literature

HIV mutation literature information.

Emerging transmitted drug resistance in treatment-naive human immunodeficiency virus-1 CRF06_cpx-infected patients in Estonia.

PMID: 20964489 2011 Scandinavian journal of infectious diseases

Abstract: A total of 2.8% of sequences harboured mutations indicating nucleoside/nucleotide reverse transcriptase inhibitor resistance (M41L, M184V, M184I, T215C and T215D), 2.1% non-nucleoside reverse transcriptase inhibitor resistance (K103N, P225H) and 2.8% protease inhibitor resistance (M46I, L90M).

Influence of major HIV-1 protease inhibitor resistance mutations on CTL recognition.

PMID: 21107269 2011 Journal of acquired immune deficiency syndromes (1999)

Abstract: CONCLUSIONS: PI mutations, G48V, M46I, and I47A, can abrogate CTL recognition, indicating potential interactions between development of drug resistance and CTL response.

Abstract: Furthermore, M46I, I47A, and I50V could impair or abolish CTL recognition in many patients.

Abstract: Recently, we identified KMIGGIGGF (KF9) as a HLA-B*1501-restricted CTL epitope, including several major PI resistance mutations (M46I/L, I47A/V, G48V, I50V).

Novel HIV-1 protease inhibitors (PIs) containing a bicyclic P2 functional moiety, tetrahydropyrano-tetrahydrofuran, that are potent against multi-PI-resistant HIV-1 variants.

PMID: 21282450 2011 Antimicrobial agents and chemotherapy

Abstract: When HIV-1(NL4-3) was selected with GRL-1398, four amino acid substitutions--leucine to phenylalanine at a position 10 (L10F), A28S, L33F, and M46I--emerged, ultimately enabling the virus to replicate in the presence of >1.0 muM the compound beyond 57 weeks of selection.

Differences in reversion of resistance mutations to wild-type under structured treatment interruption and related increase in replication capacity.

PMID: 21297946 2011 PloS one

Introduction: The authors reported a faster rate of reversion for primary resistance mutations (K70R, M184I/V, T215Y/F in RT, and D30N, M46I/L, V82A, L90M in PR) compared to secondary mutations (M41L, D67N, T69D/N, L210W, K219Q/E in RT and L10I/V, L63P, A71V/T, V77I in PR)

The L76V mutation in HIV-1 protease is potentially associated with hypersusceptibility to protease inhibitors Atazanavir and Saquinavir: is there a clinical advantage?

PMID: 21314993 2011 AIDS research and therapy

Table: M46I

Rapid development of antiretroviral drug resistance mutations in HIV-infected children less than two years of age initiating protease inhibitor-based therapy in South Africa.

PMID: 21345162 2011 AIDS research and human retroviruses

Abstract: Of 41 children without virologic suppression with posttreatment HIV genotype data available, major resistance mutations were found in 32 (78%): 14 (36%) had PI mutations including V82A, M46I, and L90M; 29 (71%) had M184V/I; and three had NNRTI mutations (K103N, Y181C, and G190A).

New trends of primary drug resistance among HIV type 1-infected men who have sex with men in Liaoning Province, China.

PMID: 21417755 2011 AIDS research and human retroviruses

Abstract: Included were V32I (0.5%), M46I (2.0%), L90M (2.0%), T215C (0.5%), and Y188L (0.5%).

The L76V drug resistance mutation decreases the dimer stability and rate of autoprocessing of HIV-1 protease by reducing internal hydrophobic contacts.

PMID: 21446746 2011 Biochemistry

Abstract: Although the L76V mutation significantly slows the N-terminal autoprocessing of the precursor TFR-PR(L76V) to give rise to the mature PR(L76V), the coselected M46I mutation counteracts the effect by enhancing this rate but renders the TFR-PR(M46I/L76V) precursor less responsive to inhibition by 6 muM LPV while preserving inhibition by SQV and DRV.

Introduction: Additionally, the effect of the mutation on the autocatalytic processing of the precursor, which is required for onset of the catalytic activity characteristic of the mature, dimeric enzyme, was assessed in vitro, and the effect of a second mutation, M46I, was examined in the precur

The impact of the nelfinavir resistance-conferring mutation D30N on the susceptibility of HIV-1 subtype B to other protease inhibitors.

PMID: 21537677 2011 Memorias do Instituto Oswaldo Cruz

Abstract: D30N also suppresses indinavir (IDV) resistance caused by the M46I mutation.

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

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