Treatment mechanism of immune triad from the repurposing drug against COVID-19

Jong hoon Lee
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Abstract

COVID-19 is an immune-mediated disease whose pathophysiology uses SAMHD1 tetramerization and cGAS–STING signaling, toll-like receptor 4 (TLR4) cascade, spike protein– inflammasome activation, and neuropilin 1 (NRP1) signaling. Variants of concern, such as SARS-CoV-2 Omicron Subvariants BQ.1, BQ.1.1, BA.4.6, BF.7, BA.2.75.2, and other mutants, have emerged. The longitudinal memory T-cell response to SARS-CoV-2 persists for eight months after symptom onset. Therefore, we must achieve viral clearance to coordinate immune cell reactions. Aspirin, dapsone, and dexamethasone as anticatalysis medicines have been used to treat COVID-19. They are shown to work harmoniously with modulating ILCs. Therefore, it needs to prescribe this immune triad to alleviate the clinical pathologic course and block exacerbation mechanisms due to diverse SARS-CoV-2 variants.

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重组药物免疫三联体抗COVID-19的治疗机制
新冠肺炎是一种免疫介导的疾病,其病理生理学使用SAMHD1四聚体和cGAS–STING信号、toll样受体4(TLR4)级联、刺突蛋白-炎症小体激活和neuropilin 1(NRP1)信号。出现了变异毒株,如SARS-CoV-2奥密克戎亚变体BQ.1、BQ.1.1、BA.4.6、BF.7、BA.2.75.2和其他变体。严重急性呼吸系统综合征冠状病毒2型的纵向记忆T细胞反应在症状出现后持续8个月。因此,我们必须实现病毒清除,以协调免疫细胞反应。阿司匹林、氨苯砜和地塞米松作为抗催化药物已被用于治疗新冠肺炎。它们被证明与调制ILC和谐地工作。因此,它需要开出这种免疫三联体来缓解临床病理过程,并阻断由多种严重急性呼吸系统综合征冠状病毒2型变异引起的恶化机制。
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来源期刊
Translational Medicine of Aging
Translational Medicine of Aging Medicine-Geriatrics and Gerontology
CiteScore
5.30
自引率
0.00%
发文量
2
审稿时长
103 days
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