TABLE 1.
Genotypic profiles and resistance phenotypes of reconstructed protease inhibitor escape virusesa
Virus | Protease inhibitor treatment | Mutation in HIV protease
|
Fold increase in IC90 | |||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
L10 | K20 | M36 | M46 | G48 | F53 | I54 | L63 | A71 | V82 | I84 | L90 | |||
202post | Ritonavir | R | I | Pb | S | 10 | ||||||||
246post | Saquinavir | I | V | Pb | M | 10 | ||||||||
401post | Ritonavir | R | I | V | A | 8.9 | ||||||||
402post | Ritonavir | Ib | R | Ib | I | L | Pb | Vb | A | 14.1 | ||||
506post | Ritonavir | R | Pb | A | M | 19 |
The amino acid substitutions conferring HIV resistance to saquinavir and ritonavir are indicated in the single-letter code. The IC90 was measured in a single-cycle resistance assay on P4 cells with the protease inhibitor included in the treatment as described in Materials and Methods. The results are expressed as the fold increase in the IC90 compared to the value for a recombinant virus carrying the parental pretherapy protease.
Already present in pretherapy virus.