key: cord-0876851-nwn8htrp authors: Park, Ae Kyung; Kim, Il-Hwan; Man Kim, Heui; Lee, Hyeokjin; Lee, Nam-Joo; Kim, Jeong-Ah; Woo, SangHee; Lee, Chae young; Lee, Jaehee; Oh, Sae Jin; Rhee, JeeEun; Yoo, Cheon-Kwon; Kim, Eun-Jin title: SARS-CoV-2 B.1.619 and B.1.620 Lineages, South Korea, 2021 date: 2022-02-03 journal: Emerg Infect Dis DOI: 10.3201/eid2802.211653 sha: c95d47ff7af32535a87878d97ebaf7e009b4886b doc_id: 876851 cord_uid: nwn8htrp We report the rapid emergence of severe acute respiratory syndrome coronavirus 2 lineages B.1.619 and B.1.620 in South Korea. The surge in frequency in a relatively short time emphasizes the need for ongoing monitoring for new lineages to track potential increases in transmissibility and disease severity and reductions in vaccine efficacy. Genomic surveillance and open data sharing of viral genome sequences have enhanced near-realtime detection, comparison, and tracking of SARS-CoV-2 variants (1). The Korea Disease Control and Prevention Agency (KDCA) has been conducting whole-genome sequencing (WGS) of SARS-CoV-2 in South Korea since the beginning of the pandemic; targeted sequencing of the spike protein is being implemented to strengthen new variant monitoring. Lineage distribution analysis in South Korea indicated that, from its discovery in March 2020 until January 2021, the B.1.497 lineage was predominant in domestic cases (7, 8) . B.1.497 formed 1 of 4 major clusters in South Korea but was the only one that had expanded and predominantly circulated in the country (9) . Sequence analysis indicated that it was originally clustered with North American viruses; additional genetic mutations in this cluster are H1113Y, T2408N, P4223S, and A5770S in open reading frame 1ab (ORF1ab) and Q52H, A222V, E556K, T716I, and A1070V in the spike protein. However, changes have been observed in lineage distribution since March 2021; increases in B.1.619 and B.1.620 are of note. We report the sudden emergence of these 2 lineages harboring the E484K mutation in the spike protein, which rapidly outcompeted the existing variants in South Korea. We collected nasopharyngeal and oropharyngeal swab samples from patients with SARS-CoV-2 cases confi rmed by real-time reverse transcription PCR (rRT-PCR We obtained WGS of 9,554 SARS-CoV-2 as of July 21, 2021, representing >5% of the total reported positive cases during this period. Specifically, we obtained WGS for 6.2% of the total positive cases during April-July, when the number of infections by B. As described previously (7) B.1.620 was prevalent in central Africa and later spread to Europe and the United States through travelers (10) . We were unable to find previous research on B.1.619 in the literature; however, we assumed that B.1.619 was a prevalent strain in central Africa and later spread to Europe because it has been identified in central Africa, according to information from GISAID. The B.1.619 and B.1.620 lineages have several characteristic spike protein mutations (Table 1) ; the E484K mutation, which is present in both Beta and Gamma variants and has been identified as an escape mutation (11) , is the only shared mutation in both lineages. The mutations in the spike protein, specifically in the RBD, have a strong influence on SARS-CoV-2 pathogenesis; B.1.619 has additional N440K mutations in the RBD and B.1.620 has S447N substitutions. The S477N mutation may evade antibody-mediated immunity (12) and increase RBD affinity for ACE2 (13) . In addition, the N440K mutation might confer resistance to monoclonal antibodies and enhance binding affinity to the ACE2 receptor (13, 14) . We observed no other specific mutation in the spike protein in B.1.619. In contrast, B.1.620 carries several mutations and deletions, previously observed individually in VOCs and VOIs ( Table 1) . The HV69/70Δ, Y144Δ, P681H, and D1118H mutations in the spike protein have been found in the Alpha variant, whereas the LAL242/243/244Δ mutation has been found in the Beta variant. Previously, we found that B.1.619 and 620 have no inhibitory effect on the neutralizing activity in vaccinated or convalescent persons (S.J. Oh et al., unpub. data). However, the combined effect of these mutations on viral pathogenicity and transmissibility needs to be elucidated. Continuous monitoring of mutations is essential to track potential vaccine efficacy reduction, increased transmissibility, and disease severity. The transmissibility of B.1.619 and B.1.620 and their likelihood to cause more severe infections are not yet confirmed. Preliminary data show that patients who recovered from non-VOC/VOI and vaccinated persons have sufficient neutralizing capacity against these lineages ( Table 2 ). The transmissibility and immune escape of these strains must be investigated further. Continuous genomic surveillance supporting public health response is required to overcome the COVID-19 pandemic. ORF1a T265I, P3884L A2123V, E2607K, del3675/3677, M3752I T403I, V1991I, del3675/3677 ORF1b P314L, Q2403L P314L P314L, A1215S S D614G I210T, N440K, E484K, D614G, D936N, S939F, T1027I P26S, del69/70, V126A, del144/145, S477N, E484K, D614G, P681H, T1027I, Global initiative on sharing all influenza data-from vision to reality Functional assessment of cell entry and receptor usage for SARS-CoV-2 and other lineage B betacoronaviruses SARS-CoV-2 spike-protein D614G mutation increases virion spike density and infectivity World Health Organization. Weekly epidemiological update on COVID-19-1 European Centre for Disease Prevention and Control. SARS-CoV-2 variants of concern as of 3 Characterization of the emerging B.1.621 variant of interest of SARS-CoV-2 Genomic surveillance of SARS-CoV-2: distribution of clades in South Korea in 2020. Osong Public Health Res Perspect A dynamic nomenclature proposal for SARS-CoV-2 to assist genomic epidemiology Genomic epidemiology reveals the reduction of the introduction and spread of SARS-CoV-2 after implementing control strategies in Republic of Korea Center for Viral Systems Biology. B.1.619.1 lineage report. 2021 COVID-19 Genomics UK (COG-UK) Consortium. SARS-CoV-2 variants, spike mutations and immune escape Identification of SARS-CoV-2 spike mutations that attenuate monoclonal and serum antibody neutralization Deep mutational scanning of SARS-CoV-2 receptor binding domain reveals constraints on folding and ACE2 binding Escape from neutralizing antibodies by SARS-CoV-2 spike protein variants We thank the authors of the originating laboratories and the submitting laboratories who have deposited and shared genome data on GISAID's EpiCoV (https://www.gisaid.org) database.