PMC:7558233 / 11816-13194 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7558233","sourcedb":"PMC","sourceid":"7558233","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7558233","text":"SARS-CoV-2 could evolve into diverse lineages with different magnitudes of virulence and transmissibility via mutations [25]. Several studies have documented a SARS-CoV-2 variant, aspartic acid (D) with substitution of glycine (G) at codon 614 in the S protein [25], [26], [27], [28], which is located on a B-cell epitope with a highly immunodominant region on the receptor binding domain. An in vitro study suggested that a D614G pseudotype variant was nine times more infectious than the D614 strains [29]. Strains carrying this mutation have become dominant since December 2019, and have been frequently observed in European countries (e.g., the Netherlands, Switzerland, and France) but not as frequently in China. Strikingly, the variant S-D614G distinguishes the SARS-CoV-2 strains that may have caused fatal infections in European populations [27]. A study on the alignment of 10 022 SARS-CoV-2 genomes from infected persons in 68 countries identified 6294 samples carrying the D614G mutation; almost all of these genomes also had another co-mutation in the proteins responsible for replication (ORF1ab P4715L; RdRp P323L) that might affect the speed of replication [28]. D614G was predicted to fine-tune the spike conformation and result in a loss of immunogenicity for B-cell recognition, a dominated process to stimulate adaptive immunity against SARS-CoV-2 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