Post-Acute Sequelae of COVID-19 or Long COVID becomes evident some weeks to months following acute COVID-19. Symptoms include cognitive impairment and varying degrees of memory loss with no definitive etiologies or efficacious therapies forthcoming even after four years of the SARS-Cov2 pandemic virus. The aim of this review is to demonstrate the important role of α7 nicotinic acetylcholine receptors in both acute COVID-19 and Long COVID. Evidence presented implicates immune mechanisms stimulated by SARS-Cov-2 S-protein fragment 674–685 that possesses homology with α7-specific ligands. Cognitive dysfunctions observed in Long COVID patients may be derived from anti-idiotypic α7-specific antibodies stimulated by (674−685)-specific antibodies. Therapeutic interventions capable of neutralizing these antibodies and restoring full functions of α7 nicotinic acetylcholine receptors appear to be of paramount importance in post-acute sequelae of COVID-19.

COVID-19 急性后遗症或长期 COVID-19 急性后遗症在急性 COVID-19 后数周至数月变得明显。症状包括认知障碍和不同程度的记忆丧失，即使在 SARS-Cov2 大流行病毒感染四年后，仍没有明确的病因或有效的治疗方法。本综述的目的是证明 α7 烟碱乙酰胆碱受体在急性 COVID-19 和长期 COVID 中的重要作用。提供的证据表明 SARS-Cov-2 S 蛋白片段 674-685 刺激的免疫机制与 α7 特异性配体具有同源性。在 Long COVID 患者中观察到的认知功能障碍可能源自 (674−685) 特异性抗体刺激的抗独特型 α7 特异性抗体。能够中和这些抗体并恢复 α7 烟碱乙酰胆碱受体全部功能的治疗干预措施似乎对于 COVID-19 的急性后遗症至关重要。