论文标题
无症状的共证于19感染和传播
Decoding asymptomatic COVID-19 infection and transmission
论文作者
论文摘要
2019年冠状病毒病（COVID-19）是一种不断毁灭性的公共卫生和世界经济。控制COVID-19爆发的主要挑战之一是其无症状的感染和传播，在大多数情况下都是难以捉摸且毫无防备的。无症状COVID-19的致病性和毒力仍然神秘。基于20656种严重急性呼吸综合征2（SARS-COV-2）基因组分离株的基因分型，我们揭示了无症状感染与SARS-COV-2 11083G> T突变有关，即liucine（l）与苯基氨基（f）替代的苯胺（f）在替代37（l37f）的l37（l37f）（l37f）。通过分析在各个国家的11083G> t的分布，我们公布了11083G> t可能与SARS-COV-2的低毒性相关。此外，我们显示了11083G> t突变比的全球衰减趋势，表明11083G> t会阻碍SARS-COV-2传输能力。序列比对发现NSP6和残留37个社区在几种冠状病毒物种上相对保守，表明它们在调节宿主细胞自噬中的重要性以破坏对病毒感染的先天细胞防御。使用机器学习和拓扑数据分析，我们证明了突变L37F使NSP6在能量上稳定。刚度和灵活性指数和几个网络模型表明，突变L37F可能损害了NSP6功能，导致SARS-COV亚型相对较弱。这项评估是我们在过去几个月中对SARS-COV-2进化和传播SARS-COV-2进化和传播的基因分型的良好同意。
Coronavirus disease 2019 (COVID-19) is a continuously devastating public health and the world economy. One of the major challenges in controlling the COVID-19 outbreak is its asymptomatic infection and transmission, which are elusive and defenseless in most situations. The pathogenicity and virulence of asymptomatic COVID-19 remain mysterious. Based on the genotyping of 20656 Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) genome isolates, we reveal that asymptomatic infection is linked to SARS-CoV-2 11083G>T mutation, i.e., leucine (L) to phenylalanine (F) substitution at the residue 37 (L37F) of nonstructure protein 6 (NSP6). By analyzing the distribution of 11083G>T in various countries, we unveil that 11083G>T may correlate with the hypotoxicity of SARS-CoV-2. Moreover, we show a global decaying tendency of the 11083G>T mutation ratio indicating that 11083G>T hinders SARS-CoV-2 transmission capacity. Sequence alignment found both NSP6 and residue 37 neighborhoods are relatively conservative over a few coronaviral species, indicating their importance in regulating host cell autophagy to undermine innate cellular defense against viral infection. Using machine learning and topological data analysis, we demonstrate that mutation L37F has made NSP6 energetically less stable. The rigidity and flexibility index and several network models suggest that mutation L37F may have compromised the NSP6 function, leading to a relatively weak SARS-CoV subtype. This assessment is a good agreement with our genotyping of SARS-CoV-2 evolution and transmission across various countries and regions over the past few months.
