<!--#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 48

HIVdb Algorithm: Comments & Scores
  • G48V causes high-level resistance to SQV, intermediate-level resistance to ATV and NFV, and low-level resistance to IDV and LPV. G48M is a less common mutation that appears to have similar effects on PI susceptibility. G48A/S/T/Q are rare nonpolymorphic PI-selected mutations that occur in patients who have received multiple PIs.
  • G48V is a nonpolymorphic substrate-cleft mutation selected by SQV and, less often, by IDV and LPV. It confers high-level resistance to SQV, intermediate-level resistance to ATV, and low-level resistance to NFV, IDV and LPV.
  • G48V is a nonpolymorphic substrate-cleft mutation selected by SQV and, less often, by IDV and LPV. It confers high-level resistance to SQV, intermediate-level resistance to ATV, and low-level resistance to NFV, IDV and LPV. G48M is a 2-base pair nonpolymorphic mutation selected in patients who have received multiple PIs. It causes high-level resistance to SQV, intermediate-level resistance to ATV and NFV and low-level resistance to IDV and LPV.

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 48 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
48 G        R 0.1  V 1.5
R 0.6
Q 0.3
M 0.3
V 3.2
M 0.5
A 0.3
S 0.1
E 0.1
Q 0.1
L 0.1
V 0.6
A 0.1
A 0.4
V 0.4
V 2.1
M 0.7
A 0.6
S 0.2
W 0.1
T 0.1
E 0.1
Q 0.1
V 1.8
Q 0.5
M 0.5
V 4.2
M 0.3
I 0.1
V 1.2
A 0.8
T 0.4
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
MutationPINumSeqNumMut% Mutantp
MutationPINumSeqNumMut% Mutantp
MutationPINumSeqNumMut% Mutantp
MutationPINumSeqNumMut% Mutantp
MutationPINumSeqNumMut% Mutantp
MutationPINumSeqNumMut% Mutantp
MutationPINumSeqNumMut% Mutantp
MutationPINumSeqNumMut% Mutantp
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 48.
Mutation patterns are listed in the frequency with which they have been reported in the published literature. The median level of fold resistance (compared with wildtype) for viruses with the mutation pattern in the first column are indicated when available. The subscripts indicate the number of viruses that were phenotyped. The drug susceptibility assay used was the PhenoSense assay (Monogram, South San Francisco). A hyperlink for each individual pattern is provided to access a complete list of mutations and fold resistances for each sequence matching the pattern of mutation.

A complete summary of additional in vitro susceptibility data for viruses with G48 obtained using other assays including the Antivirogram can be found here. A complete list of all mutation patterns with G48 (not just the top 10 most frequent patterns) can be found at this page.

Mutation PatternsNumber of
48V,90M305.321925.022.02 1.21  
48V,54T,82A,90M261651  7.61 15111.31 
Footnote: Mutation patterns were defined by the presence or absence of major PI drug resistance mutations ; Sequences containing a mixture at a major drug resistance positions were excluded; For the cutoffs defined by PhenoSense, open the sample report form provided on this page; The full list of all mutation patterns are also available 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 48.

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)
>=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.
>=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.
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
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.
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.
    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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