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.

PI-Resistance Mutations and Response to New PI-Containing Regimens

Three fundamental types of correlations form the basis of drug resistance knowledge: (i) Correlations between genotypic data with the treatments of persons from whom sequenced HIV-1 isolates have been obtained (genotype-treatment); (ii) Correlations between genotype and in vitro drug susceptibility (genotype-phenotype); and (iii) Correlations between genotype and the clinical response to a new treatment regimen (genotype-outcome). The following table summarizes the results of published studies linking genotype and the clinical response to a new PI-containing regimen.

Nearly all publications on genotype and clinical outcome have described only the results of their analyses. None have published their underlying data, in part, because until now there had been no resource for making such data publicly available. As this database has now been modified to represent such data we have written to the authors of those studies that are most relevant today to request such data.
Darunavir (DRV/r)
ReferencePrevious PIFollow-up PIOther RxNo.PtsWkEffect of Baseline Mutations on Response
Descamps (2009)
Treated. 100% PI pretreated, median PI (IQR): 4 (3-5)   OBT: NRTI +/- NNRTI +/- T20 153 48 VR: VL< 200 copies/mL at month 3 (main) and 6. Cochran-Armitage test used to detect mutations impact. Mutations associated with negative impact: K14R, K20I, E34Q, I47V, L54M, K55R, T74P and I84V. Mutations associated with positive impact : K20R, E35D and V82A. Insufficient data were available to evalute I50V and L76V
De Meyer (2008) TITAN
Treated. 69% previuosly used a PI. All LPV/r naives   OBT: at least two antiretroviral drugs (NRTIs] with or without NNRTIs) on the basis of screening resistance data and history of antiretroviral treatment 595 48 DRV vs LPV Response (defined as RNA < 50 copies/ml) according to the number of the following pre-therapy mutations: D30N, V32I, L33F, M46I/L, I47A/V, G48V, I50L/V, I54L/M, L76V, V82A/F/L/S/T, I84V, N88S, and L90M => 0 mutations: 84% vs 80%, 1 mutations: 84% vs 68%, 2 mutations: 74% vs 52%, >=3 mutations: 84% vs 38%
De Meyer (2008) POWER>=1 PI (and >=1 of 30N, 46IL, 48V,50LV, 82AFST, 84V,90M); median 5 PIs, 6 NRTIs, 1 NNRTIDRV/r (600 mg / 100 mg) BIDOB +/- T20377 (DRV/r)24V11I, V32I, L33F, I47V, I50V, I54L/M, G73S, L76V, I84V, and L89V at baseline were associated with a decreased VR to DRV/r. About 60% with 0, 45% with 1-2, and <=20% with >=3 DRMs had RNA <50 copies/ml at wk 24. In phenotypic studies, I50V, I54M, L76V, and I84V reduced susceptibility to the greatest extent. V32I emerged in 30% of failures according to prescribing information.
De Meyer (2008) POWER follow-up study combined with DUET-1 and 2   467 (DRV/r in POWER) + 604 (DRV/r + placebo-treated in DUET-1 and 2)24Ten of the 11 mutations (all except G73S) in the study above and a new mutation T74P were associated with a decreased VR (defined by RNA <50 copies/ml) at W24. In patients who did not received T20, harboring >=3 of these mutations were associated a decreased VR.
Pellegrin (2008) PREDIZISTA>=1 PI; median 5 PIs, 6 NRTIs and NNRTI-experienced (91%)DRV/r (600 mg / 100 mg) BID2 NRTIs +/- 1 PI +/- T20671226(40%) of patients resulted in VF which was defined as RNA >2.3 at W12. I13V, V32I, L33F/I/V, E35D, M36I/L/V, I47V, F53L,I62V at baseline were associated with increased VF. Adjusted OR for resulting in a VF for one addition of these mutations was 6.2. 11% with <4 , 48% with 4-5 and 100% with >5 these mutations resulted in a VF.
De Luca (2011) Retrospective >=1 PI; Median 7 PIs DRV/r OBT: T20 (23%) +/- RAL (15%) +/- NNRTI (6%) +/- MVC (5%) 21717 ( +/-9) VR defined as (i) VL decrease by >=2 log10 or to <50 copies/ml by12W; (ii) VL <50 after 12W. VR was 62% (135/217). The DRV-2009 score [V11I+L33F+R41K+I47V+2*I50V +2*I54M+K55R+D60E+L74P+L76V+ N88D+2*L89V-L10I/V -I13V-G16E- G48V-F53I/L-I62V-I66F-V77I], indicate susceptibility (<0), intermediate resistance (0-1), resistance (>=2).
