From the Department of Woman and Child Health and Public Health, Fondazione Policlinico Universitario A. Gemelli Istituti di Ricovero e Cura a Carattere Scientifico, Rome, Italy.
Pediatric Section, Department of Surgery, Dentistry, Paediatrics, and Gynaecology, University of Verona, Verona, Italy.
Allergy Asthma Proc. 2022 May 1;43(3):187-193. doi: 10.2500/aap.2022.43.220018.
Long COVID (coronavirus disease 2019) syndrome includes a group of patients who, after infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), exhibit lingering mild-to-moderate symptoms and develop medical complications that can have lasting health problems. In this report, we propose a model for the pathophysiology of the long COVID presentation based on increased proinflammatory cytokine production that results from the persistence of the SARS-CoV-2 virus or one of its molecular components. Associated with this hyperproduction of inflammatory cytokines is a heightened activity of nuclear factor κ B (NF-κB) and p38 mitogen-activated protein kinase signaling pathways that regulate cytokine production. The purpose of the present report was to review the causes of long COVID syndrome and suggest ways that can provide a basis for a better understanding of the clinical symptomatology for the of improved diagnostic and therapeutic procedures for the condition. Extensive research was conducted in medical literature data bases by applying terms such as "long COVID" associated with "persistence of the SARS-CoV-2 virus" "spike protein' "COVID-19" and "biologic therapies." In this model of the long COVID syndrome, the persistence of SARS-CoV-2 is hypothesized to trigger a dysregulated immune system with subsequent heightened release of proinflammatory cytokines that lead to chronic low-grade inflammation and multiorgan symptomatology. The condition seems to have a genetic basis, which predisposes individuals to have a diminished immunologic capacity to completely clear the virus, with residual parts of the virus persisting. This persistence of virus and resultant hyperproduction of proinflammatory cytokines are proposed to form the basis of the syndrome.
长新冠（COVID-19）综合征包括一组患者，他们在感染严重急性呼吸综合征冠状病毒 2 型（SARS-CoV-2）后，出现持续的轻度至中度症状，并出现可能导致长期健康问题的医疗并发症。在本报告中，我们基于 SARS-CoV-2 病毒或其分子成分持续存在导致促炎细胞因子过度产生的理论，提出了长新冠表现的病理生理学模型。与这种炎症细胞因子过度产生相关的是核因子 κB（NF-κB）和 p38 丝裂原活化蛋白激酶信号通路的活性增强，这些信号通路调节细胞因子的产生。本报告的目的是回顾长新冠综合征的病因，并提出可以为更好地理解该疾病的临床症状提供依据的方法，从而改善诊断和治疗方法。通过应用与 SARS-CoV-2 病毒持续存在、“刺突蛋白”、“COVID-19”和“生物疗法”相关的术语，在医学文献数据库中进行了广泛的研究。在长新冠综合征的这种模型中，假设 SARS-CoV-2 的持续存在会引发免疫系统失调，随后促炎细胞因子过度释放，导致慢性低度炎症和多器官症状。这种情况似乎具有遗传基础，使个体的免疫能力减弱，无法完全清除病毒，导致病毒的残余部分持续存在。病毒的持续存在和由此产生的促炎细胞因子的过度产生被认为是该综合征的基础。
