Zoonotic pandemics, like that caused by SARS-CoV-2, can follow the spillover of animal viruses into highly susceptible human populations. Their descendants have adapted to the human host and evolved to evade immune pressure. Coronaviruses acquire substitutions more slowly than other RNA viruses, due to a proofreading polymerase. In the spike glycoprotein, we find recurrent deletions overcome this slow substitution rate. Deletion variants arise in diverse genetic and geographic backgrounds, transmit efficiently, and are present in novel lineages, including those of current global concern. They frequently occupy recurrent deletion regions (RDRs), which map to defined antibody epitopes. Deletions in RDRs confer resistance to neutralizing antibodies. By altering stretches of amino acids, deletions appear to accelerate SARS-CoV-2 antigenic evolution and may, more generally, drive adaptive evolution.

中文翻译：

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SARS-CoV-2峰值糖蛋白驱动抗体逃逸中的反复缺失

类似于由SARS-CoV-2引起的人畜共患大流行，可以跟随动物病毒向高度易感人群的扩散。他们的后代适应了人类宿主，并逐渐逃避了免疫压力。由于校对的聚合酶，冠状病毒比其他RNA病毒更慢地获得置换。在峰值糖蛋白中，我们发现经常性缺失克服了这种缓慢的取代率。缺失变体出现在不同的遗传和地理背景中，可以高效传播，并存在于新的血统中，包括当前全球关注的那些。它们经常占据重复缺失区（RDR），其映射到确定的抗体表位。RDR中的缺失赋予对中和抗体的抗性。通过改变氨基酸的范围，