Tipranavir (TPV/r)
ReferencePrevious PIFollow-up PIOther RxNo.PtsWkEffect of Baseline Mutations on Response
Baxter (2006) RESIST-1 (1182,12; NCT00054717) and -2 (1182.48; NCT00144170) + 3 phase II studies (1182.2, 1182.4, 1182,51, 1182.52)>=2 PIs (and >=1 of 30N, 46IL, 48V,50LV, 82AFLST, 84V, 90M but <3 mutations at codons 33, 82, 84, or 90); median 4 PIs, 6 NRTIs, 1 NNRTITPV/r (500 mg / 200 mg) BIDOB +/- T20688 (TPV/r)2421 mutations at 16 positions were found to correlate with a decreased VR to TPV/r salvage therapy: L10V, I13V, K20M/R/V, L33F, E35G, M36I, K43T, M46L, I47V, I54A/M/V, Q58E, H69K, T74P, V82L/T, N83D, I84V. Each additional mutation was associated with a 0.04 log decreased 2-week and 0.16 log decreased 24 week response. The 24 week response dropped from 1.3 logs when 3 mutations were present to 0.64 logs when 4 mutations were present and was completely lost when 8 mutations were present. Note: The vast majority of isolates used to derive the list belonged to subtype B which is relevant because I13V, K20 mutations, M36I, and H69K are highly common in several non-B subtypes.
Hall (2008)
RESIST (phase II/III) follow-up study
In a weighted genotypic susceptibility score (GSS), T74P (weight=7), I47V (6), V82L/T (5), Q58E (5), N83D (4) were the best predictors of poor virologic response; whereas I54A/M/V (3), I84V (2), M36I (2), K43T (2), L10V (1), and M46V (1) were weaker predictors whereas L24I (-2), I50L/V (-4), I54L (-7), and L76V (-2) were predictors of virolgic response.
Naeger (2007)
RESIST-1 and 2 FDA analysis
Virologic response rates in TPV/r-treated participants werereduced when isolates with amino acid substitutions at positions I13, V32, M36, I47, Q58, D60, I84 or substitutions V82S/F/I/L were present at baseline
Marcelin (2008) ANRS networkMedian 4 PIs, 6 NRTIs; NNRTI-experienced (80%); T20-experienced (28%)TPV/r (500 mg / 200 mg) BIDNRTIs +/- T20 +/- NNRTI1431279 (55%) patients achieved VR defined by a decrease of >= 1 log or a BLQ in RNA level at week 12. Baseline mutations at 6 positions found to be associated with a lower VR and one with a higher VR were used for GSS: E35D/G/K/N + M36I/L/V - F53L/W/Y + Q58E + Q61D/E/G/H/N/R + H69I/K/N/Q/R/Y + L89I/M/R/T/V. 100% patients with a GSS of -1, 79% with 0, 56% with 1, 33% with 2, 21% with 3 and 0% with 4 achieved VR.
Lopinavir (LPV, LPV/r)
ReferencePrevious PIFollow-up PIOther RxNo.PtsWkEffect of Baseline Mutations on Response
Kempf (2002)>=1 PILPV/rNRTIs + EFV5072DRMs at 11 positions were associated with decreased VR: 10, 20, 24, 46, 53, 54, 63, 71, 82, 84, and 90. 21/23 with 0-5, 15/21 with 6-7 mutations, and 2/6 with 8-10 of these DRM had RNA <400 at W72.
Masquelier (2002)>=2 PIsLPV/rHighly variable681234% of pts had RNA <400. Lack of response was associated with the baseline DRMs M46I, I54V, and V82A and with >=5 of the Kempf DRMs.
Bongiovanni (2003)>=1 PILPV/rNRTIs ± NNRTIs1341271/112 pts with <5 and 5/22 pts with >=6 Kempf DRM had RNA <50 at W12.
Loutfy (2004)>=1 PILPV/rHighly variable4564-12In univariate analyses, the DRMs most predictive of VF were M46I, Q58E, V82A/F/T, and L90M. The most predictive 3-mutation combination was L10F/I/R/V, M46I, and V82A/T/F.
Delaugerre (2004)PI-naïve (21); >=1 PI (48)LPV/rNRTIs (PI-naïve) + NNRTI6924-72Among the PI-experienced pts, L10I/F, M46I, I54V/L, A71V/I, V82A/F/S/T, and L90M were associated with VF.
