Journal Article

The ongoing evolution of variants of concern and interest of SARS-CoV-2 in Brazil revealed by convergent indels in the amino (N)-terminal domain of the spike protein

Riediger, Irina, Nascimento, Fernanda, Wallau, Gabriel L, Rovaris, Darcita Buerger, Coêlho, Danilo F, Fernandes, Sandra Bianchini, Neto, Lidio Gonçalves Lima, Abbud, Adriano, Dezordi, Filipe Zimmer, Debur, Maria do Carmo, Pereira, Felicidade Mota, Khouri, Ricardo, Nascimento, Valdinete, Silva, George, Delatorre, Edson, Lopes, Renata Serrano, Mendonça, Ana Carolina da Fonseca, Souza, Victor, Sacchi, Claudio, Bernardes, André Felipe Leal, Leite, Anderson Brandao, da Costa, Cristiano Fernandes, Lins, Roberto D, Ferraz, Matheus V. F, dos Santos, Cliomar Alves, Paixão, Anna Carolina Dias, da Rocha, Alice Sampaio Barreto, Bello, Gonzalo, Mattos, Tirza, Moreira, Emerson G, da Silva, Fabiano Vieira, Appolinario, Luciana, Naveca, Felipe G, Gräf, Tiago, Resende, Paola Cristina, Siqueira, Marilda Mendonça, Motta, Fernando Couto

2021

Overview

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.

• Publisher: Oxford University Press
• Subject: Rapid Communication