of Veterinary Medicine, Sichuan Agricultural University, Wenjiang District, Chengdu City, Sichuan Province 611130, China.
College of Veterinary Medicine, Southwest University, Chongqing, China.
Vet Microbiol. 2024 Oct;297:110202. doi: 10.1016/j.vetmic.2024.110202. Epub 2024 Jul 29.
Herpesviruses-encoded microRNAs (miRNAs) have been discovered to be essential regulators in viral life cycle, participating in viral replication, latent or lytic infection, and immunological escape. However, the roles of miRNAs encoded by duck plague virus (DPV) are still unknown. Dev-miR-D28-3p is a miRNA uniquely encoded by DPV CHv strain. The aim of this study was to explore the effect of dev-miR-D28-3p on DPV replication and explore the potential mechanisms involved. Our findings demonstrated that transfection of dev-miR-D28-3p mimic into duck embryo fibroblasts (DEFs) effectively suppressed viral copies, viral titers and viral protein expressions during DPV infection, while the results above were reversed after transfection with dev-miR-D28-3p inhibitor. Subsequently, we further discovered that dev-miR-D28-3p specifically bound to DPV-encoded UL27 and inhibited its expression, suggesting that UL27 was the target gene of dev-miR-D28-3p. Finally, we investigated the role of UL27 in DPV replication and found the overexpression of UL27 increased viral copies, viral titers, and viral protein expressions; whereas the opposite results appear when knockdown of UL27. Our findings illustrated a novel mechanism that DPV regulated itself replication via dev-miR-D28-3p, paving the way for exploring the role of DPV-encoded miRNAs.
疱疹病毒编码的 microRNAs(miRNAs)已被发现是病毒生命周期中的重要调节剂,参与病毒复制、潜伏或裂解感染以及免疫逃逸。然而,鸭瘟病毒(DPV)编码的 miRNAs 的作用尚不清楚。Dev-miR-D28-3p 是 DPV CHv 株独有的 miRNA。本研究旨在探讨 dev-miR-D28-3p 对 DPV 复制的影响,并探讨涉及的潜在机制。我们的研究结果表明,在 DPV 感染过程中,转染 dev-miR-D28-3p 模拟物可有效抑制病毒拷贝、病毒滴度和病毒蛋白表达,而转染 dev-miR-D28-3p 抑制剂后则出现上述结果逆转。随后,我们进一步发现 dev-miR-D28-3p 特异性结合 DPV 编码的 UL27 并抑制其表达,表明 UL27 是 dev-miR-D28-3p 的靶基因。最后,我们研究了 UL27 在 DPV 复制中的作用,发现 UL27 的过表达增加了病毒拷贝、病毒滴度和病毒蛋白表达;而敲低 UL27 则出现相反的结果。我们的研究结果阐明了 DPV 通过 dev-miR-D28-3p 自我调节复制的新机制,为探索 DPV 编码的 miRNAs 的作用铺平了道路。