Brun, S., D. Kempf, Et Al. (2000). Analysis of Viral Isolates Following Viral Load Rebounds
Drug / SeqID / Actual Fold / Predicted
Fold / Mutations / Possible Explanation / Reference
Predicted to be Susceptible / Found to be highly resistant
NFV / 45102 / 35 / 2.7 / I13V, L19I, K20X, M46I, K55R, D60E, A71V / Unknown / (Colonno, Rose et al. 2004)
AZT / 74899 / 28 / 3.0 / A98S, K103N, V118VI, K122E, D177E, M184V, Q207E, R211K, T215Y, L228H, M230L, D250E / Unknown / (Kempf, Isaacson et al. 2001)
D4T / 75057 / 3.3 / 1.3 / L34LI, V60VI, K65R, S68G, K73M, V75A, V106VI, K122E, D123DN, I135T, S162D, T165TI, Q174H, Y181C, G190GA, T200A, Q207E, R211K, H221HY, V245VE / Rare mutation / (Mo, King et al. 2005)
TDF / 59033 / 3.4 / 1.4 / M41L, T69D, K103NK, V108I, M184V, L210W, T215Y, K219R / Unknown / Misc clinical isolates
DLV / 25066 / 200 / 2.3 / K101E, K102Q, V108I, S162C, G190A / Unknown / (Huang, Limoli et al. 1999)
DLV / 25074 / 75 / 2.5 / K102Q, E138A, S162C, Y188L / Unknown / (Huang, Limoli et al. 1999)
DLV / 26030 / 26 / 1.7 / V35I, D67N, T69D, K70R, V106A, K122E, R125KR, V189L, T200A, I202T, H208Y, R211K, T215F, D218E, K219Q, H221Y, F227L, L228H / Unknown / (Parkin, Deeks et al. 2000)
DLV / 40766 / 111 / 2.5 / R83K, K102R, V106I, S163T, K173N, Q174K, V179E, Y188C, Q207E, R211K, V245T, E248DE / Unknown / Misc clinical isolates
DLV / 52094 / 41 / 0.9 / I31L, S68GS, K103R, V179D, M184V, T200IT, R211K, F214L, T215F, V245K / K103R/V179D interaction / Misc clinical isolates
DLV / 81752 / 27 / 0.9 / K102Q, K103R, S162C, I178V, V179D / K103R/V179D interaction / (Parkin, Gupta et al. 2006)
EFV / 16579 / 150 / 0.8 / K102Q, S162C, G190T / Rare mutation / (Huang, Gamarnik et al. 2003)
EFV / 16581 / 170 / 0.8 / K102Q, S162C, G190C / Rare mutation / (Huang, Gamarnik et al. 2003)
EFV / 44025 / 400 / 0.8 / M41L, K49R, T69S_SS, L74V, R83K, A98G, M184V, G190C, Q197E, L210W, R211K, T215Y,L228H / Rare mutation / (Johnston, Dupnik et al. 2005)
EFV / 50508 / 270 / 0.8 / K20R, V35I, I50V, V60I, K65R, S68R, K73L, L74V, V75A, K101Q, K102R, K122E, D123N, I135V, Q151M, I178V, M184V, G190V, I195T, G196E, K219E / Rare mutation / (Huang, Gamarnik et al. 2003)
EFV / 50598 / 270 / 0.8 / L74V, K102Q, S162C, G190V / Rare mutation / (Huang, Gamarnik et al. 2003)
EFV / 52094 / 31 / 0.8 / I31L, S68GS, K103R, V179D, M184V, T200IT, R211K, F214L, T215F, V245K / K103R/V179D interaction / Misc clinical isolates
NVP / 16579 / 356 / 1.3 / K102Q, S162C, G190T / Rare mutation / (Huang, Gamarnik et al. 2003)
NVP / 16581 / 170 / 1.3 / K102Q, S162C, G190C / Rare mutation / (Huang, Gamarnik et al. 2003)
NVP / 44025 / 400 / 1.3 / M41L, K49R, T69S_SS, L74V, R83K, A98G, M184V, G190C, Q197E, L210W, R211K, T215Y,L228H / Rare mutation / (Johnston, Dupnik et al. 2005)
