Laboratory of Mucosal Exposome and Biomodulation, Department of Integrative Biomedical Sciences, Pusan National University, Yangsan, Republic of Korea.
Department of Medicine, Pusan National University, Yangsan, Republic of Korea.
Front Immunol. 2024 Aug 12;15:1433531. doi: 10.3389/fimmu.2024.1433531. eCollection 2024.
Post-COVID-19 condition is recognized as a multifactorial disorder, with persistent presence of viral antigens, discordant immunity, delayed viral clearance, and chronic inflammation. Obesity has emerged as an independent risk factor for both SARS-CoV-2 infection and its subsequent sequelae. In this study, we aimed to predict the molecular mechanisms linking obesity and post-COVID-19 distress. Viral antigen-exposed adipose tissues display remarkable levels of viral receptors, facilitating viral entry, deposition, and chronic release of inflammatory mediators and cells in patients. Subsequently, obesity-associated inflammatory insults are predicted to disturb cellular and humoral immunity by triggering abnormal cell differentiation and lymphocyte exhaustion. In particular, the decline in SARS-CoV-2 antibody titers and T-cell exhaustion due to chronic inflammation may account for delayed virus clearance and persistent activation of inflammatory responses. Taken together, obesity-associated defective immunity is a critical control point of intervention against post-COVID-19 progression, particularly in subjects with chronic metabolic distress.
新冠后(post-COVID-19)状况被认为是一种多因素障碍,其特征为持续存在病毒抗原、免疫失调、病毒清除延迟和慢性炎症。肥胖已成为 SARS-CoV-2 感染及其后续后遗症的独立危险因素。在这项研究中,我们旨在预测将肥胖与新冠后不适联系起来的分子机制。暴露于病毒抗原的脂肪组织表现出显著水平的病毒受体,促进病毒进入、沉积和慢性释放炎症介质和细胞。随后,肥胖相关的炎症损伤预计通过触发异常细胞分化和淋巴细胞耗竭来扰乱细胞和体液免疫。特别是,慢性炎症导致的 SARS-CoV-2 抗体滴度下降和 T 细胞耗竭可能导致病毒清除延迟和炎症反应持续激活。总之,肥胖相关的免疫缺陷是针对新冠后进展进行干预的一个关键控制点,特别是在患有慢性代谢紊乱的患者中。