Introduction: Standard population genotyping identified
Result: K65R/M184I double-mutant and wild-type were detected only once each.
Result: Of the 204 sequences, 179 (88%) contained M184V and 22 (11%) contained M184I.
Result: Of twelve clones studied, five were M184V single-mutants, one was a M184I single-mutant, and six were K65R/M184V double-mutants.
Result: The most common sequence was the K65R/M184V double-mutant in 102/204 (50%), followed by M184V single-mutant in 77/204 (38%), and M184I single-mutant in 21/204 (10%).
Prevalence and clinical significance of HIV drug resistance mutations by ultra-deep sequencing in antiretroviral-naive subjects in the CASTLE study.
Result: Considering specific TDRs that could impact virologic response to the N(t)RTI backbone, TDF/FTC, used in the study, 9 (6.4%) of the subjects had M184V/I identified by UDS at baseline.
Result: Of the 141 subjects with a UDS result, 35 (24.8%) had a nucleoside(tide) reverse transcriptase inhibitor N(t)RTI(s) TDR; 26 of these had a thymidine analog mutation (TAM), 9 had a M184V/I, and 2 had a variant with a K65R.
Result: Specific TDR patterns and levels for subjects with a M184V/I and K65R are shown in Table 4.
Table: M184I
Table: M184V/I
The effect of transmitted HIV-1 drug resistance on pre-therapy viral load.
Abstract: DISCUSSION: Our study provides clear evidence of an in-vivo fitness cost associated with the M184V/I mutation independent of drug effects which select for this mutation.
Abstract: However, patients harbouring M184V/I (n = 61) had a significantly lower viral load [adjusted mean difference -0.33 log10 copies/ml (95% CI -0.54 to -0.11), 53% lower (95% CI 22 to 71%), P = 0.002] compared to wild-type virus.
Dynamics of HIV-1 quasispecies during antiviral treatment dissected using ultra-deep pyrosequencing.
Abstract: CONCLUSIONS: With this highly sensitive UDPS protocol preexisting drug resistance was infrequently observed; only M184I, T215A and T215I were detected at very low levels.
Abstract: During treatment failure, M184V replaced M184I and dominated the population in combination with T215Y, while wild-type variants were rarely detected.
Abstract: In four of five pre-treatment samples low levels (0.07-0.09%) of the M184I mutation were observed.
Table: M184I
Discussion: 0.15% for M184V compared to 0.07% for M184I) or that these mutations are associated with a higher fitness cost.
Discussion: In addition, in
Mechanistic interplay among the M184I HIV-1 reverse transcriptase mutant, the central polypurine tract, cellular dNTP concentrations and drug sensitivity.
Result: 4D), and were transduced with the M184I (+) and (-) cPPT vectors.
Result: As seen in Figure 4B, the M184I (+) cPPT vector exhibited a high resistance to 3TC, and only a minimal decrease in transduction was seen with this vector even at 750 microM 3TC.
Result: As seen in Figure 5B, upon dC treatment, the M184I (-) cPPT vector gained a strong resistance to 3TC.
Result: As shown in Figure 2A, the M184I mutant vector showed ~70% transduction efficiency in dividing HLFs, which is only slightly reduced when compared to WT (~80%, Figure 1B).
Result: As shown in Figure 2B and 2C, a drastic decrease in the 2LTR copy number in the M184I (-) cPPT vector was observed, compared to the M184I (+) cPPT vector in nondividing HLFs, while the copy number of the late p
Partially active HIV-1 Vif alleles facilitate viral escape from specific antiretrovirals.
Abstract: Among these mutations, the lamivudine drug-resistance-associated mutation M184I in reverse transcriptase was detected in 25% of clones in the absence of any lamivudine exposure.
Proteochemometric modeling of the susceptibility of mutated variants of the HIV-1 virus to reverse transcriptase inhibitors.
Abstract: The most deleterious mutations were K65R, Q151M, M184V/I, and T215Y/F, each of them decreasing susceptibility to most of the NRTIs.
Result: For example, mutations M184V/I and K65R, which are the most deteriorating for 3TC and FTC, lead to significant increase in susceptibility to AZT, thus suggesting a benefit of combining these inhibitors.
Result: Similarly, mutation M184V/I confers high resistance to the two structurally very similar inhibitors 3TC and FTC; it also affects susceptibility to ABC, DDC, and DDI, but is unimportant or even beneficial for AZT, d4T, and TDF.
Allele-specific real-time PCR testing for minor HIV-1 drug resistance mutations: assay preparation and application to reveal dynamic of mutations in vivo.
Abstract: METHODS: We developed the allele-specific PCR assay, using the most common drug resistance mutations in Chinese AIDS patients, K103N, M184V/I, T215F/Y as a model system.
Abstract: RESULTS: The sensitivities of ASPCR assay were 0.04% for K103N, 0.30% for M184I, 0.40% for M184V, 0.03% for T215F and 0.02% for T215Y.
Selection of drug-resistant HIV-1 during the early phase of viral decay is uncommon in treatment-naive patients initiated on a three- or four-drug antiretroviral regimen including lamivudine.
Abstract: In patients on dual therapy, M184I/V mutants were found frequently.
Abstract: In this study, the extent to which selection of the HIV-1 reverse transcriptase M184I/V mutations occur during the initial phase of viral decay in treatment-naive HIV-1 infected patients receiving antiretroviral therapy (ART) was examined.
Abstract: Plasma virus from three cohorts of treatment-naive patients initiating quadruple (n = 43), triple (n = 14) or dual (n = 15) lamivudine-containing ART were analyzed for M184I/V during the first 6 months of therapy using direct sequencing and a sensitive selective real-time PCR method.
Abstract: Selection of M184I/V mutants was found to be rare during the initial phase of viral decay after initia
High rate of early virological failure with the once-daily tenofovir/lamivudine/nevirapine combination in naive HIV-1-infected patients.
PMID: 19036752
2009
The Journal of antimicrobial chemotherapy
Abstract: Resistance genotypes for the nine Group 2 failing patients showed the mutations M184V/I (n = 3), K65R (n = 6), one or more NNRTI resistance mutations in all cases.
HIV mutation literature information.
PMID: 
2010
Antiviral therapy
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