Abstract: Both D- and L-2'-fluoro-4'-thio-2',3'-unsaturated nucleosides were synthesized and their anti-HIV activity against the drug sensitive virus and lamivudine-resistant mutant (M184V) were evaluated.
Lack of persistent drug-resistant mutations evaluated within and between treatment interruptions in chronically HIV-1-infected patients.
Abstract: In the remaining six patients, the following patterns of mutations associated with viral resistance were found: one mutation (K70R), which was observed in one patient during the 1st TI and persisted during follow-up; two mutations (L90M, M184V), which were observed in four patients during the 1st TI and were intermittently present or lost following extended TI, treatment reinitiation and/or during subsequent TI; and evolution of two mutations (M184V, K219E) observed in two patients.
Studies of molecular mechanism of tenofovir against 3TC- and AZT-resistance mutant HIV-1 reverse transcriptase.
Abstract: TFV-DP is located far away from the bulky side chain of Val184 in M184V RT and tenofovir is readily translocated without steric hindrance with Asp185 after incorporation into the growing primer chain complexed with AZT-resistant RT.
Novel enzyme-linked minisequence assay for genotypic analysis of human immunodeficiency virus type 1 drug resistance.
PMID: 14605126
2003
Journal of clinical microbiology
Abstract: ELMA is a combination of hybridization and a 1-base extension reaction, and we designed the assay to detect five mutations conferring nucleoside analogue resistance (M41L, D67N, K70R, T215Y, and M184V) and six mutations conferring protease inhibitor resistance (D30N, M46I, G48V, V82A, I84V, and L90M).
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
HIV mutation literature information.
PMID: 
2003
Nucleosides, nucleotides & nucleic acids
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