King (2007) 3.1 previous PIs (excluding ATV, TPV, DRV)LPV/rOB7929-23Mutations at positions 10, 20, 24, 33, 36, 47, 48, 54, 82, and 84 were associated with decreased likelihood of 1.0 log10 RNA decrease or RNA <400. Mutations at positions 46, 53, 63, 71, 90 from the original score were not significantly associated with response in a multivariate analysis.
Marcelin (2005) Median of 3 (range 1-5)LPV/rOB11624The Genotypic Inhibitory Quotient (GIQ) defined as the median LPV Cmin concentration divided by the number of mutations at the following positions (10, 20, 24, 33, 36, 47, 48, 54, 82, 84). In a multivariate analysis, the GIQ but not the number of mutations was significantly associated with VR.
Grant (2008)LPV/r-naive (100%); ARV-experienced (97%); PI-experienced (79%).LPV/rOB1032476% patients achieved VR defined by RNA <500 at W24. Baseline mutations at positions 10, 54 and 82 and at positions 54, 84, 90 were associated with poor VR in univariate and in multivariate analyses, respectively.
Fosamprenavir (FPV, FPV/r)
ReferencePrevious PIFollow-up PIOther RxNo.PtsWkEffect of Baseline Mutations on Response
Duval (2002)>=1 PIAPV (1,200 mg BID)vs APV/r (450-900 mg / 100 mg BID)NRTIs + EFV2224Most pts had >= 1 DRM at position 46, 54, 82, or 90. 13/14 receiving APV/r vs 2/8 receiving APV had HIV-1 RNA <200 at W24.
Marcelin (2003)>=1 PIAPV/r (600 mg / 100 mg BID)NRTIs491270% of 49 pts achieved RNA <400. Lack of response was associated with >5 of the following DRM: L10F/I/V, K20M/R, E35D, R41K, I54V, L63P, V82A/F/T/S, and I84V.
Clevenbergh (2004)>=1 PIAPV/r(APV 600 mg BID, RTV 100 mg BID)Highly variable3916No. DRM in the 2002 French ANRS algorithm (L10I, V32I, M46I/L, I47V, I50V, I54L/M/V, G73S, V82A/F/I/T/S, I84V, L90M) correlated with RNA changes. Median RNA decrease was 1.4 logs in 25 pts with <=3 DRM and 0.3 logs in 14 patients with >=4 DRM.
Lastere (2004)>=1 PIAPV (1,200 mg BID)Highly variable8412In univariate and multivariate analyses DRMs at positions 10, 20, 36, 73, 82, and 90, and gag p6 PTAPP insertions were associated with poorer VR.
Pellegrin (2007)Median of 3 (range 1:5); 26% had received APVFPV/r (700/100 BID)OB1211210IFRV, 33F, 36I, 46IL, 54LMTV, 62V, 63P, 71ILVT, 73ACST, 82AFST, 84V, and 90M were associated with decreased VR. The presence of <4 mutations was associated with a median 2.3 log decrease whereas the presence of >=4 was associated with a 0.1 log decrease.
Masquelier (2008)>=1 PIFPV/r (700 mg / 100 mg) BIDOB6312L10F/I/V, L33F, M46I/L, I47V, I54L/M/V/A/T/S, A71V, G73C/S/A/T, V82A/F/C/G, and L90M were associated with a decreased VR; V77I and N88S were associated with an increased VR.
Marcelin (2007) CONTEXT and TRIAD studies>=1 PIFPV/r (700/100 BID)Usually 2 NRTIs11312The mutations I15V + M46IL + I54LMV + D60E + L63PT +I84V. Persons with 0 or 1 mutation had a mean 2 log decrease, those with 2 mutations had a median 1.5 log decrease, and those with >=3 mutations had <=0.6 log decreases. Mutations at positions 10, 33, 73, and 90 were negatively associated with response in univariate analyses. In this APV/FPV-naive population, no patient had V32I, I47V, or I50V.
Saquinavir (SQV, SQV/r)
ReferencePrevious PIFollow-up PIOther RxNo.PtsWkEffect of Baseline Mutations on Response
Harrigan (1999) PI-naïve (30); >=1 PI (37)SQV/r
(400-600 mg of each BID)
NA6724M46I/L, G48V, I54V, A71V/T, V82A/T, I84V, and L90M were weakly associated with a poor VR
Tebas (1999)NFVSQV/r
(400 mg of each BID)
NRTIs2424At baseline, 13 had D30N and 5 had L90M. 17/24 had RNA <500 and 10/24 had RNA <50 at W24. Insufficient data to establish association with baseline genotype.
