<!--#if expr="$title" --> <!--#echo var="title" --> <!--#else --> HIV Drug Resistance Database <!--#endif -->
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.

MARVEL on protease mutations at position 20


HIVdb Algorithm: Comments & Scores
  • K20I is the consensus amino acid in subtype G and CRF02_AG. In subtypes B and C, K20I is a PI-selected mutation that appears to reduce NFV susceptibility.
  • K20M/V are rare, relatively nonpolymorphic PI-selected mutations that have not been well studied.
  • K20R is a highly polymorphic, PI-selected accessory mutation that improves HIV-1 replication fitness in viruses with other PI-resistance mutations.
  • K20T is a nonpolymorphic accessory PI-selected mutation that is associated with reduced susceptibility to each of the PIs except SQV and TPV.

MutationFPV/rIDV/rNFVSQV/rLPV/rATV/rTPV/rDRV/r
K20I001000000
K20M00000000
K20R00000000
K20T551000500
K20V00500000
Footnote:Mutation scores on the left are derived from published literature linking mutations and ARVs (the complete details can be found in the HIVdb Release Notes).
Genotype-treatment correlation
Mutation frequency according to subtype and drug-class experience.
The frequency of each mutation at position 20 according to subtype and drug-class experience. Data are shown for the 8 most common subtypes. The number of persons in each subtype/treatment category is shown beneath the subtype. Mutations occurring at a frequency >0.5% are shown. Each mutation is also a hyper-link to a separate web page with information on each isolate, including literature references with PubMed abstracts, the GenBank accession number, and complete sequence and treatment records.

PosWTPI Naive Persons PI Treated Persons
A
5054
B
29747
C
10662
D
1989
F
1112
G
1687
AE
6239
AG
4331
 
A
332
B
9558
C
1209
D
299
F
1526
G
339
AE
186
AG
224
20 K R 14
I 4.5 		R 2.1 R 19 R 11
I 1.4
M 0.8 		R 30
M 1.8
I 1.3 		I 98
V 0.5 		R 16
I 2.2 		I 95
R 2.0
V 1.0 		 R 23
I 13
T 3.9 		R 13
I 7.8
T 3.7
M 2.4
V 1.1 		R 24
T 4.9
I 1.9
M 1.4 		R 24
T 10.0
M 5.3
I 4.3 		R 35
T 10.0
M 5.2
I 1.4
V 0.5 		I 93
T 4.0
V 1.9 		I 22
R 16
T 6.7 		I 90
V 3.7
R 3.2
M 0.9
T 0.5
Footnote: The query page Mutation Prevalence According to Subtype and Treatment to examine the frequency of all mutations according to subtype and treatment; The program HIVSeq provides similar output for mutations in user-submitted sequences; A complete description of the program that generates these tables can be found at Rhee et al AIDS 2006.
 

