Table 2.
Overview of the ten most frequent mutations in a subset of 2,107 SARS-CoV-2 sequences analyzed in the period March 2020–January 2023 on the territory of the Republic of Serbia.
| Position of mutation | Percentage$ (total number) | Exact change | Timespan of appearance in Serbia | Functional effects | |
|---|---|---|---|---|---|
| 1 | S:614 | 100 (2107) | D614G | March 2020* | Increases viral replication in human lung epithelial cells, boosts viral loads in the COVID-19 patients’ upper respiratory tract (Korber et al., 2020; Li et al., 2022) |
| 2 | 5’UTR | 99.9 (2015) | C241T# | March 2020* | Most likely impacts viral RNA folding, packaging and titres (Mishra et al., 2020) |
| 3 | NSP3:106 | 99.7 (2100) | F106F | March 2020* | Possibly changes the codon usage and translation efficiency of NSP3, favouring the viral infection (Majumdar and Niyogi, 2021) |
| 4 | NSP12b:314 | 99.7 (2100) | P314L | March 2020* | Increases viral transmissibility in cooperation with D614G (Wang et al., 2021) |
| <0.1 (5) | P314F | July 2022 – November 2022 | Potentially impacts viral replication due to a change of fitness (Proust et al., 2023) | ||
| 5 | N:203/204 | 84.7 (1785) | R203K & G204R | March 2020* | Increases the binding of virus to cells (Raheja et al., 2022) |
| 8.0 (168) | R203M only | April 2020 – February 2022 | Leads to increased viral mRNA packaging and delivery (Syed et al., 2021) | ||
| <0.1 (44) | G204R only | August 2021 – January 2023 | Information not available | ||
| <0.1 (4) | R203K & G204P | May 2021, August 2022 | |||
| <0.1 (1) | R203K & G204L | March 2021 | |||
| 6 | S:478 | 77.7 (1638) | T478K | End of June 2021* | Probably affects viral infectivity and pathogenesis by changing spike gene’s receptor binding motif (Jhun et al., 2021) |
| 7 | NSP4:492 | 77.6 (1636) | T492I | End of June 2021* | Boosts viral transmissibility and infectivity by increasing the replication capacity and ability to evade host immune responses (Lin et al., 2023) |
| 8 | S:681 | 76.3 (1607) | P681H | December 2020* | Initially considered to enhance resistance to interferon-β through S cleavage (Lista et al., 2022), which was later refuted, suggesting other mutations associated with it may contribute to viral replication/transmission advantages (Lubinski et al., 2022) |
| 9 | NSP6:Δ3 amino acids | 72.2 (1521) | Δ(S106/G107/F108) | December 2020* | Antagonizes type I interferon response and provides fitness advantage (Hossain et al., 2022; Bills et al., 2023) |
| 4.0 (85) | Δ(L105/S106/G107) | December 2021 – June 2022 | Facilitates autophagy by favouring interaction with membrane (Hossain et al., 2022) | ||
| 10 | S:477 | 71.2 (1500) | S477N | September 2020* | Strengthens viral binding to the human ACE2 receptor (Singh et al., 2021) |
$Percentage calculated based on the total number of 2,107 samples; *Mutation present in all samples until the end of the study period; #Nucleotide change.