Despite the fact that the new variant showed mutations: HV69/70Δ, LLA241/243Δ, S477N, E484K, and P681H, indicating it was immune evasive and it was fast spreading in clusters in various geo-locations, the WHO, US CDC, ECDC played down about the emergence of the variant and strangely a lot of data about the variant , its mutations and predominance in genomic sequencings was not found on many open access sites or if it was found, it was shown to have not much significance.
Fast forward in January 2022, the U.S.CDC along with the Korea Disease Control and Prevention Agency (KCDC), Cheongju, South Korea along with the U.S. CDC publishes a preprint study reporting that new SARS-CoV-2 B.1.619 And B.1.620 variants that most probably originated from Cameroon and Kenya are now predominant in South Korea! https://wwwnc.cdc.gov/eid/article/28/2/21-1653_article
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We collected nasopharyngeal and oropharyngeal swab samples from patients with SARS-CoV-2 cases confirmed by real-time reverse transcription PCR (rRT-PCR). We prepared WGS libraries using QIAseq SARS-CoV-2 Primer Panel and QIAseq FX DNA Library UDI Kit (QIAGEN, https://www.qiagen.comExternal Link) and sequenced them on MiSeq (Illumina, https://www.illumina.comExternal Link) with 2 × 150 bp using MiSeq reagent kit version 2 (Illumina). For phylogenetic tree analysis, we aligned whole genomic sequences using MAFFT version 7 (https://mafft.cbrc.jp/alignment/serverExternal Link), inferred maximum-likelihood phylogenetic trees with FastTree version 2.1.9 (http://www.microbesonline.org/fasttreeExternal Link), and visualized using Interactive Tree of Life version 5 (https://itol.embl.deExternal Link). The sequences have been uploaded to the GISAID EpiCoV database (https://www.gisaid.orgExternal Link).
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.1.619 and B.1.620 increased sharply. Of those, 7,585 were domestic cases. As described previously (7), the A and B.41 lineages were the most prevalent at the beginning of the pandemic in South Korea. However, B.1.497 (formerly known as B.1.3.1) gained predominance in South Korea after its emergence in March 2020 (8,9). The lineage distribution has been changing since January 2021 as VOCs have emerged.
The earliest recorded Alpha variant in South Korea was identified on December 22, 2020; its prevalence increased to 22.0% as of June 2021 (Figure 1). Simultaneously, prevalence rates of B.1.619 and B.1.620 increased rapidly; prevalence was 55.4% in March 2021 and 11.5% in June 2021. The increase in the prevalence of these 2 lineages was rapid; it reached 67% in June, but decreased slightly when the Delta variant emerged in July. The prevalence of B.1.497 decreased from 94.3% to 0.9% in June 2021.
B.1.619 and B.1.620 were identified in imported cases in South Korea in 2021; B.1.619 in a case-patient from Cameroon in February and B.1.620 in cases from Kenya and Malawi in March. The phylogenetic analysis of SARS-CoV-2 sequences isolated in South Korea showed that B.1.619 and B.1.620 were distinct from those in countries in Europe (Figure 2); this finding indicates 1 or very few introduction events for B.1.619 and B.1.620 strains into South Korea, from which strains then spread rapidly.
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.