论文标题
用细胞自动机（CA）模型分析冠状病毒包膜蛋白
Analysis of Coronavirus Envelope Protein with Cellular Automata (CA) Model
论文作者
论文摘要
与SARS COVID（2003 COV）和MERS COVID（2012 MERS）相比，SARS COVID（2019 COV-2）的可传递性明显更高的原因可以归因于结构蛋白中报道的突变，以及非结构性蛋白质（NSP）（NSP）和附属蛋白（ORFS（ORFS）（ORFS）（ORFS）（ORFS）的作用，以进行病毒重复，并进行汇集，并分配和分裂。包膜蛋白E是最小长度的四种结构蛋白之一。最近的研究证实了包膜蛋白在病毒生命周期中所起的关键作用，包括从感染细胞中导出的病毒体的组装以进行传播。然而，高度复杂的病毒 - 宿主相互作用的决定因素尚未得到充分表征。长度为75和76氨基酸的COV-2和COV包膜蛋白在四个氨基酸位置有所不同。位置70处的附加氨基酸Gly（G）使COV长度为76。氨基酸对在COV的位置69-70代替COV-2的位置69的位置，已被确定为当前研究中的主要决定因素。本文集中于计算模型的设计，以将COV-2的野生和突变体与COV的野生和突变体与蛋白质链对功能重要区域的野生和突变体进行比较。我们假设COV-2和COV的CAML模型参数的差异表征了病毒与宿主高尔基体复合物的相互作用，包膜蛋白的结构和功能偏差。而且这种差异反映在其传播性的差异中。该假设已从单点突变研究对与镰状细胞贫血相关的人HBBβ-蛋白质血红蛋白蛋白进行验证，（ii）最近出版物中报道的Covid-2感染患者的包膜蛋白突变体。
The reason of significantly higher transmissibility of SARS Covid (2019 CoV-2) compared to SARS Covid (2003 CoV) and MERS Covid (2012 MERS) can be attributed to mutations reported in structural proteins, and the role played by non-structural proteins (nsps) and accessory proteins (ORFs) for viral replication, assembly, and shedding. Envelope protein E is one of the four structural proteins of minimum length. Recent studies have confirmed critical role played by the envelope protein in the viral life cycle including assembly of virion exported from infected cell for its transmission. However, the determinants of the highly complex viral - host interactions of envelope protein, particularly with host Golgi complex, have not been adequately characterized. CoV-2 and CoV Envelope proteins of length 75 and 76 amino acids differ in four amino acid locations. The additional amino acid Gly (G) at location 70 makes CoV length 76. The amino acid pair EG at location 69-70 of CoV in place of amino acid R in location 69 of CoV-2, has been identified as a major determining factor in the current investigation. This paper concentrates on the design of computational model to compare the structure/function of wild and mutants of CoV-2 with wild and mutants of CoV in the functionally important region of the protein chain pair. We hypothesize that differences of CAML model parameter of CoV-2 and CoV characterize the deviation in structure and function of envelope proteins in respect of interaction of virus with host Golgi complex; and this difference gets reflected in the difference of their transmissibility. The hypothesis has been validated from single point mutational study on- (i) human HBB beta-globin hemoglobin protein associated with sickle cell anemia, (ii) mutants of envelope protein of Covid-2 infected patients reported in recent publications.
