Incidence of resistance in a double-blind study comparing lopinavir/ritonavir plus stavudine and lamivudine to nelfinavir plus stavudine and lamivudine.
PMID: 14702153
2004
The Journal of infectious diseases
Abstract: Primary mutations related to nelfinavir resistance (D30N and/or L90M) were observed in 43 (45%) of 96 nelfinavir-treated subjects.
GW433908/ritonavir once daily in antiretroviral therapy-naive HIV-infected patients: absence of protease resistance at 48 weeks.
Abstract: In the nelfinavir arm the key protease mutations D30N and/or L90M were frequently observed.
Molecular basis for reduced cleavage activity and drug resistance in D30N HIV-1 protease.
PMID: 15155216
2004
Antimicrobial agents and chemotherapy
Abstract: Because mutation D30N is not preferentially selected in nelfinavir-treated subtype-C-infected patients, as it is in those infected with subtype B, the consideration of using this drug initially to preserve future protease inhibitor options is less relevant for subtype-C-infected patients.
Abstract: Following nelfinavir treatment, the unique nelfinavir mutation D30N was substantially less frequent in C (7%) than in B (23%; P = 0.03) while L90M was similar (P < 0.5).
Abstract: Subtype C samples with mutation D30N showed a 50% inhibitory concentration (IC(50)) change in susceptibility to nelfinavir only.
Abstract: We confirmed the selective nature of the D30N mutation in C, and the broader cross-resistance of other common protease
Persistence of mutations during replication of an HIV library containing combinations of selected protease mutations.
Abstract: By contrast, the half lives (t(1/2)) of the D30N and N88D mutations associated with nelfinavir (NFV) resistance were only 7.2 and 1.8 days, respectively.
The influence of protease inhibitor resistance profiles on selection of HIV therapy in treatment-naive patients.
Abstract: Specific changes are characteristically linked to resistance to each of these compounds (i.e., D30N for nelfinavir, I50L for atazanavir or I50V for amprenavir).
Impact of nelfinavir resistance mutations on in vitro phenotype, fitness, and replication capacity of human immunodeficiency virus type 1 with subtype B and C proteases.
PMID: 15328124
2004
Antimicrobial agents and chemotherapy
Abstract: We showed that D30N has significantly more impact in subtype C than in subtype B counterparts, accounting for the reported low prevalence of this mutation in patients failing nelfinavir-based regimens.
Alternative, age- and viral load-related routes of nelfinavir resistance in human immunodeficiency virus type 1-infected children receiving highly active antiretroviral therapy.
PMID: 15545865
2004
The Pediatric infectious disease journal
Abstract: The prevalence of L90M was similar to that of D30N.
Drug resistance mutations and outcome of second-line treatment in patients with first-line protease inhibitor failure on nelfinavir-containing HAART.
Abstract: A pronounced accumulation of the secondary protease mutations N88D, M36I, and A71V/T was found, and D30N was strongly associated with N88D.
Abstract: CONCLUSION: In patients failing nelfinavir-containing HAART, D30N was detected frequently and L90M occasionally.
Abstract: Of eight patients with N88D, seven also harboured D30N (P < 0.01).
Abstract: Ten patients had D30N (38%), five patients had L90M (19%), two patients had V82A/F (8%) and two patients had M46I/L (8%).
HIV-1 reverse transcriptase and protease resistance mutations selected during 16-72 weeks of therapy in isolates from antiretroviral therapy-experienced patients receiving abacavir/efavirenz/amprenavir in the CNA2007 study.
Abstract: Mutations D30N, G48V, N88D/S, L90M and 154V were de-selected, and mutations I50V, I or V to 54M/L, I84V, M46I/L, L33F, I47V as well mutations at position 10 were observed in 20/49 (41%) isolates.