Zolopa (1999) >=1 PISQV/r
(400-600 mg SQV; 300-400 mg RTV BID)
NRTIs5426RNA decrease of >=0.5 occurred in patients with <= 3 of mutations at positions 46, 48, 54, 82, 84, and 90. D30N did not affect response to SQV/r.
Marcelin (2004) >=1 PISQV/r
(800 mg SQV and 100 mg RTV BID)
NRTIs7216L10F/I/R/V, L24I, M46I/L, G48V, I54V, I62V, A71V/T, V82A/T/F/S, I84V, and L90M were univariate predictors. L24I, I62V, V82A/T/F/S, I84V, and L90M were the best predictors in multivariate analyses: Patients with 0, 1, and >=2 of these 5 mutations had a median 2.2, 1.2, and 0.3 log RNA decrease.
Indinavir (IDV, IDV/r)
ReferencePrevious PIFollow-up PIOther RxNo.PtsWkEffect of Baseline Mutations on Response
Para (2000)SQV (>=12M)IDV
(800 mg TID)
NRTIs518Mutations at positions 10, 20, 48, 82, 84, and 90 predicted a decreased VR at W8. 0 mutations: 1.7 log decrease, 1 mutation: -1.1 log decrease, 2-5 mutations: 0.3 log decrease.
Saah (2003)NFVIDV
(1000 mg TID)
EFV2948D30N occurred in 17 and L90M in 11. RNA <500 occurred in 9/17 with D30N vs 2/11 with L90M.
Shulman (2002)IDV ± PIs other than RTVIDV/r
(400 mg of IDV and RTV BID)
NRTIs314810/14 vs 3/14 subjects with >=3 mutations at the following positions responded to RTV boosting: 10, 20, 30, 32, 33, 36, 46, 47, 48, 50, 54, 71, 73, 77, 82, 84, 88, 90
Campo (2003)>= 1 PI(26/28 IDV, 15/28 RTV)IDV/r
(IDV 800 mg and RTV 200 mg BID)
NRTIs ± NNRTIs2824VR correlated better with adherence than the pattern of drug-resistance mutations.
Nelfinavir (NFV, NFV/SQV)
ReferencePrevious PIFollow-up PIOther RxNo.PtsWkEffect of Baseline Mutations on Response
Lawrence (1999)SQVNFV
(750 mg TID)
NRTI1624No sustained responses were observed. L90M was associated with more rapid VF.
Walmsley (2001)>=1 PI(SQV, IDV, RTV)NFV
(750 mg TID)
NRTIs ± NNRTIs6324 -4841% and 22% had RNA declines >=0.5 logs at 24 and 48 weeks respectively. Mutations at position 48, 82, 84, and/or 90 were present in 69% and were correlated with a poor VR.
Casado (2001)IDV ± RTVNFV/SQV
(NFV 750-1250 mg; SQV 600-1000 mg BID-TID)
d4T/NVP3126 -5235% and 56% of patients had RNA <50 after 6 and 12 months. L90M (0% vs 43%) but not V82A (38% vs 36%) decreased the rate of response.
Atazanavir (ATV, ATV/r)
ReferencePrevious PIFollow-up PIOther RxNo.PtsWkEffect of Baseline Mutations on Response
Johnson (2005)>=1 PIATV/r (ATV 300 mg; RTV 100 mg QD)2-NRTI including TDF12048At baseline, 15%, 41%, 19%, and 25% of pts had a median of 0, 1-2, 3-4, or ³4 DRMs at the following positions: 10, 20, 24, 33, 36, 46, 48, 54, 63, 71, 73, 82, 84, and 90 [Colonno, 2003 #2420]. Overall, 38% achieved RNA <50 copies/ml including 44% with <4 DRM and 25% with >=4 DRMs
Naeger (2006)
AI424045 FDA's analyses
The authors selected a priori mutations at the following positions for their analysis: D30, V32, M36, M46, I47, G48, I50, I54, A71, G73, V77, V82, I84, N88, and L90. Virological response (defined as attaining RNA level < 400 copies/ml) was <30% when M36I, M46I/L/V, or V82A/F/T/S was present in combination with >=3 of the above mutations. It was <20% when G73S/A/C, I84V or L90M were present with >=3 of the above mutations.
