最新发现！中科院遗传发育所钱文峰等发现新冠病毒奥密克戎（Omicron）变异株来源于小鼠的证据
SARS-CoV-2 奥密克戎（Omicron）突变的快速积累使其爆发，引发了关于其近端起源是否发生在人类或其他哺乳动物宿主的问题。在这里，我们确定了Omicron从B.1.1谱系分化后获得的45个点突变。我们发现，Omicron刺突蛋白序列比已知在人类宿主中持续进化的任何已报道的SARS-CoV-2变异都受到了更强的阳性选择，这表明存在宿主跳跃的可能性。Omicron的祖先获得的突变分子谱(即12种碱基替换的相对频率)与在人类患者中进化的病毒的谱明显不同，但与在小鼠细胞环境中进化的病毒的谱相似。此外，Omicron刺突蛋白的突变与已知的SARS-CoV-2突变显著重叠，以促进对小鼠宿主的适应，特别是通过增强刺突蛋白与小鼠细胞进入受体的结合亲和力。总的来说，我们的研究结果表明，奥密克戎（Omicron）的祖先从人类跳到老鼠身上，迅速积累有利于感染宿主的突变，然后又跳回到人类身上，表明奥密克戎（Omicron）爆发的物种间进化轨迹。
The rapid accumulation of mutations in the SARS-CoV-2 Omicron variant that enabled its outbreak raises questions as to whether its proximal origin occurred in humans or another mammalian host. Here, we identified 45 point mutations that Omicron acquired since divergence from the B.1.1 lineage. We found that the Omicron spike protein sequence was subjected to stronger positive selection than that of any reported SARS-CoV-2 variants known to evolve persistently in human hosts, suggesting a possibility of host-jumping. The molecular spectrum of mutations (i.e., the relative frequency of the 12 types of base substitutions) acquired by the progenitor of Omicron was significantly different from the spectrum for viruses that evolved in human patients, but resembled the spectra associated with virus evolution in a mouse cellular environment. Furthermore, mutations in the Omicron spike protein significantly overlapped with SARS-CoV-2 mutations known to promote adaptation to mouse hosts, particularly through enhanced spike protein binding affinity for the mouse cell entry receptor. Collectively, our results suggest that the progenitor of Omicron jumped from humans to mice, rapidly accumulated mutations conducive to infecting that host, then jumped back into humans, indicating an inter-species evolutionary trajectory for the Omicron outbreak.
https://www.sciencedirect.com/science/article/pii/S1673852721003738#!
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