Inflammation and Epstein-Barr Virus at the Crossroads of Multiple Sclerosis and Post-Acute Sequelae of COVID-19 Infection.

Recent studies have strengthened the evidence for Epstein–Barr Virus (EBV) as an important contributing factor in the development of multiple sclerosis (MS). Chronic inflammation is a key feature of MS. EBV+ B cells can express cytokines and exosomes that promote inflammation, and EBV is known to be reactivated through the upregulation of cellular inflammasomes. Inflammation is a possible cause of the breakdown of the blood–brain barrier (BBB), which allows the infiltration of lymphocytes into the central nervous system. Once resident, EBV+ or EBV-specific B cells could both plausibly exacerbate MS plaques through continued inflammatory processes, EBV reactivation, T cell exhaustion, and/or molecular mimicry. Another virus, SARS-CoV-2, the cause of COVID-19, is known to elicit a strong inflammatory response in infected and immune cells. COVID-19 is also associated with EBV reactivation, particularly in severely ill patients. Following viral clearance, continued inflammation may be a contributor to post-acute sequelae of COVID-19 infection (PASC). Evidence of aberrant cytokine activation in patients with PASC supports this hypothesis. If unaddressed, long-term inflammation could put patients at risk for reactivation of EBV. Determining mechanisms by which viruses can cause inflammation and finding treatments for reducing that inflammation may help reduce the disease burden for patients suffering from PASC, MS, and EBV diseases.

近期研究进一步证实了爱泼斯坦 - 巴尔病毒（EBV）是多发性硬化症（MS）发展的一个重要致病因素。慢性炎症是MS的一个关键特征。EBV阳性的B细胞能够表达促进炎症的细胞因子和外泌体，并且已知EBV会通过细胞炎性小体的上调而被重新激活。炎症可能是血脑屏障（BBB）破坏的原因，这使得淋巴细胞能够渗入中枢神经系统。一旦进入，EBV阳性或EBV特异性的B细胞都有可能通过持续的炎症过程、EBV重新激活、T细胞耗竭和/或分子模拟来加重MS斑块。另一种病毒，即导致新冠肺炎的新型冠状病毒（SARS - CoV - 2），已知会在感染细胞和免疫细胞中引发强烈的炎症反应。新冠肺炎还与EBV重新激活有关，尤其是在重症患者中。在病毒清除后，持续的炎症可能是新冠肺炎感染后急性后遗症（PASC）的一个成因。PASC患者中细胞因子异常激活的证据支持这一假说。如果不加以解决，长期炎症可能会使患者面临EBV重新激活的风险。确定病毒引发炎症的机制并找到减轻炎症的治疗方法，可能有助于减轻PASC、MS和EBV相关疾病患者的疾病负担。