Vora (2006)>=1 PIATV/r(ATV 300 mg; RTV 100 mg QD)OB621213 PI mutations at baseline were associated with a reduced VR: 10F/I/V, 16E, 33F/I/V, 46I/L, 60E, 84V, 85V, and 90M. RNA decrease >1 log occurred in 100% with <2 mutations, 80% with 2 mutations, 43% with 3 mutations, and 0% with 4-5 mutations. In a follow-up study of 53 patients (Marcelin 2006), only four mutations (L10F/I/V, L33F/I, I84V, and L90M were predictive of reduced response, although the original score remained predictive.
Pellegrin (2006)>=1 PI; median 5 PIs, 6 NRTIs, 1 NNRTIATV/r (300 mg / 100 mg) QD2NRTIs (75%), 1 additional PI (17%); T20 (4%)7112L10F/I/V. K20M/R, L24I, M46I/L, Q58E, L63P, G73S/A, V77I, V82A/F/S/T, I84A/V, L90M were associated with failure to reach RNA <50 copies/ml (p<=0.1) in a univariate analysis. A score that also included I54L/M/T/V, A71I/L/V/T was significantly associated with response in that 63% of persons with <5 total mutations vs 11% with >=5 total mutations had RNA <50 copies/ml. G16E and D60E occurred at baseline in 5 and 9 persons, respectively, but were not associated with VR.
Bertoli (2006) Drug Resistance Workshop, Sitges Spain, 2006>=1 PIATV/r (300 mg / 100 mg) QD; ATV 400 mg QDOB74 ATV/r; 85 ATV12 - 24For ATV/r, L10C/I/V, V32I, E34Q, M46I/L, F53L, I54A/M/V, V82A/F/I/T, and I84V reduced probability of RNA < 50 (92%, 83%, 75%, and 0% when 0, 1, 2, or >=3 mutations were present respectively). For ATV, G16E, K20I/M/R/T/V, V32I, L33F/I/V, F53L/Y, I64L/M/V, A71I/T/V, I85V, and I93L/M reduced probability of RNA < 50 (83%, 67%, 6%, and 0% for 0, 1-2, 3, or >=4 mutations, respectively).


  • Pts: patients
  • W: week
  • M: month
  • NA: not available
  • BID: twice a day
  • BLQ: below the limit of quantification
  • DRM: drug-resistance mutation
  • OB: optimized background
  • OR: odds ratio
  • PI: protease inhibitor
  • NRTI: nucleoside RT inhibitor
  • NNRTI: non-nucleoside RT inhibitor
  • Rx: regimen
  • TAMs: thymidine analogue mutations
  • TID: three times a day
  • VR: virologic response
  • VF: virologic failure
  • APV: amprenavir
  • ATV: atazanavir
  • DRV: darunavir
  • d4T: stavudine
  • EFV: efavirenz
  • ETR: etravirine
  • IDV: indinavir
  • LPV: lopinavir
  • NFV: nelfinavir
  • NVP: nevirapine
  • RTV: ritonavir
  • SQV: saquinavir
  • TPV: tipranavir
  • TDF: tenofovir
  • Baxter J.D., Schapiro J.M., Boucher C.A., Kohlbrenner V.M., Hall D.B., Scherer J.R., Mayers D.L. Genotypic changes in human immunodeficiency virus type 1 protease associated with reduced susceptibility and virologic response to the protease inhibitor tipranavir. J Virol. 2006 Nov;80(21):10794-801.
  • Bertoli, A., M. Santoro, P. Lorenzini, F. Ceccherini-Silberstein, A. Lazzarin, G. Di Perri, D. Esposito, P. Caramello, A. Cargme, A. Cargnel, P. Narciso, G. Rizzrdini, G. Filice, L. Minoli, G. Carosi, A. Antinori, and C.F. Perno. 2006. Different patterns of mutations involved in the genotypic resistance score for atazanavir boosted versus atazanavir unboosted in multiplying failing patients. HIVDRW2006.
  • Bongiovanni M., Bini T., Adorni F., Meraviglia P., Capetti A., Tordato F., Cicconi P., Chiesa E., Cordier L., Cargnel A., Landonio S., Rusconi S., d'Arminio Monforte A. Virological success of lopinavir/ritonavir salvage regimen is affected by an increasing number of lopinavir/ritonavir-related mutations. Antivir Ther. 2003 Jun;8(3):209-14.
