ABSTRACT

Introduction:The year 2020 was defined by the 29,903 base pairs of RNA that codes for the SARS-CoV-2 genome. SARS-CoV-2 infects humans to cause COVID-19, spreading from patient-to-patient yet impacts patients very divergently.

Areas covered: Within this review, we address the known molecular mechanisms and supporting data for COVID-19 clinical course and pathology, clinical risk factors and molecular signatures, therapeutics of severe COVID-19, and reinfection/vaccination. Literature and published datasets were reviewed using PubMed, Google Scholar, and NCBI SRA tools. The combination of exaggerated cytokine signaling, pneumonia, NETosis, pyroptosis, thrombocytopathy, endotheliopathy, multiple organ dysfunction syndrome (MODS), and acute respiratory distress syndrome (ARDS) create a positive feedback loop of severe damage in patients with COVID-19 that impacts the entire body and may persist for months following infection. Understanding the molecular pathways of severe COVID-19 opens the door for novel therapeutic design. We summarize the current insights into pathology, risk factors, secondary infections, genetics, omics, and drugs being tested to treat severe COVID-19.

Expert opinion: A growing level of support suggests the need for stronger integration of biomarkers and precision medicine to guide treatment strategies of severe COVID-19, where each patient has unique outcomes and thus require guided treatment.

摘要

简介： 2020 年是由编码 SARS-CoV-2 基因组的 29,903 个碱基对的 RNA 定义的。SARS-CoV-2 感染人类并导致 COVID-19，在患者之间传播，但对患者的影响却截然不同。

涵盖的领域：在本次综述中，我们讨论了已知的分子机制以及有关 COVID-19 临床病程和病理学、临​​床危险因素和分子特征、严重 COVID-19 的治疗以及再感染/疫苗接种的支持数据。使用 PubMed、Google Scholar 和 NCBI SRA 工具对文献和已发表的数据集进行了审查。夸大的细胞因子信号传导、肺炎、NETosis、焦亡、血小板病、内皮病、多器官功能障碍综合征 (MODS) 和急性呼吸窘迫综合征 (ARDS) 的结合在 COVID-19 患者中形成了严重损害的正反馈循环，从而影响了整个身体，并可能在感染后持续数月。了解严重 COVID-19 的分子途径为新颖的治疗设计打开了大门。我们总结了当前对病理学、危险因素、继发感染、遗传学、组学和正在测试的治疗重症 COVID-19 药物的见解。

专家意见：越来越多的支持表明需要加强生物标志物和精准医学的整合来指导重症COVID-19的治疗策略，每个患者都有独特的结果，因此需要指导治疗。