Chaguza Chrispin, Hahn Anne M, Petrone Mary E, Zhou Shuntai, Ferguson David, Breban Mallery I, Pham Kien, Peña-Hernández Mario A, Castaldi Christopher, Hill Verity, Schulz Wade, Swanstrom Ronald I, Roberts Scott C, Grubaugh Nathan D
Department of Epidemiology of Microbial Diseases, Yale School of Public Health, New Haven, CT, USA.
School of Life and Environmental Sciences, University of Sydney, Sydney, NSW, Australia.
medRxiv. 2022 Jul 2:2022.06.29.22276868. doi: 10.1101/2022.06.29.22276868.
The chronic infection hypothesis for novel SARS-CoV-2 variant emergence is increasingly gaining credence following the appearance of Omicron. Here we investigate intrahost evolution and genetic diversity of lineage B.1.517 during a SARS-CoV-2 chronic infection lasting for 471 days (and still ongoing) with consistently recovered infectious virus and high viral loads. During the infection, we found an accelerated virus evolutionary rate translating to 35 nucleotide substitutions per year, approximately two-fold higher than the global SARS-CoV-2 evolutionary rate. This intrahost evolution led to the emergence and persistence of at least three genetically distinct genotypes suggesting the establishment of spatially structured viral populations continually reseeding different genotypes into the nasopharynx. Finally, using unique molecular indexes for accurate intrahost viral sequencing, we tracked the temporal dynamics of genetic diversity to identify advantageous mutations and highlight hallmark changes for chronic infection. Our findings demonstrate that untreated chronic infections accelerate SARS-CoV-2 evolution, ultimately providing opportunity for the emergence of genetically divergent and potentially highly transmissible variants as seen with Delta and Omicron.
在奥密克戎出现后,关于新型严重急性呼吸综合征冠状病毒2(SARS-CoV-2)变体出现的慢性感染假说越来越受到认可。在此,我们研究了在持续471天(且仍在进行)的SARS-CoV-2慢性感染期间B.1.517谱系的宿主体内进化和遗传多样性,在此期间持续检测到具有传染性的病毒且病毒载量很高。在感染过程中,我们发现病毒进化速率加快,每年有35个核苷酸替换,约为全球SARS-CoV-2进化速率的两倍。这种宿主体内进化导致至少三种基因上不同的基因型出现并持续存在,这表明形成了空间结构的病毒群体,并不断将不同基因型重新接种到鼻咽部。最后,我们使用独特的分子指标进行准确的宿主体内病毒测序,追踪遗传多样性的时间动态,以识别有利突变并突出慢性感染的标志性变化。我们的研究结果表明,未经治疗的慢性感染会加速SARS-CoV-2的进化,最终为出现如德尔塔和奥密克戎那样基因不同且可能具有高传播性的变体提供机会。