Abstract 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.
【저자키워드】 COVID-19, SARS-CoV-2, Pandemics, community transmission, antibody escape, 【초록키워드】 Brazil, Mutation, spike, diagnostic, variants of concern, coronavirus 2, Immune escape, RBD, P.1, Lineage, Deletion, NTD, glycoprotein, antigenicity, respiratory, epitope, Antibody neutralization, protocols, Support, domain, circulating, insertion, INDEL, B.1.1.33, transmission of SARS-CoV-2, SARS-CoV-2 lineage, widespread, Alter, predicted, generate, promote, the RBD, the receptor-binding domain, the S protein, parental, viral lineage, 【제목키워드】 Brazil, Evolution, variants of concern, domain, INDEL, the spike protein,