Department of Medical Laboratory Science, College of Medical Sciences, Ahmadu Bello University, Zaria, Nigeria.
Research Institute for Biomedical Sciences, Tokyo University of Science, Tokyo, Japan.
Scand J Immunol. 2021 Apr;93(4):e12998. doi: 10.1111/sji.12998. Epub 2020 Dec 3.
SARS-CoV-2 is a novel human coronavirus responsible for the Coronavirus disease 2019 (COVID-19) pandemic. Pneumonia and acute respiratory distress syndrome are the major complications of COVID-19. SARS-CoV-2 infection can activate innate and adaptive immune responses and result in massive inflammatory responses later in the disease. These uncontrolled inflammatory responses may lead to local and systemic tissue damage. In patients with severe COVID-19, eosinopenia and lymphopenia with a severe reduction in the frequency of CD4+ and CD8+ T cells, B cells and natural killer (NK) cells are a common feature. COVID-19 severity hinges on the development of cytokine storm characterized by elevated serum levels of pro-inflammatory cytokines. Moreover, IgG-, IgM- and IgA-specific antibodies against SARS-CoV-2 can be detected in most patients, along with the viral RNA, forming the basis for assays that aid in patient diagnosis. Elucidating the immunopathological outcomes due to COVID-19 could provide potential targets for immunotherapy and are important for choosing the best clinical management by consultants. Currently, along with standard supportive care, therapeutic approaches to COVID-19 treatment involve the use of antiviral agents that interfere with the SARS-CoV-2 lifecycle to prevent further viral replication and utilizing immunomodulators to dampen the immune system in order to prevent cytokine storm and tissue damage. While current therapeutic options vary in efficacy, there are several molecules that were either shown to be effective against other viruses such as HIV or show promise in vitro that could be added to the growing arsenal of agents used to control COVID-19 severity and spread.
SARS-CoV-2 是一种新型人类冠状病毒,引发了 2019 年冠状病毒病(COVID-19)大流行。肺炎和急性呼吸窘迫综合征是 COVID-19 的主要并发症。SARS-CoV-2 感染可激活先天和适应性免疫反应,并在疾病后期导致大量炎症反应。这些不受控制的炎症反应可能导致局部和全身组织损伤。在重症 COVID-19 患者中,嗜酸性粒细胞减少和淋巴细胞减少,CD4+和 CD8+T 细胞、B 细胞和自然杀伤(NK)细胞的频率严重降低是常见特征。COVID-19 的严重程度取决于细胞因子风暴的发展,其特征是促炎细胞因子血清水平升高。此外,大多数患者可检测到针对 SARS-CoV-2 的 IgG、IgM 和 IgA 特异性抗体,以及病毒 RNA,为辅助患者诊断的检测奠定了基础。阐明 COVID-19 引起的免疫病理结果可为免疫疗法提供潜在靶点,并有助于顾问选择最佳临床管理。目前,除了标准的支持性护理外,COVID-19 的治疗方法还包括使用抗病毒药物来干扰 SARS-CoV-2 的生命周期,以防止进一步的病毒复制,并使用免疫调节剂来抑制免疫系统,以防止细胞因子风暴和组织损伤。虽然目前的治疗选择在疗效上有所不同,但有几种分子已被证明对 HIV 等其他病毒有效,或在体外显示出有希望的结果,可加入到用于控制 COVID-19 严重程度和传播的不断增加的药物库中。