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Spike Protein Mutation Signatures in Circulating SARS-CoV-2 Variants Highlighting Immune Escape Markers and Lineage-Specific Deletion Patterns in Q1 2025

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Figshare2025-06-13 更新2026-04-08 收录
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https://figshare.com/articles/dataset/Spike_Protein_Mutation_Signatures_in_Circulating_SARS-CoV-2_Variants_Highlighting_Immune_Escape_Markers_and_Lineage-Specific_Deletion_Patterns_in_Q1_2025/29316053/1
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This dataset presents an analysis of <b>Spike protein amino acid mutations </b>in <b>SARS-CoV-2 sequences collected between January to April 2025</b>, with a focus on identifying <b>mutation signatures linked to immune escape</b>, <b>lineage-specific deletions</b>, and <b>emerging variant patterns </b>.The dataset includes:A <b>binary mutation matrix </b>of Spike AA mutations across sequencesA list of <b>lineage-specific mutations</b>Identified <b>co-occurring mutation pairs</b>A summary of hypotheses derived from mutation patternsBased on alignment and lineage assignment via <b>Nextclade</b>, this work highlights several mutations of interest:Key Hypotheses Investigated:<b>Hypothesis 1 </b>: <code>S:T20N</code> emerges as a novel mutation in the <b>HF.1.1 </b>lineage Located in the N-terminal domain (NTD), this mutation may affect antigenicity or conformational stability. <b>Hypothesis 2 </b>: <code>S:L452W</code> appears in emerging recombinant variants such as <b>KP.2 </b>and <b>LB.1</b>Linked to increased ACE2 binding and reduced neutralization, suggesting fitness advantage. <b>Hypothesis 3 </b>: <code>S:K356T</code> is a potential marker for immune escape. Found in multiple XBB and JN.1 sequences; located in a known NTD supersite targeted by monoclonal antibodies. <b>Hypothesis 4 </b>: Deletions like <code>S:H69-V70del</code> are limited to specific clusters. These deletions may help viruses evade detection or enhance replication efficiency. This dataset supports ongoing surveillance efforts and provides insight into the molecular evolution of SARS-CoV-2 during early 2025.All scripts used in data processing are included to ensure full <b>FAIR compliance</b> and promote transparency and reproducibility.<br>

本数据集针对2025年1月至4月采集的新型冠状病毒(SARS-CoV-2)序列中的刺突蛋白(Spike protein)氨基酸突变展开分析,重点鉴定与免疫逃逸相关的突变特征、谱系特异性缺失以及新兴变异株模式。数据集涵盖以下内容:覆盖所有序列的刺突蛋白氨基酸突变二元矩阵、谱系特异性突变列表、已鉴定的共现突变对,以及基于突变模式推导的假说汇总。 本研究通过Nextclade完成序列比对与谱系注释,筛选出若干重点关注的突变,核心研究假说如下: 假说1:S:T20N作为新型突变首次出现在HF.1.1谱系中。该突变位于N端结构域(N-terminal domain, NTD),可能影响病毒抗原性或构象稳定性。 假说2:S:L452W出现在KP.2、LB.1等新兴重组变异株中。该突变与血管紧张素转换酶2(Angiotensin-converting enzyme 2, ACE2)结合能力增强、中和逃逸能力提升相关,提示其具有生存优势。 假说3:S:K356T是潜在的免疫逃逸标志物。该突变在多株XBB及JN.1序列中被检出,位于单克隆抗体靶向的已知NTD超抗原表位区域。 假说4:诸如S:H69-V70del的缺失突变仅局限于特定传播簇。此类缺失突变可能帮助病毒逃避免疫检测或提升复制效率。 本数据集可为当前的新冠病毒监测工作提供支撑,并助力解析2025年初SARS-CoV-2的分子演化规律。本数据集附带所有数据处理脚本,以确保完全符合FAIR(可发现、可访问、可互操作、可复用)数据标准,并提升研究的透明度与可重复性。
提供机构:
Bhatti, Tahir Hussain
创建时间:
2025-06-13
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