literature

HIV mutation literature information.

Prevalence and resistance mutations of non-B HIV-1 subtypes among immigrants in Southern Spain along the decade 2000-2010.

PMID: 21871090 2011 Virology journal

Abstract: Major RT inhibitor resistance mutations K70R and A98G were present in one patient with subtype G, L100I in one patient with CRF01_AE, and K103N in another patient with CRF01_AE.

Result: Patient SE34, in treatment interruption, had L100I mutation associated with NNRTI resistance, and finally patient SE60, receiving HAART, had the NNRTI resistance mutation K103N.

Table: L100I

1-[2-(2-Benzoyl- and 2-benzylphenoxy)ethyl]uracils as potent anti-HIV-1 agents.

PMID: 21903401 2011 Bioorganic & medicinal chemistry

Result:

Result: For example, nevirapine and efavirenz exhibited a 15-fold and 10-fold lower activity, respectively, towards the L100I RT mutant compared to the wild-type enzyme, whereas benzophenones 17 and 20 retained almost full activity, exhibiting only a very minor degree of resistance (1.4-fold and 2.5-fold, respectively).

Result: Moreover, the resistance index for the compounds against the Y181C, Y188L and K103N/Y181C mutant RTs was comparable to that of efavirenz, and even lower for the L100I, K103N and G190A mutants, although for the V106A mutant, efavirenz was more potent than 17 and 20.

Docking analysis and resistance evaluation of clinically relevant mutations associated with the HIV-1 non-nucleoside reverse transcriptase inhibitors nevirapine, efavirenz and etravirine.

PMID: 21953939 2011 ChemMedChem

Abstract: For efavirenz resistance, K103N, G190, and L100I have the first, fourth, and eighth greatest significance, respectively, as determined in support vector regression model.

Abstract: The most common indicator of treatment failure for efavirenz was K103N mutation present in 56.7% of the patients where the drug failed, followed by V108I, L100I, and G190A.

Resistance patterns selected by nevirapine vs. efavirenz in HIV-infected patients failing first-line antiretroviral treatment: a bayesian analysis.

PMID: 22132100 2011 PloS one

Method: RT mutations were identified from the International AIDS Society USA Drug (IAS-USA) mutation tables, spring 2008 (http://www.iasusa.org/resistance_mutations): M41L, K65R, D67N, insertion 69, K70R/E, L74I/V, L100I, K103N, V106A/M, V108I, Q151M, Y181I/C, M184V, Y188C/L, G190A/S, L210W, T215Y/F,

PMID: 19933797 2010 Antimicrobial agents and chemotherapy

Abstract: NNRTI RAMs emerging in HIV-1 under selective pressure from TMC278 included combinations of V90I, L100I, K101E, V106A/I, V108I, E138G/K/Q/R, V179F/I, Y181C/I, V189I, G190E, H221Y, F227C, and M230I/L.

N348I in HIV-1 reverse transcriptase decreases susceptibility to tenofovir and etravirine in combination with other resistance mutations.

PMID: 20010074 2010 AIDS (London, England)

Introduction: Since the presence of three or more NNRTI mutations V90I, A98G, L100I, K101E/P, V106I, V179D/F, Y181C/I/V and G190A/S results in no response to etravirine treatment, the presence of two of these NNRTI mutations and N348I at baseline may also reduce etravirine efficacy in vivo.

Low frequency nonnucleoside reverse-transcriptase inhibitor-resistant variants contribute to failure of efavirenz-containing regimens in treatment- experienced patients.

PMID: 20102272 2010 The Journal of infectious diseases

Method: For single-genome sequencing analyses, a total of 27 subjects (15 NNRTI-naive and 12 NNRTI-experienced) were randomly selected from enrollees meeting the following criteria: i) entry sample negative for NNRTI-resistance mutations by standard genotype analysis (ViroSeq platform; Celera, Alameda, CA); ii) reached a protocol-defined virologic failure endpoint by study week 24, and iii) the virologic failure sample had one or more major NNRTI-resistance mutations (L100I, K101E, K103N, V106A or M, V108I, Y181C or I, Y188C, H, or L, G

In vitro resistance development for RO-0335, a novel diphenylether nonnucleoside reverse transcriptase inhibitor.

PMID: 20219553 2010 Antiviral research

Abstract: Two pathways to loss of susceptibility to RO-0335 were observed, containing patterns of amino acid changes at either V106I/A plus F227C (with additional contributions from A98G, V108I, E138K, M230L and P236L) or V106I/Y188L (with a potential contribution from L100I, E138K and Y181C).

The non-nucleoside reverse transcriptase inhibitor efavirenz stimulates replication of human immunodeficiency virus type 1 harboring certain non-nucleoside resistance mutations.

PMID: 20399480 2010 Virology

Introduction: One example of this type of mutation is L74V, which confers resi

Result: We also evaluated whether another nucleoside resistance mutation, L74V, might affect the replication of (K101E+G190S), since L74V has been shown to improve the replication fitness of at least two other NNRTI-resistant mutants, G190E and (K103N+L100I).

Discussion: L74V, in addition to improving the fitness of G190E and K103N+L100I, also has the same effect on (K101E+G190S).

Constrained patterns of covariation and clustering of HIV-1 non-nucleoside reverse transcriptase inhibitor resistance mutations.

PMID: 20462946 2010 The Journal of antimicrobial chemotherapy

Method: Of these, L100I, K101P, Y181C/I/V and M230L were considered to be major etravirine RAMs based on their marked effect on etravirine susceptibility.

Method: The complete list of etravirine RAMs was defined as V90I, A98G, L100I, K101E/H/P, V106I, E138A, V179D/F/T, Y181C/I/V, G190A/S and M230L.

Method: These mutations included: (i) 46 non-polymorphic NNRTI-selected mutations at 28 positions (

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