Viral immunology · 2026
Single-Cell and Mendelian Randomization Analyses Identify Key Genes Common to COVID-19 and Multiple Sclerosis.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Chen Shuping, Ruan Jun, Cheng Sikai, Zheng Huifang, Chang Tianyu, Bao Guichun, Zhu Zijing, Li Xinglin, Zhao Wei, Zheng Kunwen
Аннотация
The pathophysiology of multiple sclerosis (MS) bears notable similarities to the dysregulated inflammatory response occurring during coronavirus disease 2019 (COVID-19) infection. B cells play a pivotal role among immune cells in the pathogenesis of both these diseases. Consequently, clarifying the molecular mechanism underlying B cell function in COVID-19 and MS is of great significance for formulating more efficient treatment strategies. A comprehensive analysis integrating single-cell RNA sequencing (scRNA-seq), genome-wide association study, and expression quantitative trait locus data from patients with COVID-19 and MS was performed. Gene set enrichment analysis revealed pathways and functional roles associated with the key genes, while pseudotime analysis tracked their expression patterns across different B cell developmental trajectories. The results of scRNA-seq analysis showed that, in comparison with the healthy control group, the proportion of B cells rose in patients with COVID-19 and those with MS. Through differential expression analysis and Mendelian randomization analysis, DR1, IKZF3, and RUVBL2 were identified as risk factors for both COVID-19 and MS, whereas ANAPC5 was characterized as a protective factor against these two conditions. The findings of the pseudotime analysis indicated that only IKZF3 had differential expression across different branches of B cells. IKZF3's role in promoting immune inflammation and inhibiting metabolism could potentially be linked to the onset and comorbidity of COVID-19 and MS. This emphasizes not only the possible interaction mechanisms between these two diseases but also their clinical significance.