Effect of translocation defective reverse transcriptase inhibitors on the activity of N348I, a connection subdomain drug resistant HIV-1 reverse transcriptase mutant.
PMID: 23273211
2012
Cellular and molecular biology (Noisy-le-Grand, France)
8Discussion: The A62V/V75I/F77L/F116Y/Q151M set of mutations is known as the ""Q151M"" complex RT, and has been known as a multidrug-resistance mutation, since the latter mutations are known to be involved in resistant variants with reduced susceptibility to dideoxynucleotides and to AZT."
Discussion: Unlike D67N/K70R/L210Q/T215F RT, the Q151M complex decreases susceptibility to NRTIs by decreasing incorporation efficiency of the inhibitors rather than increasing excision and unblocking of chain-ter
Monitoring HIV viral load in resource limited settings: still a matter of debate?
Result: One patient carried Q151M mutation, associated with M41L, D67N, T215F and M184V, conferring pan-nucleoside resistance, except to tenofovir.
Table: Q151M
Virological failure rates and HIV-1 drug resistance patterns in patients on first-line antiretroviral treatment in semirural and rural Gabon.
PMID: 23199801
2012
Journal of the International AIDS Society
Result: Two patients had HIV-1 strains harbouring the multi-NRTI resistance Q151M mutation associated with M184V/I and Y188L.
HIV-1 reverse transcriptase (RT) polymorphism 172K suppresses the effect of clinically relevant drug resistance mutations to both nucleoside and non-nucleoside RT inhibitors.
PMID: 22761416
2012
The Journal of biological chemistry
Abstract: Q151M complex).
Multi-nucleoside reverse transcriptase inhibitor resistant HIV type-1 in a patient from Sierra Leone failing stavudine, lamivudine and nevirapine.
Abstract: We report a 33-year-old HIV type-1 (HIV-1)-infected male from Sierra Leone who harboured extensive drug resistance mutations to all nucleoside reverse transcriptase inhibitors (NRTIs) and non-NRTIs, including the multi-NRTI-resistance Q151M complex, K65R, M184I and Y181I, after using standard first-line generic fixed-dose stavudine, lamivudine and nevirapine (Triomune ) for 36 months.
Herpes simplex virus type 2 suppressive therapy with acyclovir or valacyclovir does not select for specific HIV-1 resistance in HIV-1/HSV-2 dually infected persons.
PMID: 21148504
2011
The Journal of infectious diseases
Discussion: The mutations selected in the in vitro experiments confer cross-resistance to NRTIs: V75I contributes resistance to multiple NRTIs in the presence of a concurrent Q151M mutation, T69N and other variants at position 69 are selected by didanosine and other NRTIs but their susceptibility profiles are not well-described (http://hivdb.stanford.edu/), and the variants M184I/V confer high-level resistance to lamivudine and emtricitabine.
Mechanism of resistance to GS-9148 conferred by the Q151L mutation in HIV-1 reverse transcriptase.
PMID: 21402840
2011
Antimicrobial agents and chemotherapy
Abstract: Q151L is not stably selected by any of the approved nucleoside or nucleotide analogues; however, it may be a transient intermediate that leads to the related Q151M mutation, which confers resistance to multiple compounds that belong to this class of RT inhibitors.
Clinical significance of HIV reverse-transcriptase inhibitor-resistance mutations.
Abstract: In HIV-2 infections, the high prevalence of the Q151M mutation associated with multi-NRTI resistance has been frequently observed.
Chemical system biology based molecular interactions to identify inhibitors against Q151M mutant of HIV-1 reverse transcriptase.
PMID: 21285456
2011
The Journal of infectious diseases
Abstract: Following detection, individuals with Q151M tended to have lower suppression rates and higher mortality rates, relative to control subjects.
Abstract: The 69 insertion and Q151M mutations are multi-nucleoside/nucleotide resistance mutations (MNR).
Abstract: The 69 insertion study (27 control subjects, 14 case patients) identified didanosine exposure as a risk (odds ratio, 5.0 per year; P = .019), whereas the Q151M study (which included 44 control subjects and 25 case patients) detected no associations.
Chemical system biology based molecular interactions to identify inhibitors against Q151M mutant of HIV-1 reverse transcriptase.
1Abstract: HIV-1 carrying the ""Q151M complex"" reverse transcriptase (RT) mutations (A62V/V75I/F77L/F116Y/Q151M, or Q151Mc) is resistant to many FDA-approved nucleoside RT inhibitors (NRTIs), but has been considered susceptible to tenofovir disoproxil fumarate (TFV-DF or TDF)."
Abstract: Biochemical experiments established that the increased resistance to tenofovir is not the result of enhanced excision, as K70Q/Q151Mc RT exhibited diminished, rather than enhanced ATP-based primer unblocking activity.
HIV mutation literature information.
PMID: 
2012
Cellular and molecular biology (Noisy-le-Grand, France)
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