NVP / 50508 / 400 / 1.3 / K20R, V35I, I50V, V60I, K65R, S68R, K73L, L74V, V75A, K101Q, K102R, K122E, D123N, I135V, Q151M, I178V, M184V, G190V, I195T, G196E, K219E, V276I, Q278E, A288S, E297R / Rare mutation / (Huang, Gamarnik et al. 2003)
NVP / 50598 / 400 / 1.3 / L74V, K102Q, S162C, G190V, K277R, I293V / Rare mutation / (Huang, Gamarnik et al. 2003)
NVP / 52094 / 34 / 1.3 / I31L, S68GS, K103R, V179D, M184V, T200IT, R211K, F214L, T215F, V245K / K103R/V179D interaction / Misc clinical isolates
NVP / 52912 / 400 / 1.3 / T7PT, K20R, M41L, E44D, V60I, D67N, V75M, D123E, I142V, S162Y, M184V, G196E, Q197K, E203D, H208F, L210W, R211K, T215Y, K219N / Unknown / (Shulman, Zolopa et al. 2000)
NVP / 57459 / 34 / 1.3 / V21I, T139R, M184V, T200A, Q207E, R211K, K238N / Rare mutation / (Petropoulos, Chappey et al. 2003)
NVP / 75739 / 37 / 1.3 / T39X, M41L, K43QK, E44D, D67G, T69D, V75M, F77L, A98S, K101Q, V111I, V118I, K122E, A158S, S162NDGS, M184V, I202VI, L210W, T215H / Unknown / Misc clinical isolates
NVP / 81822 / 29 / 1.3 / M41L, K43E, E44A, K49R, A62V, D67N, K70R, L74I, V75T, V118I, K122E, I135T, S162N, E169D, D177N, I178M, M184V, G196E, E203K, Q207E, L210W, R211K, T215Y, D218E, K219E, L228H, L283I / Unknown / Misc clinical isolates
Predicted to be Highly Resistant / Found to be Susceptible
LPV / 81786 / 2.9 / 30 / L33F, E34Q, N37S, I54V, Q58E, L63P, A71V, V77I, V82A, L90M, I93L / Unknown / (Resch, Parkin et al. 2005)
NFV / 27472 / 1.6 / 27 / L10I, I13V, G16A, Q18H, L33F, N37D, M46I, I54V, Q61H, L63P, A71L, I72T, L76V, V77I, N88G, L90M, I93L / Unknown / (Brun, Kempf et al. 2000)
SQV / 68072 / 1.8 / 22 / L10IL, K14RK, R41KR, M46I, I62V, L63P, I66L, G73T, V77I, I84V, L90M, I93L / Unknown / (Murphy, Marousek et al. 2004)
AZT / 52841 / 1.7 / 26 / M41L, E44D, D67N, K122E, M184V, L210W, F214L, T215Y, K219E, A272P, K277R / Unknown / (Parkin, Hellmann et al. 2004)
AZT / 56171 / 0.4 / 26 / K20R, V35I, M41L, K43E, L74V, A98G, K101H, V108IV, V118I, D123E, I135T, D177E, Y181C, V189IV, G190A, T200K, Q207ED, H208Y, L210W, R211K, T215Y, E248D, A272S, K277R, I293V / Unknown / Misc clinical isolates
AZT / 81868 / 2.7 / 29 / E6K, K20R, V35M, T39A, M41L, G45E, D67N, T69D, V118I, K122E, D123E, M184V, L210W, R211K, T215Y, L228F, A272P, L282K, E297K / Unknown / Misc clinical isolates
D4T / 81926 / 0.8 / 4.2 / P1L, V35IV, M41L, S68GS, T69T_SS, L74I, R83KR, V108I, T139M, S162D, S163T, K166R, D177E, V179I, Y181C, M184V, V189IV, I202V, L210W, R211K, T215H, A272P / Unknown / Misc clinical isolates
Nonpolymorphic treatment selected mutations (TSMs) based on the analysis in (Rhee, Fessel et al. 2005) are underlined. Drug-resistance mutations that are not nonpolymorphic TSMs but which are likely to explain observed resistance are in bold.
