<!--#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 63


HIVdb Algorithm: Comments & Scores

MutationFPV/rIDV/rNFVSQV/rLPV/rATV/rTPV/rDRV/r
L63P00000000
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 63 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
5192
B
31479
C
11223
D
2096
F
1265
G
1846
AE
6774
AG
4526
 
A
337
B
9559
C
1209
D
299
F
1526
G
339
AE
186
AG
224
63 L P 11
T 4.8
S 4.6
V 3.5
A 2.1
H 0.7
I 0.7
Q 0.4
M 0.3
C 0.3
N 0.2
F 0.1
G 0.1
P 56
A 6.8
S 6.4
T 5.7
C 2.8
Q 1.9
H 1.7
V 0.6
N 0.4
R 0.2
E 0.1
D 0.1
I 0.1
P 34
T 8.5
V 7.3
S 4.7
A 2.7
H 1.5
Q 1.1
I 0.9
C 0.5
N 0.2
M 0.2
F 0.1
E 0.1
R 0.1
G 0.1
P 33
T 7.2
S 7.0
Q 6.0
A 3.4
H 2.0
C 1.4
V 1.0
N 0.4
R 0.4
E 0.3
I 0.3
F 0.1
K 0.1
M 0.1
G 0.1
T 22
S 11
P 8.7
A 4.2
C 3.2
V 2.8
Q 1.7
I 1.0
H 0.8
G 0.7
N 0.3
R 0.3
D 0.2
F 0.1
E 0.1
M 0.1
P 19
S 2.5
T 1.2
H 1.1
A 0.9
V 0.6
Q 0.6
M 0.5
C 0.4
I 0.4
F 0.1
N 0.1
P 12
C 4.8
S 3.3
T 2.4
V 1.5
A 1.1
H 0.5
I 0.5
Q 0.3
M 0.2
F 0.1
N 0.1
R 0.1
G 0.1
P 15
S 4.2
H 1.9
T 1.6
V 1.1
A 0.8
I 0.8
Q 0.4
F 0.2
N 0.2
M 0.2
C 0.2
Y 0.1
R 0.1
 P 18
T 8.6
V 6.4
S 2.6
Q 1.3
I 1.0
A 0.6
N 0.6
H 0.6
M 0.3
D 0.3
P 74
A 3.2
S 3.0
T 2.7
Q 1.8
H 1.7
C 1.3
V 0.4
N 0.2
E 0.2
R 0.2
M 0.1
D 0.1
P 42
T 8.3
V 8.3
S 3.0
A 2.2
H 1.5
Q 1.2
C 0.7
I 0.7
N 0.2
R 0.2
E 0.1
M 0.1
D 0.1
P 59
T 7.1
S 4.2
A 3.9
C 3.5
H 2.1
V 1.8
Q 1.8
R 0.7
G 0.7
N 0.4
E 0.4
D 0.4
P 24
T 9.2
C 5.3
S 4.8
A 3.8
V 2.4
Q 1.2
G 1.0
H 0.9
I 0.7
N 0.4
D 0.4
E 0.1
M 0.1
R 0.1
P 24
S 1.3
Q 0.6
C 0.6
I 0.6
V 0.6
H 0.3
A 0.3
T 0.3
P 20
C 7.3
T 5.6
V 2.2
H 1.1
I 1.1
S 0.6
A 0.6
Q 0.6
R 0.6
P 21
S 3.8
T 1.4
H 1.4
V 1.0
R 1.0
A 0.5
M 0.5
C 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
L63A06661930784.60 
L63A>=1138994373.100.000
L63AAPV7368.200.236
L63AIDV1174363.000.014
L63ALPV1258342.700.002
L63ANFV1172342.900.007
L63ASQV457173.700.422
L63AATV215104.600.888
L63ATPV00  
L63ADRV80  
MutationPINumSeqNumMut% Mutantp
L63C06661913091.90 
L63C>=1138992351.600.035
L63CAPV7311.300.956
L63CIDV117460.500.001
L63CLPV1258221.700.656
L63CNFV117270.500.001
L63CSQV45781.700.872
L63CATV21520.900.397
L63CTPV00  
L63CDRV80  
MutationPINumSeqNumMut% Mutantp
L63D066619700.10 
L63D>=113899230.100.077
L63DAPV730  
L63DIDV117410.000.805
L63DLPV125830.200.319
L63DNFV11720  
L63DSQV4570  
L63DATV2150  
L63DTPV00  
L63DDRV80  
MutationPINumSeqNumMut% Mutantp
L63E066619440.00 
L63E>=113899250.100.000
L63EAPV730  
L63EIDV117410.000.749
L63ELPV12580  
L63ENFV117210.000.751
L63ESQV45730.600.000
L63EATV2150  
L63ETPV00  
L63EDRV80  
MutationPINumSeqNumMut% Mutantp
L63F066619700.10 
L63F>=11389930.000.005
L63FAPV730  
L63FIDV11740  
L63FLPV125810.000.872
L63FNFV11720  
L63FSQV4570  
L63FATV2150  
L63FTPV00  
L63FDRV80  
MutationPINumSeqNumMut% Mutantp
L63G066619570.00 
L63G>=113899250.100.002
