Department of Biotechnology, College of Science, University of Tehran, Tehran, Iran.
Department of Biology, Faculty of Sciences, University of Maragheh, Maragheh, Iran.
Microb Pathog. 2021 May;154:104831. doi: 10.1016/j.micpath.2021.104831. Epub 2021 Mar 13.
The third pandemic of coronavirus infection, called COVID-19 disease, began recently in China. The newly discovered coronavirus, entitled SARS-CoV-2, is the seventh member of the human coronaviruses. The main pathogenesis of SARS-CoV-2 infection is severe pneumonia, RNAaemia, accompanied by glass turbidity, and acute cardiac injury. It possesses a single-stranded positive-sense RNA genome which is 60-140 nm in diameter, and has a size of 26-32 kbp. Viral pathogenesis is accomplished with spike glycoprotein through the employment of a membrane-bound aminopeptidase, called the ACE2, as its primary cell receptor. It has been confirmed that various factors such as different national rules for quarantine and various races or genetic backgrounds might influence the mortality and infection rate of COVID-19 in the geographic areas. In addition to various known and unknown factors and host genetic susceptibility, mutations and genetic variabilities of the virus itself have a critical impact on variable clinical features of COVID-19. Although the SARS-CoV-2 genome is more stable than SARS-CoV or MERS-CoV, it has a relatively high dynamic mutation rate with respect to other RNA viruses. It's noteworthy that, some mutations can be founder mutations and show specific geographic patterns. Undoubtedly, these mutations can drive viral genetic variability, and because of genotype-phenotype correlation, resulting in a virus with more/lower/no decrease in natural pathogenic fitness or on the other scenario, facilitating their rapid antigenic shifting to escape the host immunity and also inventing a drug resistance virus, so converting it to a more infectious or deadly virus. Overall, the detection of all mutations in SARS-CoV-2 and their relations with pathological changes is nearly impossible, mostly due to asymptomatic subjects. In this review paper, the reported mutations of the SARS-CoV-2 and related variations in virus structure and pathogenicity in different geographic areas and genotypes are widely investigated. Many studies need to be repeated in other regions/locations for other people to confirm the findings. Such studies could benefit patient-specific therapy, according to genotyping patterns of SARS-CoV-2 distribution.
最近在中国爆发了第三次冠状病毒感染疫情，即 COVID-19 疾病。新发现的冠状病毒被命名为 SARS-CoV-2，是人类冠状病毒的第七个成员。SARS-CoV-2 感染的主要发病机制是严重肺炎、RNAaemia，伴有玻璃混浊和急性心脏损伤。它具有一个直径为 60-140nm 的单链正链 RNA 基因组，大小为 26-32kbp。病毒发病机制是通过使用一种称为 ACE2 的膜结合氨肽酶来实现的，它是病毒的主要细胞受体。已经证实，不同国家的隔离规定、不同种族或遗传背景等各种因素可能会影响地理区域 COVID-19 的死亡率和感染率。除了各种已知和未知的因素以及宿主遗传易感性外，病毒本身的突变和遗传变异性对 COVID-19 的不同临床特征也有重要影响。尽管 SARS-CoV-2 基因组比 SARS-CoV 或 MERS-CoV 更稳定，但相对于其他 RNA 病毒，它具有相对较高的动态突变率。值得注意的是，一些突变可能是创始突变，并表现出特定的地理模式。毫无疑问，这些突变可以驱动病毒遗传变异性，并且由于基因型-表型相关性，导致天然致病性适应性更高/更低/没有降低的病毒，或者在其他情况下，促使它们快速抗原漂移以逃避宿主免疫，还发明了耐药病毒，从而将其转化为更具传染性或更致命的病毒。总体而言，由于无症状患者的存在，几乎不可能检测到 SARS-CoV-2 的所有突变及其与病理学变化的关系。在本文综述中，广泛研究了不同地理区域和基因型中 SARS-CoV-2 的报告突变及其与病毒结构和致病性的关系。需要在其他地区/地点由其他人重复进行许多研究来验证这些发现。根据 SARS-CoV-2 分布的基因分型模式，这些研究可以为患者的特异性治疗带来益处。
