Identifying Markers of Emerging SARS-CoV-2 Variants in Patients With Secondary Immunodeficiency.
Identifying Markers of Emerging SARS-CoV-2 Variants in Patients With Secondary Immunodeficiency.
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DOI：
10.3389/fmicb.2022.933983
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发表时间：
2022
影响因子：
5.2
通讯作者：
中科院分区：
文献类型：
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作者：
自2019年底以来，世界一直受到2019冠状病毒病（COVID-19）大流行的挑战。随着COVID-19病例在全球范围内的上升，严重急性呼吸综合征冠状病毒2型（SARS-CoV-2）继续演变，导致感兴趣（VOI）和关注（VOC）变体的出现。在数亿感染者中，免疫缺陷患者是最容易感染这种病毒的弱势群体之一。这些人包括那些先前存在健康状况和/或正在接受免疫抑制治疗（继发性免疫缺陷）的人。在这些病例中，一些研究人员报告了抗covid -19治疗存在的慢性感染，这可能导致宿主内病毒的进化。这种变异发生在多种病毒蛋白中，包括与发病机制有关的关键结构蛋白，如刺突蛋白。将这些突变与普通人群中出现的突变进行跟踪和比较，可能会提供有关SARS-CoV-2基因组功能位点的信息。在这项研究中，我们回顾了目前关于免疫功能低下患者中SARS-CoV-2进化的具体特征的文献，并发现这些患者的病毒分离株中复发性从头氨基酸变化可能在SARS-CoV-2发病和进化中发挥重要作用。
Since the end of 2019, the world has been challenged by the coronavirus disease 2019 (COVID-19) pandemic. With COVID-19 cases rising globally, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues to evolve, resulting in the emergence of variants of interest (VOI) and of concern (VOC). Of the hundreds of millions infected, immunodeficient patients are one of the vulnerable cohorts that are most susceptible to this virus. These individuals include those with preexisting health conditions and/or those undergoing immunosuppressive treatment (secondary immunodeficiency). In these cases, several researchers have reported chronic infections in the presence of anti-COVID-19 treatments that may potentially lead to the evolution of the virus within the host. Such variations occurred in a variety of viral proteins, including key structural ones involved in pathogenesis such as spike proteins. Tracking and comparing such mutations with those arisen in the general population may provide information about functional sites within the SARS-CoV-2 genome. In this study, we reviewed the current literature regarding the specific features of SARS-CoV-2 evolution in immunocompromised patients and identified recurrent de novo amino acid changes in virus isolates of these patients that can potentially play an important role in SARS-CoV-2 pathogenesis and evolution.