Mutation frequency according to treatment with individual ARVs.
The first row shows the frequency of the mutation in persons who are PI-naive (indicated in green). The second row shows the frequency of the mutation in persons who have received one or more PIs. The following rows show the frequency of the mutation in persons who have received only a single PI. Mutation rates that differ significantly between treated and untreated isolates are indicated in yellow.
MutationPINumSeqNumMut% Mutantp
K20E061159120.00 
K20E>=11374240.000.715
K20EAPV730  
K20EIDV11760  
K20ELPV11160  
K20ENFV116910.000.601
K20ESQV4550  
K20EATV2160  
K20ETPV00  
K20EDRV80  
MutationPINumSeqNumMut% Mutantp
K20I061159688811.20 
K20I>=113742146910.600.056
K20IAPV7334.100.081
K20IIDV117619016.100.000
K20ILPV11161059.400.058
K20INFV116911710.000.194
K20ISQV455347.400.013
K20IATV21641.800.000
K20ITPV00  
K20IDRV80  
MutationPINumSeqNumMut% Mutantp
K20L061159260.00 
K20L>=113742180.100.000
K20LAPV730  
K20LIDV11760  
K20LLPV111610.000.975
K20LNFV116920.100.174
K20LSQV45510.200.499
K20LATV2160  
K20LTPV00  
K20LDRV80  
MutationPINumSeqNumMut% Mutantp
K20M0611592300.30 
K20M>=1137423772.700.000
K20MAPV7311.300.668
K20MIDV1176141.100.000
K20MLPV111670.600.269
K20MNFV1169121.000.001
K20MSQV455153.200.000
K20MATV2160  
K20MTPV00  
K20MDRV80  
MutationPINumSeqNumMut% Mutantp
K20Q061159110.00 
K20Q>=11374290.000.005
K20QAPV730  
K20QIDV11760  
K20QLPV11160  
K20QNFV11690  
K20QSQV4550  
K20QATV2160  
K20QTPV00  
K20QDRV80  
MutationPINumSeqNumMut% Mutantp
K20R06115955769.10 
K20R>=113742254818.500.000
K20RAPV73912.300.454
K20RIDV1176897.500.075
K20RLPV111622420.000.000
K20RNFV1169726.100.001
K20RSQV455378.100.518
K20RATV216136.000.144
K20RTPV00  
K20RDRV8225.000.344
MutationPINumSeqNumMut% Mutantp
K20T061159530.00 
K20T>=1137426854.900.000
K20TAPV7322.700.000
K20TIDV1176110.900.000
K20TLPV1116100.800.000
K20TNFV11691018.600.000
K20TSQV45581.700.000
K20TATV21662.700.000
K20TTPV00  
K20TDRV80  
MutationPINumSeqNumMut% Mutantp
K20V061159620.10 
K20V>=1137421290.900.000
K20VAPV730  
K20VIDV117640.300.041
K20VLPV111620.100.739
K20VNFV116950.400.003
K20VSQV4550  
K20VATV2160  
K20VTPV00  
K20VDRV80  
Footnote: Data are not shown for TPV or DRV because there are no data available from persons who have developed virological failure after receiving just one of these PIs; About one-half of the untreated isolates belong to non-subtype B isolates; About 20% of the treated isolates belong to non-subtype B isolates; A page containing summaries for all of the mutations at this position can be found here.

Genotype-phenotype correlation
Phenotypes of top 10 common patterns of drug resistance mutations with mutations at position 20.
Mutation pattern data is not available for K20.

A complete summary of additional in vitro susceptibility data for viruses with K20 obtained using other assays including the Antivirogram can be found here.

 

Phenotypic coefficients using machine learning
Least Square Regression (LSR) was used to learn the relative contribution of each mutation to the fold decrease in susceptibility for an ARV. The figure on the left (click to enlarge the figure) shows the regression coefficients (which correlate with the contribution to resistance) for the 35 nonpolymorphic PI-resistance mutations shown to contribute decreased susceptibility to at least one PI. A complete description of the method that generates this figure can be found at Rhee et al PNAS 2006.

 

Genotype-clinical outcome correlation
Studies correlating baseline genotype and virological response to an ARV therapy with or without mutations at 20.

ReferencePreviousPIFollowUpPIOther RxNo.PtsWeeksEffect 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.
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 >4 DRMs at the following positions: 10, 20, 24, 33, 36, 46, 48, 54, 63, 71, 73, 82, 84, and 90. Overall, 38% achieved RNA <50 copies/ml including 44% with <4 DRM and 25% with >=4 DRMs
Bertoli(2006)>=1 PIATV/r (300 mg / 100 mg) QD; ATV 400 mg QDOB7412-24For 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).
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.
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.
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 +/- T2037724V11I, 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		   46724Ten of the 11 mutations (all except G73S: V11I, V32I, L33F, I47V, I50V, I54L/M, G73S, L76V, I84V, and L89V) in the previous De Meyer 2008 study 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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Lawrence(1999)SQVNFV (750 mg TID)NRTI1624No sustained responses were observed. L90M was associated with more rapid VF.
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.
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.
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
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 +/- T206882421 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		>=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 +/- T206888/48In 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.
Marcelin(2008)Median 4 PIs, 6 NRTIs; NNRTI-experienced (80%); T20-experienced (28%)TPV/r (500 mg / 200 mg) BIDNRTIs +/- T20 +/- NNRTI6881279 (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.
Abbreviations:
    DRM - drug-resistance mutation; OB - optimized background; BID - twice a day; VR - virologic response; VF - virologic failure; OR - odds ratio; BLQ - below the limit of quantification;

References:
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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., 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • 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

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