Table 1.
Summary of characteristic of variants of interest (VOIs) and concern (VOCs)
| Variants | Mutations in the S protein | Potential drugsa | |||
|---|---|---|---|---|---|
| NTD | RBD | S1-CTD | S2 domain | ||
|
Alpha (B.1.1.7) |
Δ69–70, ΔY144, | N501Y, | A570D, P681H | T716I, S982A, D1118H | Most of RBD-directed mAbs |
|
Beta (B.1.351) |
L18F, D80A, D215G, R246I, | K417N, E484K, N501Y | D614G, | A701V | Some mAbs (such as C135, COVA1–16, S309, REGN10987, AZD1061, AZD7442, mAb222, Casirivimab and imdevimab),360,361 and PF-07321332362 |
|
Gamma (P.1) |
L18F, T20N, P26S, D138Y, R190S, | K417T, E484K, N501Y, | D614G, H655Y, | T1027I, | Some mAbs (such as S309, mAb222, AZD7442, AZD1061, and REGN10987, Casirivimab and imdevimab)360,363 |
| Delta (B.1.617.2) | T19R, G142D, Δ156–157, R158G, | L452R, T478K, | D614G, P681R, | D950N | Some mAbs (such as Sotrovimab, BRII-198, BRII-196, Bamlanivimab, Etesevimab, Casirivimab, and imdevimab)364,365 and Molnupiravir366 |
|
Epsilon (B.1.427/9) |
S13I, W152C | L452R | D614G | / | Nucleoside analog Sangivamycin367 |
|
Zeta (P.2) |
L18F, T20N, P26S, F157L, | E484K, | D614G, | S929I, V1176F | Nucleoside analog Sangivamycin; and PF-07321332362 |
|
Eta (B.1.525) |
Q52R, A67V, Δ69–70, Δ144, | E484K, | D614G, D677H | F888L | Some mAbs, such as Casirivimab and imdevimab |
|
Lota (B.1.526) |
L5F, T95I, D253G, | S477N, E484K, | D614G | A701V | Some mAbs, such as Casirivimab and imdevimab |
|
Kappa (B.1.617.1) |
G142D, E154K | L452R, E484Q, | D614G, P681R, | Q1071H | Some mAbs, such as Casirivimab and imdevimab; Molnupiravir366 |
|
Lambda (C.47) |
G75V, T76I, Δ246–252, | L452Q, F490S, | D614G | T859N | Some mAbs (such as Casirivimab and imdevimab) and PF-07321332 |
|
Mu (B.1.621) |
T95I, Y144S, Y145N, | R346K, E484K, N501Y, | D614G, P681H | D950N | Molnupiravir366 |
| Omicron (B.1.1.529) | A67V, Δ69–70, T95I, G142D, Δ143–145, Δ211, Y145D, L212I, ins214EPE, | G339D, S371L, S373P, S375F, K417N, N440K, G446S, S477N, T478K, E484A, Q493R, G496S, Q498R, N501Y, Y505H, | T547K, D614G, H655Y, N679K, P681H, | N764K, D796Y, N856K, Q954H, N969K, L981F |
(1) Some mAbs: VIR-7831, VIR-7832, DXP-604 and BRII-198 (2) Ribonucleoside analogs that target to Nsp12 (3) Protease inhibitors that target to Nsp3, Nsp5 and other protease participated in virus infection |
aVaccines in this table are not listed, and vaccines efficacy and effectiveness against variants can be obtained at https://www.who.int/publications/m/item/draft-landscape-of-covid-19-candidate-vaccines. Moreover, booster vaccination is still the best strategy to prevent SARS-CoV-2 variants at present
S13I, L18F, 69–70del, 141–143del, 144del, W152C R246I/M, K417N/T/M, L452R, N440K, S477G/N/R, E484K/A/Q/P, Q493K/R, N501Y, H655Y mutations are associated with antibody evasion
S477G/N/R, N501Y, D614G mutations increase the binding affinity of S protein to ACE2
L452R, P681H/R mutation increase virus transmissibility
69–70del, P681H/R increase virus infectivity
69–70del, K417N mutation is related to the conformational change of S protein