  • Campo R.E., Moreno J.N., Suarez G., Miller N., Kolber M.A., Holder D.J., Shivaprakash M., DeAngelis D.M., Wright J.L., Schleif W.A., Emini E.A., Condra J.H. Efficacy of indinavir-ritonavir-based regimens in HIV-1-infected patients with prior protease inhibitor failures. AIDS. 2003 Sep 5;17(13):1933-9.
  • Casado J.L., Dronda F., Hertogs K., Sabido R., Antela A., Marti-Belda P., Dehertogh P., Moreno S. Efficacy, tolerance, and pharmacokinetics of the combination of stavudine, nevirapine, nelfinavir, and saquinavir as salvage regimen after ritonavir or indinavir failure. AIDS Res Hum Retroviruses. 2001 Jan 20;17(2):93-8.
  • Clevenbergh P., Boulme R., Kirstetter M., Dellamonica P. Efficacy, safety and predictive factors of virological success of a boosted amprenavir-based salvage regimen in heavily antiretroviral-experienced HIV-1-infected patients. HIV Med. 2004 Jul;5(4):284-8.
  • Delaugerre C., Teglas J.P., Treluyer J.M., Vaz P., Jullien V., Veber F., Rouzioux C., Chaix M.L., Blanche S. J Acquir Immune Defic Syndr. 2004 Oct 1;37(2):1269-75. Predictive factors of virologic success in HIV-1-infected children treated with lopinavir/ritonavir.
  • de Meyer S., Vangeneugden T., van Baelen B., de Paepe E., van Marck H., Picchio G., Lefebvre E., de Bethune M.P. Resistance profile of darunavir: combined 24-week results from the POWER trials. AIDS Res Hum Retroviruses. 2008 Mar;24(3):379-88.
  • de Meyer S., Dierynck I., Lathouwers E., van Baelen B., Vangeneugden T., Spinosa-Guzman S., Peeters M., Picchio G., de Bethune M-P. Phenotypic and genotypic determinants of resistance to darunavir: analysis of data from treatment-experienced patients in POWER 1,2,3 and DUET-1 and 2 [abstract 31]. Antiviral Therapy. 2008; 13 Suppl 3:A33
  • Duval X., Lamotte C., Race E., Descamps D., Damond F., Clavel F., Leport C., Peytavin G., Vilde J.L. Amprenavir inhibitory quotient and virological response in human immunodeficiency virus-infected patients on an amprenavir-containing salvage regimen without or with ritonavir. Antimicrob Agents Chemother. 2002 Feb;46(2):570-4.
  • Grant P, Wong EC, Rode R, Shafer R, Deluca A, Nadler J, Hawkins T, Cohen C, Harrington R, Kempf D, Zolopa A. Virologic Response to Lopinavir/Ritonavir-Based Antiretroviral Regimens in a Multi-Center International Clinical Cohort: Comparison of Genotypic Interpretation Scores. Antimicrob Agents Chemother. 2008 Aug 18.
  • Hall D.B., Baxter J., Schapiro J., Boucher C.A.B., Tilke C., Scherer J. Mutations 24I, 50L/V, 54L, and 76V, selected by other protease inhibitors, predict durable response to tipranavir in treatment experienced patients when two or more are present [abstract 124]. Antiviral Therapy. 2008; 13 Suppl 3:A136.
  • Harrigan P.R., Hertogs K., Verbiest W., Pauwels R., Larder B., Kemp S., Bloor S., Yip B., Hogg R., Alexander C., Montaner J.S. Baseline HIV drug resistance profile predicts response to ritonavir-saquinavir protease inhibitor therapy in a community setting. AIDS. 1999 Oct 1;13(14):1863-71
  • Johnson M., Grinsztejn B., Rodriguez C., Coco J., DeJesus E., Lazzarin A., Lichtenstein K., Rightmire A., Sankoh S., Wilber R. Atazanavir plus ritonavir or saquinavir, and lopinavir/ritonavir in patients experiencing multiple virological failures. AIDS. 2005 Apr 29;19(7):685-94. Corrected and republished from: AIDS. 2005 Jan 28;19(2):153-62.
  • Kempf D.J., Isaacson J.D., King M.S., Brun S.C., Sylte J., Richards B., Bernstein B., Rode R., Sun E. Analysis of the virological response with respect to baseline viral phenotype and genotype in protease inhibitor-experienced HIV-1-infected patients receiving lopinavir/ritonavir therapy. Antivir Ther. 2002 Sep;7(3):165-74.
