Wang Rui, Chen Jiahui, Hozumi Yuta, Yin Changchuan, Wei Guo-Wei
Department of Mathematics, Statistics, and Computer Science, University of Illinois at Chicago, Chicago, Illinois 60607, United States.
J Phys Chem Lett. 2020 Dec 3;11(23):10007-10015. doi: 10.1021/acs.jpclett.0c02765. Epub 2020 Nov 12.
One of the major challenges in controlling the coronavirus disease 2019 (COVID-19) outbreak is its asymptomatic transmission. The pathogenicity and virulence of asymptomatic COVID-19 remain mysterious. On the basis of the genotyping of 75775 SARS-CoV-2 genome isolates, we reveal that asymptomatic infection is linked to SARS-CoV-2 11083G>T mutation (i.e., L37F at 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 the SARS-CoV-2 transmission capacity. Artificial intelligence, sequence alignment, and network analysis are applied to show that NSP6 mutation L37F may have compromised the virus's ability to undermine the innate cellular defense against viral infection via autophagy regulation. This assessment is in good agreement with our genotyping of the SARS-CoV-2 evolution and transmission across various countries and regions over the past few months.
控制2019冠状病毒病(COVID-19)疫情的主要挑战之一是其无症状传播。无症状COVID-19的致病性和毒力仍然不明。基于对75775个严重急性呼吸综合征冠状病毒2(SARS-CoV-2)基因组分离株的基因分型,我们发现无症状感染与SARS-CoV-2的11083G>T突变(即非结构蛋白6(NSP6)中的L37F)有关。通过分析11083G>T在各国的分布情况,我们揭示11083G>T可能与SARS-CoV-2的低毒性相关。此外,我们发现11083G>T突变率呈现全球下降趋势,表明11083G>T会阻碍SARS-CoV-2的传播能力。我们应用人工智能、序列比对和网络分析表明,NSP6的L37F突变可能损害了病毒通过自噬调节破坏细胞对病毒感染的固有防御能力。这一评估与我们对过去几个月SARS-CoV-2在各国和各地区的进化及传播情况的基因分型结果高度一致。