covid - 19后疲劳的炎症预测因素

IF 3.5 Q2 IMMUNOLOGY

Brain, behavior, & immunity - health Pub Date : 2025-09-17 DOI:10.1016/j.bbih.2025.101109

A. Nuber-Champier , G. Breville , P. Voruz , I. Jacot de Alcântara , P.H. Lalive , G. Allali , L. Benzakour , K.-O. Lövblad , O. Braillard , M. Nehme , M. Coen , J. Serratrice , J.-L. Reny , J. Pugin , I. Guessous , B.N. Landis , A. Cionca , F. Assal , J.A. Péron

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引用次数: 0

摘要

新冠肺炎后综合征主客观疲劳的生物学机制尚不清楚。本研究探讨SARS-CoV-2感染急性期的免疫反应是否能预测感染后6-9个月的疲劳维度。我们分析了54例住院患者（平均年龄：58.69±10.90岁，女性：31%）的血清免疫标志物，并使用一般线性混合模型评估其与慢性疲劳的关系。急性感染期间IL-1RA、IFNγ、TNFα和单核细胞百分比的升高预示着身体和总疲劳的增加。此外，较高的TNFα水平（r = - 0.40, p = 0.019）与认知疲劳意识降低相关。这些发现强调了急性炎症在covid后疲劳持续中的作用。

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Inflammatory predictors of Post-COVID fatigue

The biological mechanisms underlying objective and subjective fatigue in post-COVID syndrome remain unclear. This study investigates whether immune responses during the acute phase of SARS-CoV-2 infection predict fatigue dimensions 6–9 months post-infection. We analyzed serum immune markers from 54 hospitalized patients (mean age: 58.69 ± 10.90 yrs; female: 31 %) and assessed their association with chronic fatigue using general linear mixed models. Elevated levels of IL-1RA, IFNγ, TNFα, and monocyte percentage during acute infection predicted increased physical and total fatigue. Additionally, higher TNFα levels (r = −0.40, p = .019) correlated with reduced awareness of cognitive fatigue. These findings highlight the role of acute inflammation in the persistence of post-COVID fatigue.

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来源期刊

Brain, behavior, & immunity - health Biological Psychiatry, Behavioral Neuroscience

CiteScore

8.50

自引率

0.00%

发文量

审稿时长

97 days