  • King M.S., Rode R., Cohen-Codar I., Calvez V., Marcelin A.G., Hanna G.J., Kempf D.J. Predictive genotypic algorithm for virologic response to lopinavir-ritonavir in protease inhibitor-experienced patients. Antimicrob Agents Chemother. 2007 Sep;51(9):3067-74. Erratum in: Antimicrob Agents Chemother. 2008 Feb;52(2):811.
  • Lastere S., Dalban C., Collin G., Descamps D., Girard P.M., Clavel F., Costagliola D., Brun-Vezinet F. Impact of insertions in the HIV-1 p6 PTAPP region on the virological response to amprenavir. Antivir Ther. 2004 Apr;9(2):221-7.
  • Lawrence J., Schapiro J., Winters M., Montoya J., Zolopa A., Pesano R., Efron B., Winslow D., Merigan T.C. Clinical resistance patterns and responses to two sequential protease inhibitor regimens in saquinavir and reverse transcriptase inhibitor-experienced persons. J Infect Dis. 1999 Jun;179(6):1356-64.
  • Loutfy M.R., Raboud J.M., Walmsley S.L., Saskin R., Montaner J.S., Hogg R.S., Thompson C.A., Harrigan P.R. Predictive value of HIV-1 protease genotype and virtual phenotype on the virological response to lopinavir/ritonavir-containing salvage regimens. Antivir Ther. 2004 Aug;9(4):595-602.
  • Marcelin A.G., Dalban C., Peytavin G., Lamotte C., Agher R., Delaugerre C., Wirden M., Conan F., Dantin S., Katlama C., Costagliola D., Calvez V. Clinically relevant interpretation of genotype and relationship to plasma drug concentrations for resistance to saquinavir-ritonavir in human immunodeficiency virus type 1 protease inhibitor-experienced patients. Antimicrob Agents Chemother. 2004 Dec;48(12):4687-92.
  • Marcelin A.G., Flandre P., Molina J.M., Katlama C., Yeni P., Raffi F., Wirden M., Antoun Z, Khaled M.A., Vincent Calvez V. Genotypic Analysis of the Virological Response to Fosamprenavir/Ritonavir in Clinical Trials: Context and Triad 14th Conference on Retroviruses and Opportunistic Infections, CROI, Los Angeles, Feb. 25-28, 2007.
  • Marcelin A.G., Lamotte C., Delaugerre C., Ktorza N., Ait Mohand H., Cacace R., Bonmarchand M., Wirden M., Simon A., Bossi P., Bricaire F., Costagliola D., Katlama C., Peytavin G., Calvez V. Genotypic inhibitory quotient as predictor of virological response to ritonavir-amprenavir in human immunodeficiency virus type 1 protease inhibitor-experienced patients. Antimicrob Agents Chemother. 2003 Feb;47(2):594-600.
  • Marcelin AG, Masquelier B, Descamps D, Izopet J, Charpentier C, Alloui C, Bouvier-Alias M, Signori-Schmuck A, Montes B, Chaix ML, Amiel C, Santos GD, Ruffault A, Barin F, Peytavin G, Lavignon M, Flandre P, Calvez V. Tipranavir-ritonavir genotypic resistance score in protease inhibitor-experienced patients. Antimicrob Agents Chemother. 2008 Sep;52(9):3237-43
  • Masquelier B., Assoumou K.L., Descamps D., Bocket L., Cottalorda J., Ruffault A., Marcelin A.G., Morand-Joubert L., Tamalet C., Charpentier C., Peytavin G., Antoun Z., Brun-Vezinet F., Costagliola D. Clinically validated mutation scores for HIV-1 resistance to fosamprenavir/ritonavir. J Antimicrob Chemother. 2008 Jun;61(6):1362-1368.
  • Masquelier B., Breilh D., Neau D., Lawson-Ayayi S., Lavignolle V., Ragnaud J.M., Dupon M., Morlat P., Dabis F., Fleury H. Human immunodeficiency virus type 1 genotypic and pharmacokinetic determinants of the virological response to lopinavir-ritonavir-containing therapy in protease inhibitor-experienced patients. Antimicrob Agents Chemother. 2002 Sep;46(9):2926-32.
