hsa-miR-223-5p 和 SARS-CoV-2 S 基因突变在 COVID-19 中的作用。

Zeyad Sadeg Sabbar, Ashraf Kariminik, Maryam Ghane
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摘要

背景:促炎分子增加是感染 SARS-CoV-2 的患者出现严重症状的主要原因。本研究评估了住院的 SARS-CoV-2 感染者中 SARS-CoV-2 S 基因突变与 hsa-miR-223-5p、白细胞介素 2 受体 α(IL-2Rα)和 CCL16 趋化因子的表达情况:设计:这是一项横断面研究:本研究包括 75 名症状严重的 SARS-CoV-2 感染者和 75 名年龄性别匹配的健康对照者。采用实时聚合酶链反应技术评估 hsa-miR-223-5p、IL-2Rα 和 CCL16 趋化因子的表达水平。利用 Sanger 技术对 SARS-CoV-2 的 S 基因 23,274 至 23,641 位进行了测序:结果:在 SARS-CoV-2 感染者中,hsa-miR-223-5p 的相对表达量明显增加,而 IL-2Rα 的表达量则明显减少。在 SARS-CoV-2 的 S 基因 23,403 位(p.Asp23403Gly)和 23,525 位(p.His23525Tyr)发现了两个突变:结论:hsa-miR-223-5p 的增加可能是导致 IL-2Rα 下调的主要原因,而 IL-2Rα 是 T 调节淋巴细胞的主要开发者。SARS-CoV-2感染者的S基因突变可能会影响对该分子的免疫反应,并改变病毒与人体细胞相互作用的热度。
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The roles played by hsa-miR-223-5p and mutations in the S gene of SARS-CoV-2 in COVID-19.

Background: Increased proinflammatory molecules are a main reason for severe symptoms in patients infected with SARS-CoV-2. This study evaluated mutations in the S gene of SARS-CoV-2 and the expression of hsa-miR-223-5p, interleukin 2 receptor α (IL-2Rα), and CCL16 chemokine in hospitalized SARS-CoV-2 infected patients.

Design: This is a cross-sectional study.

Methods: This study included 75 SARS-CoV-2-infected patients with severe symptoms and 75 age-sex-matched healthy controls. Real-time polymerase chain reaction techniques were used to evaluate the expression levels of hsa-miR-223-5p, IL-2Rα, and CCL16 chemokine. The Sanger technique was used to sequence the S gene of SARS-CoV-2 from positions 23,274 to 23,641.

Results: The relative expression of hsa-miR-223-5p was significantly increased whereas that of IL-2Rα was significantly decreased in the SARS-CoV-2 infected patients. Two mutations were found in the S gene of SARS-CoV-2 at positions 23,403 (p.Asp23403Gly) and 23,525 (p.His23525Tyr) of the S gene of SARS-CoV-2.

Conclusion: Increased hsa-miR-223-5p may be a main cause for the downregulation of IL-2Rα, which is a main developer of T-regulatory lymphocytes. The mutations in the S gene of SARS-CoV-2-infected patients may affect immune responses to the molecule and alter the avidity of virus-human cell interactions.

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