L63GAPV730  
L63GIDV11740  
L63GLPV12580  
L63GNFV11720  
L63GSQV4570  
L63GATV21520.900.003
L63GTPV00  
L63GDRV80  
MutationPINumSeqNumMut% Mutantp
L63H06661914292.10 
L63H>=1138992261.600.000
L63HAPV7311.300.956
L63HIDV1174171.400.124
L63HLPV1258292.300.772
L63HNFV1172141.100.033
L63HSQV457132.800.386
L63HATV21562.700.677
L63HTPV00  
L63HDRV80  
MutationPINumSeqNumMut% Mutantp
L63I0666194390.60 
L63I>=113899470.300.000
L63IAPV7311.300.975
L63IIDV117420.100.060
L63ILPV1258161.200.014
L63INFV117220.100.060
L63ISQV45720.400.769
L63IATV21510.400.944
L63ITPV00  
L63IDRV80  
MutationPINumSeqNumMut% Mutantp
L63M066619910.10 
L63M>=113899110.000.109
L63MAPV730  
L63MIDV11740  
L63MLPV125820.100.862
L63MNFV117210.000.944
L63MSQV4570  
L63MATV2150  
L63MTPV00  
L63MDRV80  
MutationPINumSeqNumMut% Mutantp
L63N0666192270.30 
L63N>=113899330.200.061
L63NAPV730  
L63NIDV11740  
L63NLPV125810.000.180
L63NNFV117220.100.459
L63NSQV4570  
L63NATV21510.400.784
L63NTPV00  
L63NDRV80  
MutationPINumSeqNumMut% Mutantp
L63P0666192614939.20 
L63P>=113899854561.400.000
L63PAPV733041.000.840
L63PIDV117466656.700.000
L63PLPV125851240.600.311
L63PNFV117267657.600.000
L63PSQV45725956.600.000
L63PATV21511754.400.000
L63PTPV00  
L63PDRV8225.000.643
MutationPINumSeqNumMut% Mutantp
L63Q0666199111.30 
L63Q>=1138992041.400.379
L63QAPV7322.700.614
L63QIDV1174151.200.893
L63QLPV1258181.400.944
L63QNFV1172161.300.906
L63QSQV45761.300.920
L63QATV21520.900.797
L63QTPV00  
L63QDRV80  
MutationPINumSeqNumMut% Mutantp
L63R0666191060.10 
L63R>=113899380.200.005
L63RAPV7311.300.263
L63RIDV117420.100.784
L63RLPV125860.400.016
L63RNFV117270.500.001
L63RSQV45720.400.371
L63RATV21510.400.790
L63RTPV00  
L63RDRV80  
MutationPINumSeqNumMut% Mutantp
L63S06661934455.10 
L63S>=1138994122.900.000
L63SAPV7368.200.363
L63SIDV1174504.200.182
L63SLPV1258483.800.036
L63SNFV1172363.000.002
L63SSQV457122.600.019
L63SATV215188.300.050
L63STPV00  
L63SDRV80  
MutationPINumSeqNumMut% Mutantp
L63T06661938295.70 
L63T>=1138995543.900.000
L63TAPV7322.700.394
L63TIDV1174605.100.386
L63TLPV1258846.600.180
L63TNFV1172342.900.000
L63TSQV457183.900.120
L63TATV21583.700.259
L63TTPV00  
L63TDRV80  
MutationPINumSeqNumMut% Mutantp
L63V06661914862.20 
L63V>=1138992311.600.000
L63VAPV7334.100.490
L63VIDV1174110.900.004
L63VLPV1258745.800.000
L63VNFV1172181.500.133
L63VSQV45751.000.138
L63VATV2150  
L63VTPV00  
L63VDRV80  
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 63.
Mutation pattern data is not available for L63.

A complete summary of additional in vitro susceptibility data for viruses with L63 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 63.

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;

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