HIV mutation literature information.


  Polymorphisms of HIV-2 integrase and selection of resistance to raltegravir.
 PMID: 21114823       2010       Retrovirology
Abstract: The N155 H INI resistance-associated mutation (RAM) was detected in the virus population from one ARV-treated, INI-naive patient, and the 72I and 201I polymorphisms were detected in samples from 36 and 38 patients respectively.
Introduction: In HIV-1-infected patients failing an INI-containing regimen, three distinct resistance pathways involving Y143R, Q148H/R/K or N155 H have been described.
Introduction: RAL resistance is not well documented for HIV-2, although cases of therapy failure have been associated with the emergence of variants carrying the Y143C, Q148K/R, or


  Extended use of raltegravir in the treatment of HIV-1 infection: optimizing therapy.
 PMID: 21694899       2010       Infection and drug resistance
Abstract: The development of resistance to raltegravir mainly involved three resistance mutations in integrase gene: Q148H/K/R, N155H, and Y143C/H/R.
Discussion: However, 39 (29%) of the patients in the raltegravir arm of the EASIER study displayed at least one episode of low-level viremia on treatment and significant integrase resistance-associated mutations were detected in three subject (7.7%), including N155H in two subjects and P145S in one subject.
Discussion: Indeed, the level of phenotypic resistance to raltegravir associated with N155H is always much lower than that associated with Q148 or Y143 mutation (>100 times higher).


  The G140S mutation in HIV integrases from raltegravir-resistant patients rescues catalytic defect due to the resistance Q148H mutation.
 PMID: 19129221       2009       Nucleic acids research
Introduction: Finally, we found that the G140S/Q148H mutant was much more resistant than the N155H mutant.
Introduction: We investigated the impact of the two main genetic resistance pathways (N155H and G140S/Q148H), on viral replication and the catalytic properties of recombinant INs.
Method: In parallel, the E92Q, G140S, Q148H, N155H and G140S/Q148H mutations were obtained by site-directed mutagenesis from pET-15b, containing the WT sequence.

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