Kinetics of Archived M184V Mutation in Treatment-Experienced Virally Suppressed HIV-Infected Patients.
PMID: 14624368
2003
The Journal of infectious diseases
Abstract: In 14 of 25 and in 3 of 25 subjects, the M184V and the L90M mutations, respectively, were detected as minor populations, at different times during STI.
Abstract: Minor populations of drug-resistant variants were detected by quantitative real-time polymerase chain reaction, by use of allele-discriminating oligonucleotides for 2 key resistance mutations: L90M (protease) and M184V (reverse transcriptase).
Drug resistance mutations during structured treatment interruptions.
Abstract: Among the 74 patients receiving lamivudine, the M184V/I mutation was detected in 13/74 (17.6%) patients.
Abstract: CONCLUSIONS: The M184V/I mutation is frequently selected during repeated treatment interruptions.
Abstract: The relative risk for virological failure was 2.55-fold higher in patients with the M184V/I mutation than in patients without detectable mutation (P=0.007).
Change to abacavir-lamivudine-tenofovir combination treatment in patients with HIV-1 who had complete virological suppression.
Abstract: Reversion of the M184V mutation alone did not change viral replicative capacity (RC), but it led to enhanced resistance to zidovudine and tenofovir.
A review of HIV-1 resistance to the nucleoside and nucleotide inhibitors.
PMID: 14754429
2003
Current drug targets. Infectious disorders
Abstract: There are several major genetic mutational patterns of resistance and cross-resistance that evolve with the NRTIs including the thymidine analog mutations M41L, D67N, K70R, L210W, T215Y, and K219Q/E/W, the non-thymidine mutations M184V, L74V, and K65R, and the multidrug resistant Q151M complex, as well as others.
HIV fitness and resistance as covariates associated with the appearance of mutations under antiretroviral treatment.
PMID: 15000581
2003
Scandinavian journal of infectious diseases. Supplementum
Abstract: A deep molecular analysis (90 clones) conducted on proviral DNA of lymphocytes demonstrates that M184V strains are no longer detected in plasma and proviral DNA shortly after interruption of therapeutic regimens including lamivudine (even if a new therapeutic regimen has been started).
Abstract: At the time of interruption of specific viral pressure (lamivudine in the case of M184V), wild-type virus easily overgrows mutated strains.
Abstract: In the case of M184V (a mutation involving the catalytic site of HIV reverse transcriptase), no pathways of viral escape have been defined so far; it is thus conceivable that the mutated virus maintains a relatively low replicative capacity.
Abstract: This supports the concept that the low fitness of M184V strains is not easily compensated by additional
Sexual transmission of HIV-1 isolate showing G-->A hypermutation.
Abstract: The patient's viral genotype showed several mutations related to antiretroviral drug resistance in RT (T69N, M184V, T215F, K219Q) and protease (M36I, G48V, I54V, T63L, V82A) genes.
Prevalence of the mutational pattern E44D/A and/or V118I in the reverse transcriptase (RT) gene of HIV-1 in relation to treatment with nucleoside analogue RT inhibitors.
Abstract: It has been reported that a new pattern of mutations, E44D/A and/or V118I, in the reverse transcriptase (RT) gene of HIV-1 confers a moderate level of resistance to lamivudine in the absence of the M184V mutation.
Abstract: No relationship was observed between this mutational pattern and the lamivudine-specific resistance mutation M184V.
Persistence and fitness of multidrug-resistant human immunodeficiency virus type 1 acquired in primary infection.
Abstract: In two of these PHI cases, a rebound to higher levels of plasma viremia only occurred when the M184V mutation in reverse transcriptase could no longer be detected and, in a third case, nondetection of M184V was associated with an inability to isolate virus.
Efficacy and safety of stavudine plus didanosine in asymptomatic HIV-infected children with plasma HIV RNA below 50,000 copies per milliliter.
Abstract: Resistance mutations linked to didanosine (L74V or M184V) or stavudine (V75T) were not recognized and neither were multinucleoside resistant genotypes (151 complex or 69 inserts).
HIV mutation literature information.
PMID: 
2003
The Journal of infectious diseases
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