Drug resistance mutations in patients infected with HIV-2 living in Spain.
PMID: 21558334
2011
The Journal of antimicrobial chemotherapy
Abstract: No major mutations associated with drug resistance in HIV-1 were recognized in 29 PR, 20 RT and 5 INT sequences from antiretroviral-naive HIV-2 individuals, although natural polymorphisms with potential effects on susceptibility to PR inhibitors were recognized at 10 positions (L10V/I, V32I, M36I, M46I, I47V, Q58E, A71V/I, G73A, V82I and L89I/V) and for nucleoside reverse transcriptase inhibitors at three positions (T69N, V75I
HIV-1 drug resistance at antiretroviral treatment initiation in children previously exposed to single-dose nevirapine.
Result: The major PI mutations M46I/L and I47V were present in 4 samples, and minor PI mutations L10I/V, V11I, A71T, I85V, and N88D were also detected.
Transmission of HIV drug resistance and non-B subtype distribution in the Spanish cohort of antiretroviral treatment naive HIV-infected individuals (CoRIS).
Abstract: The most prevalent resistance mutations were: T215 revertants (3.8%), D67NG (1.3%), K219QENR (1.2%) and M41L (1%), for NRTIs; K103N (3.2%), for NNRTIs; I54VLMSAT, M46I and L90M (0.7%), for PIs.
The new and less toxic protease inhibitor saquinavir-NO maintains anti-HIV-1 properties in vitro indistinguishable from those of the parental compound saquinavir.
Abstract: The following recombinant viruses were generated and tested: L33F, M46I, G48V, I54V, I84V + L90M, M46I + L90M, G48V + L90M, M46I + I54V + L90M, L33F + M46I + L90M.
Prevalence of antiretroviral drug resistance mutations and HIV-I subtypes among newly-diagnosed drug-naive persons visiting a voluntary testing and counselling centre in northeastern South Africa.
PMID: 21957668
2011
Journal of health, population, and nutrition
Abstract: Four (7.4%) of these were nucleoside RT inhibitor mutations (D67G, D67E, T69D, and T215Y), and one (1.9%) was a PR inhibitor mutation (M46I).
Discussion: Mutations in D67E, D67G, and T69D were detected in three women while T215Y and M46I were detected in two men.
Discussion: The only protease inhibitor (PI) mutation observed :M46I:causes intermediate resistance to nelfinavir, with a potential for low-level resistance to ritonavir-boosted doses of atazanavi
Can linear regression modeling help clinicians in the interpretation of genotypic resistance data? An application to derive a lopinavir-score.
Abstract: About 60% of tests reported L10FIRVC, M36ILV, M46IL, I54VLAMTS, V82AFTSLI, and L90M mutations in the protease region.
Impact of reduced dosing of lopinavir/ritonavir in virologically controlled HIV-infected patients: the Kaledose trial.
PMID: 19919951
2010
The Journal of antimicrobial chemotherapy
Abstract: In the 15 patients with transient viraemia, analysis of proviral DNA for antiretroviral resistance showed that mutations had occurred when compared with baseline genotypes in three patients: I47M (n = 2) and M46I (n = 1).
Design and synthesis of novel P2 substituents in diol-based HIV protease inhibitors.
PMID: 19926360
2010
European journal of medicinal chemistry
Abstract: These inhibitors were also tested against an HIV protease inhibitor resistant strain carrying the M46I, V82F, and I84V mutations.
Characterization of HIV type 1 genotypes and drug resistance mutations among drug-naive HIV type 1-infected patients in Northern Vietnam.
PMID: 20156106
2010
AIDS research and human retroviruses
Abstract: Major protease inhibitor resistance mutations, such as L33F, M46I, and M46L, were found in three patients (1.7%).
HIV mutation literature information.
PMID: 
2011
The Journal of antimicrobial chemotherapy
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