• J. Intern. Med. · Sep 2024

    SARS-CoV-2 spike protein acts as a β-adrenergic receptor agonist: A potential mechanism for cardiac sequelae of long COVID.

    • Xiangning Deng, Hongtu Cui, Hao Liang, Xinyu Wang, Haiyi Yu, Jingjia Wang, Wenyao Wang, Dongyang Liu, Youyi Zhang, Erdan Dong, Yida Tang, and Han Xiao.
    • Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, Beijing, China.
    • J. Intern. Med. 2024 Sep 1; 296 (3): 291297291-297.

    BackgroundCurrently, pathophysiological mechanisms of post-acute sequelae of coronavirus disease-19-cardiovascular syndrome (PASC-CVS) remain unknown.Methods And ResultsPatients with PASC-CVS exhibited significantly higher circulating levels of severe acute respiratory syndrome-coronavirus-2 spike protein S1 than the non-PASC-CVS patients and healthy controls. Moreover, individuals with high plasma spike protein S1 concentrations exhibited elevated heart rates and normalized low frequency, suggesting cardiac β-adrenergic receptor (β-AR) hyperactivity. Microscale thermophoresis (MST) assay revealed that the spike protein bound to β1- and β2-AR, but not to D1-dopamine receptor. These interactions were blocked by β1- and β2-AR blockers. Molecular docking and MST assay of β-AR mutants revealed that the spike protein interacted with the extracellular loop 2 of both β-ARs. In cardiomyocytes, spike protein dose-dependently increased the cyclic adenosine monophosphate production with or without epinephrine, indicating its allosteric effects on β-ARs.ConclusionSevere acute respiratory syndrome-coronavirus-2 spike proteins act as an allosteric β-AR agonist, leading to cardiac β-AR hyperactivity, thus contributing to PASC-CVS.© 2024 The Association for the Publication of the Journal of Internal Medicine.

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