SARS-CoV-2 Spike Protein and Lung Vascular Cells

S. Suresh, Yuichiro J. Suzuki
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引用次数: 10

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is causing the current pandemic of coronavirus disease 2019 (COVID-19), and COVID-19 vaccines focus on its spike protein. However, in addition to facilitating the membrane fusion and viral entry, the SARS-CoV-2 spike protein promotes cell growth signaling in human lung vascular cells, and patients who have died of COVID-19 have thickened pulmonary vascular walls, linking the spike protein to a fatal disease, pulmonary arterial hypertension (PAH). In addition to SARS-CoV spike proteins, gp120, the viral membrane fusion protein of human immunodeficiency virus (HIV), has been reported to promote cell signaling, and long-term surviving HIV-positive patients have a high incidence of developing PAH. This article describes the findings of the SARS-CoV-2 spike protein affecting lung vascular cells and explains how the spike protein possibly increases the incidence of PAH. Since the SARS-CoV-2 spike protein will be administered to millions of people as COVID-19 vaccines, it is critical to understand the biological effects of this protein on human cells to ensure that it does not promote long-term adverse health consequences.
SARS-CoV-2刺突蛋白与肺血管细胞
严重急性呼吸综合征冠状病毒2 (SARS-CoV-2)正在导致当前的冠状病毒病2019 (COVID-19)大流行,COVID-19疫苗的重点是其刺突蛋白。然而,除了促进膜融合和病毒进入外,SARS-CoV-2刺突蛋白还促进人肺血管细胞中的细胞生长信号,死于COVID-19的患者肺血管壁增厚,将刺突蛋白与一种致命疾病肺动脉高压(PAH)联系起来。除了SARS-CoV刺突蛋白外,人类免疫缺陷病毒(HIV)的病毒膜融合蛋白gp120也被报道能促进细胞信号传导,并且长期存活的HIV阳性患者发生PAH的几率很高。本文描述了SARS-CoV-2刺突蛋白影响肺血管细胞的发现,并解释了刺突蛋白如何可能增加多环芳烃的发病率。由于SARS-CoV-2刺突蛋白将作为COVID-19疫苗接种给数百万人,因此了解这种蛋白对人体细胞的生物学效应至关重要,以确保它不会促进长期的不良健康后果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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