literature

HIV mutation literature information.

HIV-1 integrase sequence variability in antiretroviral naive patients and in triple-class experienced patients subsequently treated with raltegravir.

PMID: 20961278 2010 AIDS research and human retroviruses

Abstract: Four ARV-naive (5.3%) and two ARV-treated patients (2.7%) had one of the following minor INI-resistance mutations: L74M, E157Q, G163R, and R263K but there was no association between baseline raltegravir genotype and subsequent response to raltegravir treatment.

The HIV-1 integrase genotype strongly predicts raltegravir susceptibility but not viral fitness of primary virus isolates.

PMID: 19770695 2010 AIDS (London, England)

Abstract: The first had the mutations G140S+Q148H+S230N, the second had Y143R+G163R and the third had no evidence of genotypic resistance in integrase.

G140S/Q148R and N155H mutations render HIV-2 Integrase resistant to raltegravir whereas Y143C does not.

PMID: 20436677 2010 PloS one

Result: In all three patients, the initial selection of the N155H mutation was followed by its disappearance and replacement by a pattern comprising the Y143H/R/C mutations with other mutations (T97A in 3 patients, L74M in 2 patients and G163R and S230R in one patient each); RAL was stopped between months 6 and 12 in patient 1, with disappearance of the selected mutations.

Discussion: The Y143C/H/R mutation was associated with T97A in 3 patients, with L74M in 2 patients and with G163R and S230R in one patient each.

Discussion: When the viruses of these three patients replicated

The HIV-1 integrase mutations Y143C/R are an alternative pathway for resistance to Raltegravir and impact the enzyme functions.

PMID: 20436677 2010 PloS one

Method: We followed-up the 50 mutations of resistance present at 32 positions: associated with in vitro or in vivo resistance to HIV-1 integrase inhibitors: H51Y, T66I/A/K, V72I, L74I/A/M, E92Q, T97A, T112I, F121Y, T125K, A128T, E138 K/A/D, G140R/C/H, Y143C/H/R, Q146K/P, S147G, Q148K/R/H, V151I,

PMID: 20634701 2010 Journal of acquired immune deficiency syndromes (1999)

Result: Introduction of E92Q or G163R into an N155H backbone resulted in a virus with greater fitness than N155H mutant both in the absence and presence of RAL.

Result: The addition of secondary mutations L74M or E92Q to N155H resulted in 28- and 55-fold resistance, respectively, but addition of G163R did not result in any substantial change in raltegravir resistance.

Result: The relative fitness difference for N155H/G163R versus N155H was 3.4-fold in absence of drug, and 2.1-fold in the presence of RAL.

Result: To determine how the secondary RAL resistance mutations

PMID: 20817922 2010 The Journal of antimicrobial chemotherapy

Abstract: Similarly, V165I and G163R mutations were associated with the RT resistance mutations F227L and M230L, respectively, and the T206S polymorphism was associated with the RT resistance mutation L210W.

Dynamic escape of pre-existing raltegravir-resistant HIV-1 from raltegravir selection pressure.

PMID: 20883724 2010 Antiviral research

Abstract: Double 148R+N155H mutants were also detected in 1.7% of viruses at virological failure in association with E138K and/or G163R.

Effects of HIV type-1 immune selection on susceptability to integrase inhibitor resistance.

PMID: 19918099 2009 Antiviral therapy

Result: There were 18 codons at which at least one sequence contained a (non-primary) drug resistance-associated mutation and in nine of these codons, the prevalence of the resistance mutation exceeded 5% in either the SHCS or WAHCS (M50I prevalence 18.0% and 14.8%, V72I 52.2% and 58.8%, T112I 5.6% and 6.3%, S119G 6.2% and 7.3%, K156N 5.7% and 8.0%, G163A/E/Q/T/R 5.1% and 4.4%, V201I 48.1% and 46.8%, T206S 15.6% and 9.3%, and S230N 9.4% and 6.2% for the SHCS and the WAHCS, respectively; Figure 2A).

The dynamics of appearance and disappearance of HIV-1 integrase mutations during and after withdrawal of raltegravir therapy.

PMID: 19571721 2009 AIDS (London, England)

Abstract: In three other patients, viruses with N155H emerged at viral rebound either alone (2 months), followed by V151I (8 months) or alone (10 months), or together with V151I/G163RG (7 months).

Abstract: Mutations Q148R (2 months) followed by G140A/Q148R and then G140A/Y143CHR/Q148R/G163R were detected in the virus from one patient, and these reverted to wild type when treatment was withdrawn, although clonal analysis identified maintenance of RAL resistance minority species at this time point.

Abstract: RAL treatment was restarted after 6 months, and 2 weeks later,

PMID: 19447792 2009 The Journal of antimicrobial chemotherapy

Abstract: The secondary mutations L74M, T97A, V151I and G163R were observed with a frequency of <4%.

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