2021 年 38 巻 1 号 p. 14-19
Coronavirus disease 2019 (COVID–19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS–CoV–2). This review summarizes the knowledge about SARS–CoV–2 immunology and discusses the policy of clinical practice for neuroimmune diseases at the time of the SARS–CoV–2 pandemic. The human defense systems against SARS–CoV–2 infection begin to work through innate immunity. Most neuroimmune diseases are caused by impairment of adaptive immunity, which preserves the function of innate immunity. Therefore, patients with neuroimmune diseases are not typically susceptible to COVID–19 and will not experience severe symptoms. However, patients with multiple sclerosis are at risk if their score on the Expanded Disability Status Scale is high. In the context of the COVID–19 pandemic, various neuroimmune disease practice guidelines have been published assessing the risk COVID–19 poses with each immunotherapeutic agent. Some immunotherapeutics may reduce immunity to viral infections. In particular, B–cell depletion therapy (rituximab, ocrelizumab, and inebilizumab) should be avoided because it can cause severe COVID–19 outcomes and decrease immune response to vaccination. On the other hand, some immunotherapeutics such as dexamethasone and tocilizumab may prevent severe COVID–19 symtpoms by suppressing cytokine storms. In most neuroimmune diseases, infection is known as a risk factor for acute exacerbation, so there is a risk of exacerbation of neuroimmune diseases by SARS–CoV–2 infection. In diseases such as myasthenia gravis, where respiratory function is impaired, COVID–19 has a high risk of being fatal. In addition to treatment of viral infections, these patients should be carefully monitored with immunotherapy. The efficacy and safety of COVID–19 vaccines in patients with neuroimmune diseases is still unclear and awaits further study.
