College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai'an, PR China.
Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Tai'an, PR China.
J Gen Virol. 2022 Feb;103(2). doi: 10.1099/jgv.0.001719.
Avian leukosis virus (ALV) is a retrovirus that induces tumours in infected birds; ALV is divided into different subgroups according to the gene and cellular tropism. In general, ALV subgroup J (ALV-J) is considered to be the most pathogenic and prevalent subgroup while subgroup K (ALV-K), a newly identified subgroup, only causes mild symptoms. To illuminate the roles of the viral gene and LTR sequence in pathogenic differences between ALV-J and ALV-K, rescued ALV-J strain rSDAU1005, rescued ALV-K strain rJS11C1, and recombinant strains rENV(J)-LTR(K) and rENV(K)-LTR(J) were characterized and investigated in this study. Among rescued viruses, rSDAU1005 had the highest replication efficiency while rJS11C1 replicated the slowest (replication efficiency rankings were rSDAU1005 >rENV(K)-LTR(J)>rENV(J)-LTR(K)>rJS11 C1). The luciferase reporter gene assay results showed that the promoter activity of ALV-K LTR was lower than that of the ALV-J LTR promoter, which may have accounted for the slower replication efficiency of ALV-K. Pathogenicity of the four rescued viruses was determined via inoculating the yolk sacs of specific-pathogen-free chickens. The results demonstrated that all four viruses were pathogenic; rSDAU1005 caused the most severe growth retardation and immunosuppression. rENV(J)-LTR(K) was more pathogenic when compared to rENV(K)-LTR(J), indicating that and the LTR sequence play important roles in pathogenicity between ALV-K and ALV-J. Additionally, seemed to especially play a role in ALV-K pathogenesis. This study provided scientific data and insight to improve detection methods and judgement criteria in ALV clearance and surveillance.
禽白血病病毒（ALV）是一种逆转录病毒，可引起感染鸟类的肿瘤；ALV 根据基因和细胞嗜性分为不同亚群。一般来说，ALV 亚群 J（ALV-J）被认为是最具致病性和最普遍的亚群，而新发现的亚群 K（ALV-K）仅引起轻微症状。为了阐明病毒基因和 LTR 序列在 ALV-J 和 ALV-K 致病差异中的作用，本研究对拯救的 ALV-J 株 rSDAU1005、拯救的 ALV-K 株 rJS11C1 以及重组株 rENV(J)-LTR(K) 和 rENV(K)-LTR(J)进行了特征和研究。在拯救的病毒中，rSDAU1005 的复制效率最高，而 rJS11C1 的复制最慢（复制效率排名为 rSDAU1005>rENV(K)-LTR(J)>rENV(J)-LTR(K)>rJS11C1）。荧光素酶报告基因检测结果表明，ALV-K LTR 的启动子活性低于 ALV-J LTR 启动子，这可能是 ALV-K 复制效率较慢的原因。通过接种 SPF 鸡的卵黄囊来确定四种拯救病毒的致病性。结果表明，四种病毒均具有致病性；rSDAU1005 引起的生长迟缓和免疫抑制最为严重。与 rENV(K)-LTR(J)相比，rENV(J)-LTR(K)的致病性更高，表明 和 LTR 序列在 ALV-K 和 ALV-J 的致病性中起重要作用。此外，似乎在 ALV-K 发病机制中起特殊作用。本研究为改进 ALV 清除和监测的检测方法和判断标准提供了科学数据和见解。
