Corrêa-Dias Laura Cardoso, Lopes-Ribeiro Ágata, Mendes Gabriel Eduardo Ribeiro, Marques-Ferreira Geovane, Wilker-Teixeira Caio, Clarindo Felipe Alves, de Melo Rocha Victor, Martuchele-Félix Maria Eduarda, Retes Henrique Morais, Santos Thaiza Aline Pereira, Azevedo Gabriela Lorrany Aparecida, Pereira Verônica Evelyn Viana, de Fátima Silva Moraes Thais, de Sousa Reis Erik Vinicius, Gomes-de-Pontes Letícia, Rabelo Lívia Frota, Dos Santos Eduardo Augusto Sartori, Pereira Carlos Lorran Dias, Coelho Fernanda Daniela Santos, Coelho Rafael Pacheco, Santos Raiany Araújo, Coelho Gabriel Pacheco, da Fonseca Flávio Guimarães, Coelho-Dos-Reis Jordana Grazziela Alves
Long COVID Study Group, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Laboratório de Virologia Básica e Aplicada, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Avenida Antônio Carlos, 6627 - Pampulha, Belo Horizonte, Minas Gerais, 31270-901, Brazil.
Inflamm Res. 2025 Sep 16;74(1):127. doi: 10.1007/s00011-025-02085-6.
Long COVID is a debilitating illness with multi-systemic symptoms that affects at least 10% of individuals who have had COVID-19. Symptoms include respiratory, dermatological, gastrointestinal, cardiovascular, and most frequently reported, neurological sequelae. The most common neurological manifestations include fatigue, brain fog, memory issues, attention disorder, and headaches.
In this review, we explore the current literature and highlight key findings regarding not only the clinical presentations of neurological commitment during long COVID but mainly the mechanisms that culminate in neuroinflammation, such as autoimmunity, viral reservoirs, and lack of surveillance of T-cells.
Neuroinflammation is a complex multicellular response that directly impacts microglial cells and includes inflammasome activation, trafficking of immune cells, and increased circulating autoantibodies, cytokines, and chemokines in the central nervous system, directly impacting the tissue homeostasis. This review provides important information beyond the clinical manifestations of long COVID. Here, we highlight multifactorial neuroinflammation as the main mechanism involved in long COVID, bringing together several studies that address the different mechanisms that culminate in inflammation of the central nervous system, and highlight possible biomarkers involved in this syndrome and potential therapeutic approaches that have been studied.
Thus, this review strengthens research into long COVID and provides new possibilities for future studies.
新冠后综合征是一种具有多系统症状的使人衰弱的疾病,影响至少10%的新冠病毒感染者。症状包括呼吸系统、皮肤、胃肠道、心血管方面的症状,以及最常报告的神经后遗症。最常见的神经表现包括疲劳、脑雾、记忆问题、注意力障碍和头痛。
在本综述中,我们探讨了当前的文献,并强调了关于新冠后综合征期间神经损伤的临床表现的关键发现,但主要是导致神经炎症的机制,如自身免疫、病毒储存库和T细胞监测不足。
神经炎症是一种复杂的多细胞反应,直接影响小胶质细胞,包括炎性小体激活、免疫细胞的运输,以及中枢神经系统中循环自身抗体、细胞因子和趋化因子的增加,直接影响组织稳态。本综述提供了超出新冠后综合征临床表现的重要信息。在这里,我们强调多因素神经炎症是新冠后综合征的主要机制,汇集了几项研究,这些研究探讨了导致中枢神经系统炎症的不同机制,并强调了该综合征可能涉及的生物标志物以及已研究的潜在治疗方法。
因此,本综述加强了对新冠后综合征的研究,并为未来的研究提供了新的可能性。