Stanford University HIV Drug Resistance Database - A curated public database designed to represent, store, and analyze the divergent forms of data underlying HIV drug resistance.

A curated public database designed to represent, store, and analyze the divergent forms of data underlying HIV drug resistance.

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PI Resistance Notes

Last updated on Jun 10, 2008
Resistance Matrix Resistance Mutation Comments Resistance Mutation Scores Drug Summaries
Protease Inhibitor (PI) Resistance Mutations
 232430323346474850†53547376†82848890
ConsLLDVVMIGIFIGLVINL
ATVr I  FILVVMLLVTALMST ATFSVACDSM
DRVr§   IF VA V LMSTV VAC M
FPVr I IFILVA V VTALMSTVATFSVAC M
IDVr I I ILV  LVTALMSTVAFTSVACSM
LPVr I IFILVAVMV VTALM VAFTSVAC M
NFVIIN FILVVM LVTALMST AFTSVACDSM
SQVr I     VM LVTALMST ATVACSM
TPVr   IFILV   VAM  ATFSLVAC M
LEGEND Mutations in bold have been shown to reduce in vitro suscep tib ility or in vivo virological response. Mutations in bold underline are relative contraindications to the use of specific PIs.
ADDITIONAL MUTATIONS Several additional uncommon mutations at the 17 positions in this table are also selected by PIs but have not been evaluated phenotypically including L24F, L33I, M46V, F53Y, I54S, G73CA, V82MC, and N88TG (S Rhee JID 2005). In constrast, V82I and L33V are polymorphisms that are not associated with PI therapy (http://hivdb.stanford.edu/cgi-bin/PRPosMutSummary.cgi).
ACCESSORY MUTATIONS Accessory protease mutations that are not in the table include the polymorphic mutations L10IV, I13V, K20RMI, M36I, D60E, I62V, L63P, A71VT, V77I, and I93L (F Mammano JV 1998, M Nijuis AIDS 1999, J Martinez-Picado JV 1999, N Hoffman Virology 2003) and the nonpolymorphic mutations L10FR, V11I, E34Q, E35G, K43T, K45I, K55R, Q58E, A71IL, T74PAS, V75I, N83D, P79AS, I85V, L89V, T91S, Q92K and C95F (T Wu JV 2003, N Parkin AIDS 2003, V Svicher AAC 2005).
†HYPERSUSCEPTIBILITY I50L increases susceptibility to all PIs except ATV (R Colonno JID 2004); I50V and I54L increase TPV susceptibility (R Elston HIVDRW 2006); N88S increases FPV susceptibility (R Ziermann 2006); L76V increases ATV, SQV, and TPV susceptibility (S Mueller HIVDRW 2004, H Vermeiren 2007).
§ A GSS for DRVr derived from the POWER trials identified 11 mutations at 10 positions: V11I, V32I, L33F, I47V, I50V, I54LM, G73S, L76V, I84V, L89V (S De Meyer ARHR 2008). In a subsequent update the substitution of T74P for G73S led to an improved model (S De Meyer Eur HIVDRW 2008).
A GSS for TPVr derived from the RESIST trials identified 21 mutations at 16 positions: L10V, I13V, K20MRV, L33F, E35G, M36I, K43T, M46L, I47V, I54AMV, Q58E, H69K, T74P, V82LT, N83D, and I84V (J Baxter JV 2006). An updated TPVr GSS excluded I13V, K20MRV, E35G, and H69K; reclassified I47V, I54AMV, Q58E, T74P, V82LT, and N83D as major mutations; reclassified L10V, M36I, K43T, M46L, and I84V as minor mutations; and included L24I, I50LV, I54L, and L76V as mutations likely to improve TPV susceptibility and virological response (J Scherer Eur HIV AIDS Conf 2007). A list of studies of genotypic PI response predictors can be found at http://hivdb.stanford.edu/pages/geno_clinical_review/PI.html.

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