<!--#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 10F10101005005 10I00000000 10R00000000 10V00000000 10Y00000000 11I50000005 11L50000005 13V00000000 20I001000000 20M00000000 20R00000000 20T551000500 20V00500000 23I001500000 24I101010101010-50 24F55555500 24M55555500 30N006000000 32I30151501515515 33F1005055105 33V00000000 33I00000000 35G00500050 36I00000000 36L00000000 36V00000000 36T00000000 43T000000100 46I1010205101050 46L10102051010100 46V101020551050 47V30151501553010 47A60153006053010 48V0103060103000 48M0103060103000 48A0103060101000 48S0103060101000 48T0103060101000 48Q0103060101000 48L0103060101000 50V6001515300-520 50L-5-5-5-5-1060-5-10 53L0001501000 53Y00000000 54L601020151515-1020 54M6015201515152020 54S101520151015200 54T101520151015200 54V101520151515200 54A101520151015200 58E005005150 63P00000000 71T00000000 71V00000000 71I50550500 71L50550500 73C510151551000 73S510151551000 73T510151551000 73A510151551000 73V55555500 74P10101510510205 74S001500000 76V60300-530-5-520 77I00000000 82A15303015301500 82F303030103015015 82I00000000 82S103030102525250 82T103030102525450 82M103030102510100 82L151010101010450 82C101010101010100 83D0101010010200 84A6060606060606030 84V6060606030603015 84C6060606030603010 85V00000000 88D003050500 88S-101560150600-5 88T0030001500 88G0030001500 89V55500005 89I00000000 89M00000000 89T00000000 90M20306040152500 93L00000000
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
4155
B
25465
C
9974
D
1649
F
1084
G
1380
AE
5827
AG
3694
 
A
214
B
9433
C
1063
D
241
F
1522
G
260
AE
115
AG
140
20 K R 14
I 4.4 		R 2.0 R 19 R 11
I 1.6
M 0.6 		R 30
M 1.8
I 1.3 		I 98
V 0.6 		R 16
I 2.3 		I 95
R 2.0
V 1.1 		 R 29
I 13
T 4.0
M 0.5
P 0.5 		R 13
I 7.8
T 3.8
M 2.4
V 1.1 		R 24
T 5.1
I 1.8
M 1.5 		R 23
T 12
M 6.2
I 4.4 		R 34
T 10.0
M 5.3
I 1.4
V 0.5 		I 93
T 4.8
V 1.2 		I 22
R 13
T 9.0 		I 88
R 4.4
V 3.6
M 1.5
T 0.7
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
K20E053954110.00 
K20E>=11316540.000.716
K20EAPV600  
K20EIDV11740  
K20ELPV8970  
K20ENFV115310.000.616
K20ESQV4530  
K20EATV2050  
K20ETPV00  
K20EDRV80  
MutationPINumSeqNumMut% Mutantp
K20I053954596511.00 
K20I>=11316512789.700.000
K20IAPV6023.300.089
K20IIDV117419016.100.000
K20ILPV897242.600.000
K20INFV11531149.800.228
K20ISQV453347.500.020
K20IATV20510.400.000
K20ITPV00  
K20IDRV80  
MutationPINumSeqNumMut% Mutantp
K20L053954240.00 
K20L>=113165170.100.001
K20LAPV600  
K20LIDV11740  
K20LLPV8970  
K20LNFV115320.100.190
K20LSQV45310.200.520
K20LATV2050  
K20LTPV00  
K20LDRV80  
MutationPINumSeqNumMut% Mutantp
K20M0539542030.30 
K20M>=1131653752.800.000
K20MAPV6011.600.565
K20MIDV1174141.100.000
K20MLPV89770.700.095
K20MNFV1153121.000.001
K20MSQV453153.300.000
K20MATV2050  
K20MTPV00  
K20MDRV80  
MutationPINumSeqNumMut% Mutantp
K20Q053954110.00 
K20Q>=11316590.000.010
K20QAPV600  
K20QIDV11740  
K20QLPV8970  
K20QNFV11530  
K20QSQV4530  
K20QATV2050  
K20QTPV00  
K20QDRV80  
MutationPINumSeqNumMut% Mutantp
K20R05395449879.20 
K20R>=113165247318.700.000
K20RAPV60610.001.000
K20RIDV1174897.500.058
K20RLPV89719721.900.000
K20RNFV1153716.100.000
K20RSQV453378.100.480
K20RATV205125.800.121
K20RTPV00  
K20RDRV8225.000.353
MutationPINumSeqNumMut% Mutantp
K20T053954460.00 
K20T>=1131656745.100.000
K20TAPV6011.600.050
K20TIDV1174110.900.000
K20TLPV89780.800.000
K20TNFV1153998.500.000
K20TSQV45381.700.000
K20TATV20562.900.000
K20TTPV00  
K20TDRV80  
MutationPINumSeqNumMut% Mutantp
K20V053954570.10 
K20V>=1131651220.900.000
K20VAPV600  
K20VIDV117440.300.051
K20VLPV8970  
K20VNFV115350.400.004
K20VSQV4530  
K20VATV2050  
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:
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  • 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.
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  • 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.
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  • 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.
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  • 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.
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