Severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2) infection is associated with proinflammatory cytokine release as mediators of host antiviral response to the infection. Cytokine persistent elevation leads to post-Coronavirus disease-2019 (COVID-19) post-COVID-19 sequela (PCS) reported in about 60% of patients affecting individual's normal life after recovery. This study evaluates relationship of cytokines and chemokines pattern during and postinfection to PCS events. Serum samples collected from 82 individuals with symptomatic, asymptomatic, or no SARS-CoV-2 infection were classified as recently or formerly infected groups according to levels of anti-2019nCoV Immunoglobulin G/Immunoglobulin M. Levels of interleukin (IL)-1α, IL-1β, IL-6, IL-8, interferon alpha (IFN-α), tumor necrosis factor alpha (TNF-α), granulocyte macrophage colony-stimulating factor (GM-CSF), and monocyte chemoattractant protein-1 were assessed via ELISA for each individual. All asymptomatic groups showed nonsignificant differences in cytokines' levels than control group. Significant elevation of IFN-α, TNF-α, and GM-CSF levels were observed in recent symptomatic, while IFN-α and TNF-α levels were significant in former symptomatic groups. We observed an association between fever with IL-1α and IFN-α levels, fatigue with TNF-α and GM-CSF, dyspnea with IFN-α, TNF-α, and GM-CSF, and chest-wheezing with GM-CSF. Individuals were surveyed 12 months postsampling for PCS events. Among 35 responders to survey, 8 (22.8%) reported PCS events, 6 of which were females. Upon studying PCS events, IL-8, IFN-α, TNF-α, and GM-CSF levels showed significant elevation in active infection, that was not seen in a resolved state of infection. Cytokines patterns suggest that either a persistent elevation in levels or damage caused during infection contributes to PCS. Although with the limited sample size, our study emphasizes the importance to conduct medical approaches targeting the associated cytokines to improve the PCS symptoms.

中文翻译：

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轻度症状和无症状 SARS-CoV-2 感染埃及个体的促炎细胞因子谱及其与 COVID-19 后遗症的拟议关系。

严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 感染与促炎细胞因子的释放有关，促炎细胞因子是宿主对感染的抗病毒反应的介质。约 60% 的患者报告称，细胞因子持续升高会导致 2019 年冠状病毒病 (COVID-19) 后遗症 (PCS)，影响患者康复后的正常生活。本研究评估了感染期间和感染后细胞因子和趋化因子模式与 PCS 事件的关系。从 82 名有症状、无症状或无 SARS-CoV-2 感染者采集的血清样本根据抗 2019nCoV 免疫球蛋白 G/免疫球蛋白 M 水平分为最近感染组或既往感染组。白细胞介素 (IL)-1α、IL 水平-1β、IL-6、IL-8、干扰素 α (IFN-α)、肿瘤坏死因子 α (TNF-α)、粒细胞巨噬细胞集落刺激因子 (GM-CSF) 和单核细胞趋化蛋白-1 通过评估对每个人进行 ELISA。所有无症状组的细胞因子水平与对照组相比均无显着差异。在近期症状组中观察到 IFN-α、TNF-α 和 GM-CSF 水平显着升高，而在先前症状组中 IFN-α 和 TNF-α 水平显着升高。我们观察到发烧与 IL-1α 和 IFN-α 水平之间的关联，疲劳与 TNF-α 和 GM-CSF 之间的关联，呼吸困难与 IFN-α、TNF-α 和 GM-CSF 之间的关联，以及胸闷与 GM-CSF 之间的关联。采样后 12 个月对个人进行了 PCS 事件调查。在 35 名受访者中，8 名（22.8%）报告了 PCS 事件，其中 6 名是女性。在研究 PCS 事件后，IL-8、IFN-α、TNF-α 和 GM-CSF 水平在活动性感染中显示出显着升高，而在感染缓解状态下则未见这种情况。细胞因子模式表明，细胞因子水平持续升高或感染期间造成的损伤都会导致 PCS。尽管样本量有限，但我们的研究强调了针对相关细胞因子进行医疗方法以改善 PCS 症状的重要性。