  • Marcelin A.G., Cohen-Codar I., King M.S., Colson P., Guillevic E., Descamps D., Lamotte C., Schneider V., Ritter J., Segondy M., Peigue-Lafeuille H., Morand-Joubert L., Schmuck A., Ruffault A., Palmer P., Chaix M.L., Mackiewicz V., Brodard V., Izopet J., Cottalorda J., Kohli E., Chauvin J.P., Kempf D.J., Peytavin G., Calvez V. Virological and pharmacological parameters predicting the response to lopinavir-ritonavir in heavily protease inhibitor-experienced patients. Antimicrob Agents Chemother. 2005 May;49(5):1720-6.
  • Para M.F., Glidden D.V., Coombs R.W., Collier A.C., Condra J.H., Craig C., Bassett R., Leavitt R., Snyder S., McAuliffe V., Boucher C. Baseline human immunodeficiency virus type 1 phenotype, genotype, and RNA response after switching from long-term hard-capsule saquinavir to indinavir or soft-gel-capsule saquinavir in AIDS clinical trials group protocol 333. J Infect Dis. 2000 Sep;182(3):733-43.
  • Pellegrin I., Breilh D., Coureau G., Boucher S., Neau D., Merel P., Lacoste D., Fleury H., Saux M.C., Pellegrin J.L., Lazaro E., Dabis F., Thiebaut R. Interpretation of genotype and pharmacokinetics for resistance to fosamprenavir-ritonavir-based regimens in antiretroviral-experienced patients. Antimicrob Agents Chemother. 2007 Apr;51(4):1473-80.
  • Pellegrin I., Breilh D., Ragnaud J.M., Boucher S., Neau D., Fleury H., Schrive M.H., Saux M.C., Pellegrin J.L., Lazaro E., Vray M. Virological responses to atazanavir-ritonavir-based regimens: resistance-substitutions score and pharmacokinetic parameters (Reyaphar study). Antivir Ther. 2006;11(4):421-9.
  • Pellegrin I, Wittkop L, Joubert LM, Neau D, Bollens D, Bonarek M, Girard PM, Fleury H, Winters B, Saux MC, Pellegrin JL, Thiébaut R, Breilh D; ANRS Co3 Aquitaine Cohort. Virological response to darunavir/ritonavir-based regimens in antiretroviral-experienced patients (PREDIZISTA study). Antivir Ther. 2008;13(2):271-9.
  • Saah A.J., Haas D.W., DiNubile M.J., Chen J., Holder D.J., Rhodes R.R., Shivaprakash M., Bakshi K.K., Danovich R.M., Graham D.J., Condra J.H. Treatment with indinavir, efavirenz, and adefovir after failure of nelfinavir therapy. J Infect Dis. 2003 Apr 1;187(7):1157-62.
  • Shulman N., Zolopa A., Havlir D., Hsu A., Renz C., Boller S., Jiang P., Rode R., Gallant J., Race E., Kempf D.J., Sun E. Virtual inhibitory quotient predicts response to ritonavir boosting of indinavir-based therapy in human immunodeficiency virus-infected patients with ongoing viremia. Antimicrob Agents Chemother. 2002 Dec;46(12):3907-16.
  • Tebas P., Patick A.K., Kane E.M., Klebert M.K., Simpson J.H., Erice A., Powderly W.G., Henry K. Virologic responses to a ritonavir--saquinavir-containing regimen in patients who had previously failed nelfinavir. AIDS. 1999 Feb 4;13(2):F23-8. Comment in: AIDS. 2000 Mar 10;14(4):466-8.
  • Vora S., Marcelin A.G., Gunthard H.F., Flandre P., Hirsch H.H., Masquelier B., Zinkernagel A., Peytavin G., Calvez V., Perrin L., Yerly S. Clinical validation of atazanavir/ritonavir genotypic resistance score in protease inhibitor-experienced patients. AIDS. 2006 Jan 2;20(1):35-40.
  • Walmsley S.L., Becker M.I., Zhang M., Humar A., Harrigan P.R. Predictors of virological response in HIV-infected patients to salvage antiretroviral therapy that includes nelfinavir. Antivir Ther. 2001 Mar;6(1):47-54.
  • Zolopa A.R., Shafer R.W., Warford A., Montoya J.G., Hsu P., Katzenstein D., Merigan T.C., Efron B. HIV-1 genotypic resistance patterns predict response to saquinavir-ritonavir therapy in patients in whom previous protease inhibitor therapy had failed. Ann Intern Med. 1999 Dec 7;131(11):813-21.