Parry Rhys H, Lytras Spyros, Petrone Mary E, Wille Michelle, Crits-Christoph Alexander, Gifford Robert J, Saito Akatsuki, Smura Teemu, Peacock Thomas P
School of Chemistry and Molecular Biosciences, The University of Queensland, St Lucia, Queensland, Australia.
Division of Systems Virology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
J Virol. 2024 Dec 17;98(12):e0146824. doi: 10.1128/jvi.01468-24. Epub 2024 Nov 4.
Understanding the origin and evolution of mutations in SARS-CoV-2 variants of concern (VOCs) is a critical area of research. B. Cao, X. Wang, W. Yin, Z. Gao, and B. Xia (mBio 15:e03187-23, 2024, https://doi.org/10.1128/mbio.03187-23) proposed that these mutations originated from bacterial sequences incorporated into the viral genome through stochastic template-switching by the viral RNA-dependent RNA polymerase (RdRp). Their analysis suggested that 62% of the viral mutation fragments (VMFs) in key SARS-CoV-2 proteins were identical to bacterial protein sequences. Given the implications of this finding, we re-examined the methods employed and argue that they resulted in false-positive findings. Specifically, the short query length of VMFs, seven amino acids, leads to spurious matches in large protein databases, as indicated by high BLAST Expect values. Furthermore, we analyzed the nucleotide sequence of VMFs, revealing no unique homology between SARS-CoV-2 and bacterial sequences. Consequently, the evidence does not support the hypothesis that bacterial sequences contribute to the evolution of SARS-CoV-2 VOCs. Instead, the emergence of these variants is more plausibly attributed to factors intrinsic to viral replication and evolution, such as the error-prone nature of RdRp, intrahost diversity, and recombination of related viral sublineages.
了解严重急性呼吸综合征冠状病毒2(SARS-CoV-2)变异株(VOCs)中突变的起源和进化是一个关键的研究领域。曹博、王雪、尹伟、高泽和夏博(《mBio》15:e03187-23,2024,https://doi.org/10.1128/mbio.03187-23)提出,这些突变源自通过病毒RNA依赖性RNA聚合酶(RdRp)的随机模板切换整合到病毒基因组中的细菌序列。他们的分析表明,SARS-CoV-2关键蛋白中62%的病毒突变片段(VMFs)与细菌蛋白序列相同。鉴于这一发现的影响,我们重新审视了所采用的方法,并认为这些方法导致了假阳性结果。具体而言,VMFs的短查询长度(七个氨基酸)导致在大型蛋白质数据库中出现虚假匹配,如高BLAST期望值所示。此外,我们分析了VMFs的核苷酸序列,发现SARS-CoV-2与细菌序列之间没有独特的同源性。因此,证据不支持细菌序列促成SARS-CoV-2 VOCs进化的假说。相反,这些变异株的出现更可能归因于病毒复制和进化的内在因素,如RdRp的易出错性质、宿主内多样性以及相关病毒亚谱系的重组。