Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, SE-10691 Stockholm, Sweden.
Department of Clinical Microbiology, Virology, Umeå University, SE-90185 Umeå, Sweden.
Viruses. 2021 Oct 13;13(10):2056. doi: 10.3390/v13102056.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to the coronavirus disease 2019 (COVID-19) pandemic, severely affecting public health and the global economy. Adaptive immunity plays a crucial role in fighting against SARS-CoV-2 infection and directly influences the clinical outcomes of patients. Clinical studies have indicated that patients with severe COVID-19 exhibit delayed and weak adaptive immune responses; however, the mechanism by which SARS-CoV-2 impedes adaptive immunity remains unclear. Here, by using an in vitro cell line, we report that the SARS-CoV-2 spike protein significantly inhibits DNA damage repair, which is required for effective V(D)J recombination in adaptive immunity. Mechanistically, we found that the spike protein localizes in the nucleus and inhibits DNA damage repair by impeding key DNA repair protein BRCA1 and 53BP1 recruitment to the damage site. Our findings reveal a potential molecular mechanism by which the spike protein might impede adaptive immunity and underscore the potential side effects of full-length spike-based vaccines.
严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)导致了 2019 年冠状病毒病(COVID-19)大流行,严重影响了公共卫生和全球经济。适应性免疫在对抗 SARS-CoV-2 感染中起着至关重要的作用,并直接影响患者的临床结局。临床研究表明,重症 COVID-19 患者表现出适应性免疫应答延迟和减弱;然而,SARS-CoV-2 阻碍适应性免疫的机制尚不清楚。在这里,我们通过使用体外细胞系报告称,SARS-CoV-2 刺突蛋白显著抑制 DNA 损伤修复,这是适应性免疫中有效 V(D)J 重组所必需的。在机制上,我们发现刺突蛋白定位于细胞核内,并通过阻碍关键 DNA 修复蛋白 BRCA1 和 53BP1 募集到损伤部位来抑制 DNA 损伤修复。我们的研究结果揭示了刺突蛋白可能阻碍适应性免疫的潜在分子机制,并强调了全长刺突蛋白疫苗的潜在副作用。