HIV-1 subtypes and primary antiretroviral resistance mutations in antiretroviral therapy naive HIV-1 infected individuals in Turkey.
PMID: 23883841
2013
Japanese journal of infectious diseases
Abstract: The patients had primary antiretroviral resistance mutations to nucleos(t)ide reverse transcriptase (RT) inhibitors (NRTIs) (M41L, T215C, T215D, and K219Q), non-nucleoside RT inhibitors (NNRTIs; K103N), and protease inhibitors (PIs; I47V, G73S).
Persistence of HIV-1 transmitted drug resistance mutations.
PMID: 23904291
2013
The Journal of infectious diseases
Table: I47 V
Simultaneous detection of major drug resistance mutations in the protease and reverse transcriptase genes for HIV-1 subtype C by use of a multiplex allele-specific assay.
PMID: 23985909
2013
Journal of clinical microbiology
Abstract: All the wild-type and mutant alleles were unequivocally distinguished with plasmid templates, and the limits of detection were 1.56% for K219Q and K219E, 3.13% for L76V, 6.25% for K65R, K70R, L74V, L100I, K103N, K103R, Q151M, Y181C, and I47V, and 12.5% for M41L, K101P, K101E, V106A, V106M, Y115F, M184V, PMID: 24093951
2013
Journal of the International AIDS Society
Method: Sequences were analyzed to identify mutations associated with reduced susceptibility to protease and RT inhibitors, as reported by the International AIDS Society-USA in 2010: RT-M41L, A62V, K65R, D67N, 69 insert, K70R, L74V,V75I, F77L, L100I, K101P, K103N, V106A, V106M, V108I, Y115F, F116Y,
Virological response to darunavir in patients infected with HIV is linked to darunavir resistance-associated mutations corrected by the count of mutations with positive impact and is not associated with pharmacological and combined virological/pharmacological parameters.
PMID: 21545648
2012
Fundamental & clinical pharmacology
Abstract: Darunavir GIQ is defined as the ratio between darunavir trough plasma concentration and the count of darunavir resistance-associated mutations (V11I, V32I, L33F, I47V, I50V, I54L/M, T74P, L76V, I84V, L89V) corrected or not corrected by the count of mutations with positive impact (V82A and E35D).
Critical differences in HIV-1 and HIV-2 protease specificity for clinical inhibitors.
Abstract: Furthermore, we analyzed the PR1 mutant (PR(1M) ) with substitutions V32I, I47V, and V82I that mimic the inhibitor binding site of PR2.
Interaction of I50V mutant and I50L/A71V double mutant HIV-protease with inhibitor TMC114 (darunavir): molecular dynamics simulation and binding free energy studies.
PMID: 22239286
2012
The journal of physical chemistry. B
Result: This result is quite similar to the earlier study on JE-2147 bound I47V mutant.
Potent antiviral HIV-1 protease inhibitor GRL-02031 adapts to the structures of drug resistant mutants with its P1'-pyrrolidinone ring.
PMID: 22401672
2012
Journal of medicinal chemistry
Abstract: Crystal structures at resolutions of 1.25-1.55 A were analyzed for complexes of 1 with the PR containing major drug resistant mutations, PR(I47V), PR(L76V), PR(V82A), and PR(N88D).
Abstract: Mutations of I47V and V82A alter residues in the inhibitor-binding site, while L76V and N88D are distal mutations having no direct contact with the inhibitor.
Abstract: Substitution of a smaller amino acid in PR(I47V) and PR(
HIV-1 protease with 20 mutations exhibits extreme resistance to clinical inhibitors through coordinated structural rearrangements.
5Result: Four ""first shell"" mutations D30N, V32I, I47V and I84V alter residues making direct contacts with DRV and SQV inhibitors."
Result: First, mutation of four (D30N, V32I, I47V and I84V) of the seven residues forming the S2/S2' subsites alters their size, shape and charge.
Result: In the Result: In the PR20/SQV complex, the P2' group of SQV shifts more than 1.5 A towards the shorter I84'V to compensate for the larger S2' subsite and maintain interactions with D30N, V32I, I47V and I84V (Figure 5E).
Transmitted drug resistance and phylogenetic relationships among acute and early HIV-1-infected individuals in New York City.
PMID: 22592583
2012
Journal of acquired immune deficiency syndromes (1999)
4Method: ARV resistance was defined by mutations at the following positions: M41L, A62V, K65R, D67N, T69ins, K70R, L74VI, Y115F, F116Y, Q151M, M184VI, T210W, T215YF and K219QE for Nucleoside Reverse Transcriptase Inhibitors (NRTI), L100I, K101EP, K103NS, V106AM