TABLE 7.
INSTI resistance mutations and estimated INSTI resistance levels for sequences with differences in genotypic resistance testing results by Sanger sequencing and NGS
| Sample group and sample identifier | DRM detected by: |
Sanger sequencing score → NGS scorea |
||||
|---|---|---|---|---|---|---|
| Sanger sequencing and NGS | Sanger sequencing alone | NGS alone | DTG | EVG | RAL | |
| Samples for which NGS reported higher levels of resistance to ≥1 INSTIs | ||||||
| B3-17 | 148H | 140S | 3 → 4 | 5 | 5 | |
| B3-41 | 97A, 138A, 143C | 155H | 3 | 4 → 5 | 5 | |
| Samples for which Sanger sequencing or NGS detected different DRMs but for which levels of INSTI resistance were the same | ||||||
| B1-33b | 138A, 140A, 148R | 163R | 5 | 5 | 5 | |
| B3-07 | 155H | 157Q | 2 | 5 | 5 | |
| B3-09 | 155H, 163K | 97A | 2 | 5 | 5 | |
| B3-25b | 155H | 97A, 163K | 2 | 5 | 5 | |
a
Predicted levels of drug resistance according to the HIVDB genotypic resistance interpretation system, which were scored as follows: 1 for susceptible, 2 for potential low-level resistance, 3 for low-level resistance, 4 for intermediate resistance, and 5 for high-level resistance. DTG, dolutegravir; EVG, elvitegravir; RAL, raltegravir.
b
Samples B1-33 and B3-25 had weak evidence for an APOBEC-mediated G-to-A hypermutation. G163R and G163K are accessory INSTI resistance mutations that occur in the APOBEC dinucleotide context.