Novel human immunodeficiency virus type 1 protease mutations potentially involved in resistance to protease inhibitors.
PMID: 15855527
2005
Antimicrobial agents and chemotherapy
Abstract: On the other hand, C95F, which was associated with treatment with saquinavir and indinavir, was highly expressed in clusters with either L90M and I93L or V82A and G48V.
Substitutions in the Reverse Transcriptase and Protease Genes of HIV-1 Subtype B in Untreated Individuals and Patients Treated With Antiretroviral Drugs.
PMID: 19825125
2005
Journal of the International AIDS Society
Table: G48V
Effect of polymorphisms on the replicative capacity of protease inhibitor-resistant HIV-1 variants under drug pressure.
PMID: 14759236
2004
Clinical microbiology and infection
Abstract: Using HIV-1 variants resistant to the protease inhibitors saquinavir (G48V/L90M) or indinavir (A71V/V82T/I84V), viral replication was studied in the presence or absence of inhibitor and a mutation at position 63.
The influence of protease inhibitor resistance profiles on selection of HIV therapy in treatment-naive patients.
Abstract: Other mutations (D30N, G48V, I50V or I50L) are relatively specific for particular PIs and are less likely to produce cross resistance.
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.
Elucidation of HIV-1 protease resistance by characterization of interaction kinetics between inhibitors and enzyme variants.
Abstract: The kinetics of the interaction between drug-resistant variants of HIV-1 protease (G48V, V82A, L90M, I84V/L90M, and G48V/V82A/I84V/L90M) and clinically used inhibitors (amprenavir, indinavir, nelfinavir, ritonavir, and saquinavir) were determined using biosensor technology.
Novel enzyme-linked minisequence assay for genotypic analysis of human immunodeficiency virus type 1 drug resistance.
PMID: 14605126
2003
Journal of clinical microbiology
Abstract: ELMA is a combination of hybridization and a 1-base extension reaction, and we designed the assay to detect five mutations conferring nucleoside analogue resistance (M41L, D67N, K70R, T215Y, and M184V) and six mutations conferring protease inhibitor resistance (D30N, M46I, G48V, V82A, I84V, and L90M).
Sexual transmission of HIV-1 isolate showing G-->A hypermutation.
Abstract: The patient's viral genotype showed several mutations related to antiretroviral drug resistance in RT (T69N, M184V, T215F, K219Q) and protease (M36I, G48V, I54V, T63L, V82A) genes.
Evolution of primary protease inhibitor resistance mutations during protease inhibitor salvage therapy.
PMID: 11897594
2002
Antimicrobial agents and chemotherapy
Abstract: Among 78 patients meeting study selection criteria, baseline primary PI resistance mutations included L90M (42% of patients), V82A/F/T (27%), D30N (21%), G48V (6%), and I84V (4%).
Abstract: HIV-1 isolates from 38 (49%) patients failing PI salvage therapy developed new primary PI resistance mutations including L90M, I84V, V82A, and G48V.
Abstract: The persistence of L90M, V82A/F/T, G48V, and I84V during sa
HIV-1 Vif-derived peptide inhibits drug-resistant HIV proteases.
PMID: 11944889
2002
Biochemical and biophysical research communications
Abstract: In agreement with the in vitro experiments, Vif88-98 has no effect on the production of infectious particles in cells infected with a G48V mutated virus.
Abstract: Variants of HIV protease bearing the mutation G48V are resistant to inhibition by this Vif-derived peptide, as shown by in vitro assays.
HIV mutation literature information.
PMID: 
2005
Antimicrobial agents and chemotherapy
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