Department of Experimental Medicine, University of Tor Vergata, Rome, Italy.
Department of Otorhinolaryngology, University of Rome "Tor Vergata", Rome, Italy.
Int Immunopharmacol. 2024 Mar 10;129:111599. doi: 10.1016/j.intimp.2024.111599. Epub 2024 Feb 7.
Olfactory impairment, particularly hyposmia and anosmia, has emerged as a distinctive early symptom of SARS-CoV-2. Drawing on the historical association of autoimmune diseases with olfactory function, this study delves into the connections between COVID-19, autoimmunity, and persistent olfactory dysfunctions, focusing on individuals experiencing long-lasting smell disorders (3-18 months post-SARS-CoV-2 infection).
The study comprised 36 Long Covid patients with persistent olfactory dysfunctions, alongside two control groups. Olfactory functionality was assessed using the Sniffin' Sticks extended test. Non-invasive olfactory mucosa brushing and nasal secretions were processed for nasal samples, while serum samples were obtained through peripheral venous sampling. A panel of autoantibodies, including Immunocirculating Complexes, ANA, ENA, and AECA, was investigated in serum and brush supernatant samples.
Contrary to expectations, the absence of traditional autoantibodies challenges the proposed autoimmune etiology of Long Covid-associated olfactory dysfunction. However, the presence and potential pathogenic role of AECA suggest viral cytopathic and inflammatory involvement in specific anatomical districts. One hypothesis explores the impact of inflammation and cytokine release induced by the viral infection, altering neuronal signaling and contributing to persistent hyposmia.
This research contributes to our understanding of the complex relationships between autoimmunity, olfactory impairment, and COVID-19. The absence of classical autoantibodies challenges prevailing theories, while the prominence of AECA hints at unique viral-induced pathogenic mechanisms. By unraveling these complexities, this study enhances our comprehension of post-acute sequelae, offering valuable perspectives on immune-mediated responses in the aftermath of the pandemic.
嗅觉障碍，特别是嗅觉减退和嗅觉丧失，已成为 SARS-CoV-2 的一种明显的早期症状。鉴于自身免疫性疾病与嗅觉功能之间的历史关联，本研究深入探讨了 COVID-19、自身免疫与持续性嗅觉功能障碍之间的联系，重点关注经历持续性嗅觉障碍（SARS-CoV-2 感染后 3-18 个月）的个体。
本研究纳入了 36 名持续性嗅觉障碍的长新冠患者，并设立了两个对照组。采用 Sniffin' Sticks 扩展测试评估嗅觉功能。通过非侵入性嗅黏膜刷检和鼻分泌物处理获取鼻样本，同时通过外周静脉采血获取血清样本。在血清和刷检上清样本中检测了一系列自身抗体，包括免疫循环复合物、ANA、ENA 和 AECA。
与预期相反，传统自身抗体的缺失对长新冠相关嗅觉功能障碍的自身免疫病因提出了挑战。然而，AECA 的存在及其潜在的致病性提示病毒细胞毒性和炎症可能参与了特定解剖区域。一种假说探讨了病毒感染引起的炎症和细胞因子释放对神经元信号的影响，导致持续性嗅觉减退。
本研究有助于我们理解自身免疫、嗅觉障碍与 COVID-19 之间的复杂关系。传统自身抗体的缺失对现有理论提出了挑战，而 AECA 的显著存在则提示了独特的病毒诱导的致病机制。通过揭示这些复杂性，本研究增进了我们对急性后期后遗症的理解，为大流行后免疫介导反应提供了有价值的视角。
