Table 1.
HIV-1 group M viruses developing integrase mutations during in vitro passage experimentsa
| Position (Cons) |
|||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|
| 51 | 66 | 92 | 118 | 138 | 140 | 147 | 148 | 153 | 263 | ||
| AuthorYr | Parent virusb | (H) | (T) | (E) | (G) | (E) | (G) | (S) | (Q) | (S) | (R) |
| Kobayashi11 | NL43 | F/Y | |||||||||
| Quashie12 | clinical (n = 3) | K | |||||||||
| clinical | K | K | |||||||||
| clinical | Y | K | |||||||||
| clinical (C) | Y | R | |||||||||
| clinical (C) | Y | T | |||||||||
| clinical (02) | R | ||||||||||
| clinical (02) | Y | K | |||||||||
| Oliveira14 | NL43 | K | |||||||||
| NL43-118R | I | K | |||||||||
| NL43-51Y/263K | K | ||||||||||
| Anstett15 | NL43 | K | |||||||||
| NL43-92Q | K | ||||||||||
| NL43-140S | R | ||||||||||
| NL43-140S/148R | Y | ||||||||||
| NL43-155H | K | ||||||||||
| Departureaux15 | NL43 | Y | |||||||||
| Seki15 | NL43 | Q | |||||||||
| NL43-148H | K | S | |||||||||
| NL43-148K | K | ||||||||||
| NL43-148R | K | S | |||||||||
| Brenner16 | NL43-118R | I | K | ||||||||
| clinical-118R (C) | A | K | |||||||||
| Oliveira16 | NL43 | F | K | ||||||||
| Brenner17 | clinical | Y | |||||||||
| clinical (n = 6) | K | ||||||||||
| clinical | F | K | |||||||||
| clinical (n = 2) | Y | ||||||||||
| Andreatta18 | LAI (n = 2) | Y | |||||||||
| LAI-155H | N | ||||||||||
| LAI-148R | K | ||||||||||
| Oliveira18 | NL43 | K | |||||||||
| NL43-157Q | K | ||||||||||
| clinical | Y | ||||||||||
| clinical (n = 6) | K | ||||||||||
| clinical | Y | G | |||||||||
| clinical | F | ||||||||||
| clinical (C) | K | ||||||||||
| clinical (01) | K | ||||||||||
| clinical (02) | K | ||||||||||
| clinical-157Q (n = 3) | K | ||||||||||
| clinical-157Q (D) | K | ||||||||||
| clinical-157Q (D) | F | ||||||||||
Cons, consensus subtype B amino acid.
Columns contain established non-polymorphic INSTI resistance mutations. Mutations not shown include: M50I in two non-mutated viruses (Quashie12 and Oliveria14); E157Q in two viruses (Oliveira18); 101I/124A (Kobayashi11); 262K with NL43-51Y (Oliveira14); 75I/97A/154I in addition to 138K/140S in NL43-148H (Seki15); 193E with 51Y/153T in Clinical (C) (Quashie12) and with 92Q in NL43 (Seki15); 234F with 153Y in LAI (Andreatta18); 144D in LAI with the RT mutation 184V; 95K/146R in Clinical (Oliveira18).
Clinical: virus isolates obtained from INSTI-naive individuals lacking known INSTI resistance mutations. NL43 and LAI are WT laboratory strains. Drug-resistance mutations in laboratory strains were placed by site-directed mutagenesis. Non-B subtypes are indicated in parentheses: C, D, CRF01_AE (01), and CRF02_AG (02). Replicate experiments yielding the same results are followed by the number of experiments (n) in parentheses. Notes: 22 subtype B are not shown including one developing polypurine tract mutations and 21 that did not develop mutations, including those with parent viruses 92Q (2), 92Q/155H (1), 51Y/118R (1), 143C (1), 143R (1), 148R (1), 155H (1), 263K (2), RT-65R (1), RT-184V/I (2) and 8 without mutations.