Description
Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), the causative agent of COVID-19, has undergone continuous genomic evolution since its emergence in late 2019. Many of these changes occur in the viral spike (S) glycoprotein, which mediates host cell entry through binding to the angiotensin-converting enzyme 2 (ACE2) receptor. Mutations within the spike receptor-binding domain (RBD) can alter viral infectivity, transmissibility, and immune recognition, thereby shaping the epidemiology of circulating variants (Huang et al., 2020; Harvey et al., 2021).
This study conducted a meta-analysis to assess the prevalence of major spike mutations and their potential effects on infectivity. Approximately 5,000 adult SARS-CoV-2 genomic sequences covering the full spike region were obtained from the Global Initiative on Sharing All Influenza Data (GISAID) database, including 1,000 sequences each from the United States, Germany, Ghana, Brazil, and China. Pediatric cases were excluded. Mutations were identified by comparative genomic analysis using the wild-type SARS-CoV-2 genome as the reference and were grouped by geographic origin. The study focused on mutations associated with increased infectivity or immune escape, including D614G, N501Y, L452R/W, E484K/Q, K417N/T, N439K, Y453F, and T478K, as well as emerging Omicron-associated substitutions.
D614G was the most prevalent mutation across all regions, occurring in 80–90% of sequences and consistent with its known role in enhancing infectivity through improved spike stability and ACE2 interaction (Korber et al., 2020; Yurkovetskiy et al., 2020). N501Y was common in Germany, Brazil, and the United States, while L452R and T478K were frequent in the United States and Brazil. E484K and K417N were more prevalent in Brazil and Ghana. These findings highlight the widespread distribution of spike mutations linked to infectivity and immune evasion and underscore the importance of continued genomic surveillance.