宿主桥粒体蛋白与人细小病毒B19基因组DNA相互作用。

IF 1.9 4区 医学 Q3 GENETICS & HEREDITY
Virus Genes Pub Date : 2026-02-01 Epub Date: 2025-11-29 DOI:10.1007/s11262-025-02202-x
Sakika Kimura, Toshitsugu Fujita, Yasushi Hata, Kotaro Ishida, Hirotaka Ebina, Hodaka Fujii, Eiji Morita
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引用次数: 0

摘要

人细小病毒B19 (B19V)主要靶向红细胞祖细胞,并与多种血液学疾病相关。然而,其生命周期的详细机制,特别是病毒组装过程,在很大程度上仍然未知。在这项研究中,我们使用体外工程化dna结合分子介导的染色质免疫沉淀(In vitro enChIP)来鉴定感染UT7/Epo-S1细胞中与B19V基因组相关的宿主蛋白。利用靶向病毒末端发夹区的引导rna,我们成功地富集了病毒基因组DNA。质谱分析显示,沉淀部分的桥粒蛋白特异性富集,包括桥粒蛋白(DSP)、桥粒蛋白-1、桥粒蛋白-1和连接板红蛋白,这表明整个桥粒复合物的成分可能与B19V基因组有关。免疫荧光显微镜显示,病毒VP2蛋白强烈定位于核外病灶,在那里它与DSP共定位。下拉实验进一步表明,VP2而不是VP1与DSP相互作用,这表明VP1唯一的n端区域(VP1u)可能抑制这种相互作用。值得注意的是,b19v感染的细胞表现出细胞间粘附和细胞聚集减少,这意味着这些相互作用可能参与了感染期间细胞粘附的破坏。这些发现揭示了B19V利用宿主桥粒机制促进病毒在感染细胞内繁殖的新机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Host desmosomal proteins interacting with human parvovirus B19 genomic DNA.

Human parvovirus B19 (B19V) primarily targets erythroid progenitor cells and is associated with various hematological disorders. However, the detailed mechanisms underlying its life cycle, particularly the viral assembly process, remain largely unknown. In this study, we used in vitro engineered DNA-binding molecule-mediated chromatin immunoprecipitation (in vitro enChIP) to identify host proteins associated with the B19V genome in infected UT7/Epo-S1 cells. Using guide RNAs targeting the viral terminal hairpin region, we successfully enriched viral genomic DNA. Mass spectrometry analysis of the precipitated fractions revealed specific enrichment of desmosomal proteins, including desmoplakin (DSP), desmoglein-1, desmocollin-1, and junction plakoglobin, suggesting that the components of the entire desmosome complex may be associated with the B19V genome. Immunofluorescence microscopy showed that the viral VP2 protein was strongly localized to the extranuclear foci, where it colocalized with DSP. Pull-down assays further demonstrated that VP2, but not VP1, interacted with DSP, indicating that the VP1-unique N-terminal region (VP1u) may inhibit this interaction. Notably, B19V-infected cells displayed reduced cell-cell adhesion and diminished cellular aggregation, implying that these interactions may be involved in the disruption of cell adhesion during infection. These findings revealed a novel mechanism by which B19V exploits the host desmosomal machinery to facilitate viral propagation in infected cells.

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来源期刊
Virus Genes
Virus Genes 医学-病毒学
CiteScore
3.30
自引率
0.00%
发文量
76
审稿时长
3 months
期刊介绍: Viruses are convenient models for the elucidation of life processes. The study of viruses is again on the cutting edge of biological sciences: systems biology, genomics, proteomics, metagenomics, using the newest most powerful tools. Huge amounts of new details on virus interactions with the cell, other pathogens and the hosts – animal (including human), insect, fungal, plant, bacterial, and archaeal - and their role in infection and disease are forthcoming in perplexing details requiring analysis and comments. Virus Genes is dedicated to the publication of studies on the structure and function of viruses and their genes, the molecular and systems interactions with the host and all applications derived thereof, providing a forum for the analysis of data and discussion of its implications, and the development of new hypotheses.
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