Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwanoha, Kashiwa-shi, Chiba, Japan.
Laboratory of Functional Analysis in silico, Human Genome Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Hum Genomics. 2017 Jul 11;11(1):15. doi: 10.1186/s40246-017-0112-8.
Human T cell leukemia virus type 1 (HTLV-1) causes adult T cell leukemia (ATL) in a proportion of infected individuals after a long latency period. Development of ATL is a multistep clonal process that can be investigated by monitoring the clonal expansion of HTLV-1-infected cells by isolation of provirus integration sites. The clonal composition (size, number, and combinations of clones) during the latency period in a given infected individual has not been clearly elucidated.
We used high-throughput sequencing technology coupled with a tag system for isolating integration sites and measuring clone sizes from 60 clinical samples. We assessed the role of clonality and clone size dynamics in ATL onset by modeling data from high-throughput monitoring of HTLV-1 integration sites using single- and multiple-time-point samples.
From four size categories analyzed, we found that big clones (B; 513-2048 infected cells) and very big clones (VB; >2048 infected cells) had prognostic value. No sample harbored two or more VB clones or three or more B clones. We examined the role of clone size, clone combination, and the number of integration sites in the prognosis of infected individuals. We found a moderate reverse correlation between the total number of clones and the size of the largest clone. We devised a data-driven model that allows intuitive representation of clonal composition.
This integration site-based clonality tree model represents the complexity of clonality and provides a global view of clonality data that facilitates the analysis, interpretation, understanding, and visualization of the behavior of clones on inter- and intra-individual scales. It is fully data-driven, intuitively depicts the clonality patterns of HTLV-1-infected individuals and can assist in early risk assessment of ATL onset by reflecting the prognosis of infected individuals. This model should assist in assimilating information on clonal composition and understanding clonal expansion in HTLV-1-infected individuals.
人类 T 细胞白血病病毒 1 型(HTLV-1)在感染个体经过长时间潜伏期后导致成人 T 细胞白血病(ATL)。ATL 的发生是一个多步骤的克隆过程,可以通过分离原病毒整合位点来监测 HTLV-1 感染细胞的克隆扩张来研究。在给定感染个体的潜伏期内,克隆组成(大小、数量和克隆组合)尚未明确阐明。
我们使用高通量测序技术结合标签系统从 60 个临床样本中分离整合位点并测量克隆大小。我们通过使用单时间点和多时间点样本对 HTLV-1 整合位点进行高通量监测的数据建模,评估了克隆性和克隆大小动态在 ATL 发病中的作用。
在分析的四个大小类别中,我们发现大克隆(B;513-2048 个感染细胞)和非常大克隆(VB;>2048 个感染细胞)具有预后价值。没有样本含有两个或更多 VB 克隆或三个或更多 B 克隆。我们研究了克隆大小、克隆组合和整合位点数量在感染个体预后中的作用。我们发现克隆总数与最大克隆的大小之间存在中度负相关。我们设计了一种数据驱动的模型,可以直观地表示克隆组成。
这种基于整合位点的克隆性树模型代表了克隆性的复杂性,并提供了克隆性数据的全局视图,有助于在个体间和个体内尺度上分析、解释、理解和可视化克隆的行为。它完全是数据驱动的,直观地描绘了 HTLV-1 感染个体的克隆模式,并通过反映感染个体的预后,有助于早期评估 ATL 发病的风险。该模型应有助于整合克隆组成信息并理解 HTLV-1 感染个体中的克隆扩张。