HIV mutation literature information.


  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: M46L


  HIV-1 drug resistance at antiretroviral treatment initiation in children previously exposed to single-dose nevirapine.
 PMID: 21633285       2011       AIDS (London, England)
Result: The major PI mutations M46I/L and I47V were present in 4 samples, and minor PI mutations L10I/V, V11I, A71T, I85V, and N88D were also detected.


  Increase of transmitted drug resistance among HIV-infected sub-Saharan Africans residing in Spain in contrast to the native population.
 PMID: 22046345       2011       PloS one
Result: Among SSA, RT-M184I/V and PR-M46L were the most frequent mutations, respectively, meanwhile in both Spanish natives and CSA, RT-T215rev and PR-V82A were the most prevalent substitutions.


  Does GSS still maintain relevance on HAART outcome after the introduction of newest active antiretroviral drugs? 48 weeks results.
 PMID: 22211659       2011       Current HIV research
Abstract: About 60% of tests reported L10FIRVC, M36ILV, M46IL, I54VLAMTS, V82AFTSLI, and L90M mutations in the protease region.


  Characterization of HIV type 1 genotypes and drug resistance mutations among drug-naive HIV type 1-infected patients in Northern Vietnam.
 PMID: 20156106       2010       AIDS research and human retroviruses
Abstract: Major protease inhibitor resistance mutations, such as L33F, M46I, and M46L, were found in three patients (1.7%).


  HIV drug resistance surveillance using pooled pyrosequencing.
 PMID: 20174661       2010       PloS one
Abstract: Using Sanger sequencing, two TDR mutations, M46L and I84V, were each detected as mixtures at a frequency of 1.04% (1/96).
Result: The M46L and I84V mutations overwhelmingly clustered with the appropriate Sanger sequences that had the mixtures identified on the electropherograms ( Figure 3 ).
Result: Two of these TDR mutations: M46L and I84V, detected at frequencies of 0.29% and 0.34% respectively, were also found in two Sanger sequences as mixed base calls ( Figure 2 ).


  Novel protease inhibitors (PIs) containing macrocyclic components and 3(R),3a(S),6a(R)-bis-tetrahydrofuranylurethane that are potent against multi-PI-resistant HIV-1 variants in vitro.
 PMID: 20439612       2010       Antimicrobial agents and chemotherapy
Abstract: At passage 50 with GRL-216 (the HIV isolate selected with GRL-216 at up to 0.16 microM [HIV216-0.16 microM]), HIV-1NL4-3 containing the L10I, L24I, M46L, V82I, and I84V mutations remained relatively sensitive to PIs, including darunavir, with the EC50s being 3- to 8-fold-greater than the EC50 of each drug for HIV-1NL4-3.


  Tissue culture drug resistance analysis of a novel HIV-1 protease inhibitor termed PL-100 in non-B HIV-1 subtypes.
 PMID: 20541566       2010       Antiviral research
Abstract: One of these involved the V82A and L90M resistance mutations while the other involved a mutation at position T80I, with other mutations being observed at positions M46I/L, I54M, K55R, L76F, P81S and I85V.


  HIV type-1 genotypic resistance profiles in vertically infected patients from Argentina reveal an association between K103N+L100I and L74V mutations.
 PMID: 20587857       2010       Antiviral therapy
Abstract: RESULTS: In protease (PR), resistance-associated mutations M46I/L, I54M/L/V/A/S and V82A/F/T/S/M/I were associated with each other and with minor mutations at codons 10, 24 and 71.



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