Mutations at both the receptor-binding domain (RBD) and the amino (N)-terminal domain (NTD) of the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Spike (S) glycoprotein can alter its antigenicity and promote immune escape. We identified that SARS-CoV-2 lineages circulating in Brazil with mutations of concern in the RBD independently acquired convergent deletions and insertions in the NTD of the S protein, which altered the NTD antigenic-supersite and other predicted epitopes at this region. Importantly, we detected the community transmission of different P.1 lineages bearing NTD indels ∆69-70 (which can impact several SARS-CoV-2 diagnostic protocols), ∆144 and ins214ANRN, and a new VOI N.10 derived from the B.1.1.33 lineage carrying three NTD deletions (∆141–144, ∆211, and ∆256–258). These findings support that the ongoing widespread transmission of SARS-CoV-2 in Brazil generates new viral lineages that might be more resistant to antibody neutralization than parental variants of concern.

中文翻译：

---

巴西 SARS-CoV-2 令人关注和感兴趣的变体的持续演变通过刺突蛋白氨基 (N) 末端结构域中的会聚插入缺失揭示

严重急性呼吸系统综合症冠状病毒 2 (SARS-CoV-2) 刺突 (S) 糖蛋白的受体结合域 (RBD) 和氨基 (N) 末端域 (NTD) 的突变可改变其抗原性并促进免疫逃脱。我们发现在巴西流行的 SARS-CoV-2 谱系在 RBD 中具有相关突变，独立地获得了 S 蛋白 NTD 中的聚合缺失和插入，这改变了该区域的 NTD 抗原超位点和其他预测表位。重要的是，我们检测到带有 NTD 插入缺失 Δ69-70（这会影响多种 SARS-CoV-2 诊断方案）、Δ144 和 ins214ANRN 以及源自 B 的新 VOI N.10 的不同 P.1 谱系的社区传播.1.1.33 谱系携带三个 NTD 缺失（Δ141–144、Δ211 和 Δ256–258）。