literature

HIV mutation literature information.

Role of atazanavir in the treatment of HIV infection.

PMID: 19436623 2009 Therapeutics and clinical risk management

Introduction: Mutations more significant to be included in the GIQ model are the following: L10F/I/V, K20M/R, L24I, D30N, V32I, L33F, M36I/L, I47V/A, G48V, I50V, I50L, F53L, I54V/L/A/M/T/S, L63P, A71V/T, G73S, V77I, V82A/F/T, I84V, N88D/S and

HIV type-1 clade C resistance genotypes in treatment-naive patients and after first virological failure in a large community antiretroviral therapy programme.

PMID: 19578237 2009 Antiviral therapy

Result: The most frequent protease mutations remained M36I (86%), L63P (60%), H69K (94%) and L89I/M (82%), similar to the consensus sequence noted for clade C (differing amino acids compared to clade B subtypes at positions M361, R41K, H69K AND L89M).

Result: The most frequent protease mutations were L89I/M (89%), H69K (88%), L63P (52%) and M36I (87%).

Discussion: The impact of these on viral drug susceptibility is uncertain, but many, including L10I/V, K20R

Virological efficacy and emergence of drug resistance in adults on antiretroviral treatment in rural Tanzania.

PMID: 19583845 2009 BMC infectious diseases

Table: L63P

Genetic diversity and drug resistance of HIV type 1 circulating recombinant Form_BC among drug users in Guangdong Province.

PMID: 19698024 2009 AIDS research and human retroviruses

Abstract: Five high polymorphisms were found in CRF_07BC isolates; there were E35D (88%), R41K (100%), D60E (96%), L63P (99%), and I93L (91%).

Abstract: Four of the identified polymorphism positions (R41K, D60E, L63P, and I93L) were the same in the PR region of both subtypes.

Abstract: The polymorphisms L19I, M36I, R41K, D60E, L63P, H69K, and I93L were complete substitutions, and were followed by

Rapid and persistent selection of the K103N mutation as a majority quasispecies in a HIV1-patient exposed to efavirenz for three weeks: a case report and review of the literature.

PMID: 21092074 2009 Journal of medical case reports

Table: L63P

Conformational analysis of TMC114, a novel HIV-1 protease inhibitor.

PMID: 18173253 2008 Journal of chemical information and modeling

Abstract: All 43 conformers were subject to both rigid and flexible ligand docking in the wild-type and a triple mutant (L63P/V82T/I84V) of HIV-1 protease.

Genotypic resistance profiles in antiretroviral-naive HIV-1 infections before and after initiation of first-line HAART: impact of polymorphism on resistance to therapy.

PMID: 18182278 2008 International journal of antimicrobial agents

Abstract: At baseline, the differences between CRF01_AE and B strain were mainly observed in the minor mutations L10I/V, M36I and L63P/I/H (P<0.001, chi(2)).

Characterization of a novel human immunodeficiency virus type 1 protease inhibitor, A-790742.

PMID: 18212102 2008 Antimicrobial agents and chemotherapy

Abstract: During in vitro selection, A-790742 selected two primary mutations (V82L and I84V) along with L23I, L33F, K45I, A71V/A, and V77I in the pNL4-3 background and two other mutations (A71V and V82G) accompanied by M46I and L63P in the HIV-1 RF background.

Multiple independent origins of a protease inhibitor resistance mutation in salvage therapy patients.

PMID: 18221530 2008 Retrovirology

Introduction: Primary drug resistance mutations that alone confers moderate resistance such as V82A and L90M are initially selected followed by the addition of secondary mutations often located outside of the active site of the PR, such as L10I, M36I, M46I, L63P, or A71V leading to higher levels of resistance.

Prevalence of genotypic resistance to nucleoside analogues, nonnucleoside analogues, and protease inhibitors in HIV-infected persons in Athens, Greece.

PMID: 18275347 2008 AIDS research and human retroviruses

Abstract: Mutations in the protease gene showed that the ARM at residue L63P was the most prevalent present in 119 samples (50.9%).

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