All but three of the mutation lists are for RT genes. The first three in the second part of the table are for protease genes.
Brun, S., D. Kempf, et al. (2000). Analysis of viral isolates following viral load rebounds on therapy with ABT-378/ritonavir (ABT-378/r) [abstract 2112]. 40th Interscience Conference on Antimicrobial Agents and Chemotherapy, Toronto, Canada.
Colonno, R., R. Rose, et al. (2004). "Identification of I50L as the signature atazanavir (ATV)-resistance mutation in treatment-naive HIV-1-infected patients receiving ATV-containing regimens." J Infect Dis189(10): 1802-10.
Huang, W., A. Gamarnik, et al. (2003). "Amino acid substitutions at position 190 of human immunodeficiency virus type 1 reverse transcriptase increase susceptibility to delavirdine and impair virus replication." J Virol77(2): 1512-23.
Huang, W., K. Limoli, et al. (1999). "Complex interactions involving multiple amino acid substitutions alter NNRTI susceptibility [abstract 73]." Antivir Ther4(Suppl 1): 50-51.
Johnston, E., K. M. Dupnik, et al. (2005). "Panel of prototypical infectious molecular HIV-1 clones containing multiple nucleoside reverse transcriptase inhibitor resistance mutations." Aids19(7): 731-3.
Kempf, D. J., J. D. Isaacson, et al. (2001). "Identification of genotypic changes in human immunodeficiency virus protease that correlate with reduced susceptibility to the protease inhibitor lopinavir among viral isolates from protease inhibitor-experienced patients." J Virol75(16): 7462-9.
Mo, H., M. S. King, et al. (2005). "Selection of resistance in protease inhibitor-experienced, human immunodeficiency virus type 1-infected subjects failing lopinavir- and ritonavir-based therapy: mutation patterns and baseline correlates." J Virol79(6): 3329-38.
Murphy, M. D., G. I. Marousek, et al. (2004). "HIV protease mutations associated with amprenavir resistance during salvage therapy: importance of I54M." J Clin Virol30(1): 62-7.
Parkin, N. T., S. G. Deeks, et al. (2000). "Loss of antiretroviral drug susceptibility at low viral load during early virological failure in treatment-experienced patients." AIDS14(18): 2877-2887.
Parkin, N. T., S. Gupta, et al. (2006). "The K101P and K103R/V179D Mutations in Human Immunodeficiency Virus Type 1 Reverse Transcriptase Confer Resistance to Nonnucleoside Reverse Transcriptase Inhibitors." Antimicrob Agents Chemother50(1): 351-4.
Parkin, N. T., N. S. Hellmann, et al. (2004). "Natural variation of drug susceptibility in wild-type HIV-1." Antimicrob Agents Chemother48(2): 437-43.
Petropoulos, C., C. Chappey, et al. (2003). High-level resistance to HIV-1 non-nucleoside reverse transcriptase inhibitors (NNRTIs) in the absence of known resistance mutations [H-451]. 43rd Interscience Conference on Antimicrobial Agents and Chemotherapy, Chicago, IL.
Resch, W., N. Parkin, et al. (2005). "Evolution of human immunodeficiency virus type 1 protease genotypes and phenotypes in vivo under selective pressure of the protease inhibitor ritonavir." J Virol79(16): 10638-49.
Rhee, S. Y., W. J. Fessel, et al. (2005). "HIV-1 protease and reverse-transcriptase mutations: correlations with antiretroviral therapy in subtype B isolates and implications for drug-resistance surveillance." J Infect Dis192(3): 456-65.
Shulman, N. S., A. R. Zolopa, et al. (2000). "Efavirenz- and adefovir dipivoxil-based salvage therapy in highly treatment-experienced patients: clinical and genotypic predictors of virologic response." J Acquir Immune Defic Syndr23(3): 221-6.