Dioxolane guanosine 5'-triphosphate, an alternative substrate inhibitor of wild-type and mutant HIV-1 reverse transcriptase. Steady state and pre-steady state kinetic analyses.
PMID: 12651859
2003
The Journal of biological chemistry
Abstract: HIV-1 with the reverse transcriptase mutations K65R, L74V, and/or Q151M were less sensitive to DXG, whereas the mutation K103N re-sensitized the virus to the inhibitory effect of DXG.
K65R with and without S68: a new resistance profile in vivo detected in most patients failing abacavir, didanosine and stavudine.
Abstract: D-d4FC is highly effective at inhibiting subsets of lamivudine- and zidovudine-resistant variants but, like other NRTIs, seems less potent against multi-NRTI-resistant viruses, particularly those carrying the Q151M complex of mutations.
Pathways for the emergence of multi-dideoxynucleoside-resistant HIV-1 variants.
Abstract: CONCLUSION: HIV-1(Q151M) probably develops through a poorly replicating HIV-1(Q151L); however, it is also possible that it occurs through two concurrent base changes.
Abstract: DESIGN AND METHODS: Propagation assays and competitive HIV-1 replication assays were used to evaluate the fitness of various infectious clones, including two putative intermediates (HIV-1(Q151K(AAG)) and HIV-(1Q151L(CTG))) for HIV-1(Q151M(ATG)), in terms of sensitivity to zidovudine and didanosine.
Abstract: HIV-1(Q151M) was less susceptible to drugs, while HIV-1(Q151L/M230I) was as sensitive as HIV-1(WT).
Abstract: OBJECTIVE: To investigate the mechanism by which the Q151M mutation in PMID: 12908931
2003
AIDS research and human retroviruses
Abstract: Instead, a E219D mutation evolved in virus from two patients and a Q151M mutation evolved in two other patients.
Chemical system biology based molecular interactions to identify inhibitors against Q151M mutant of HIV-1 reverse transcriptase.
Abstract: At week 96, among the switchers, i.e., group A d4T/ddI to ZDV/3TC, group B ZDV/3TC to d4T/ddI, and group C ZDV/3TC/ddI to d4T/3TC/abacavir: NAM, 12/21 (57%), 4/7 and 1/3; Q151M, 4/21 (19%), 0% and 1/3, respectively.
Abstract: CONCLUSIONS: Multi-NRTI resistance (NAM and Q151M) and M184V (only in 3TC failure) are commonly found in HIV-1 subtype A/E infection associated with NRTI failure.
Abstract: RESULTS: Resistance mutations found in the d4T/ddI, ZDV/3TC, and ZDV/3TC/ddI groups: none at baseline; at week 48, nucleoside analogue mutations (NAM), 2/17 (12%), 2/10 (20%), and 1/8; Q151M complex, 3/17 (18%), 0%, and 0%; M184V, 0%, 10/10 (P < 0.001), 3/8; V75T, 3/17 (18%), 0%, and 0%; PMID: 14522102
2003
International journal of antimicrobial agents
Abstract: Finally Q151M, the marker mutation able to confer resistance to all nucleoside analogues, was detected in seven patients with a viral load of between 1 x 10(4) and 9 x 10(4) HIV-1 RNA copies/ml.
Antiretroviral therapy in HIV-2-infected patients: changes in plasma viral load, CD4+ cell counts, and drug resistance profiles of patients treated in Abidjan, Cote d'Ivoire.
Abstract: Three patients had the multi-drug-resistant mutation, Q151M, two of whom showed reduced susceptibility to zidovudine, didanosine, stavudine and zalcitabine.
Clinical, immunological and virological response to different antiretroviral regimens in a cohort of HIV-2-infected patients.
Abstract: Development of mutations proved to be similar to that observed in HIV-1-infected patients, with the exception of a higher occurrence of the Q151M mutation within the reverse transcriptase gene.
Long-term outcome of HIV-infected patients with multinucleoside-resistant genotypes.
Abstract: BACKGROUND: Multiple resistance to nucleoside analogs mediated by the Q151M complex and/or codon 67-69 inserts/deletions represents a growing problem among HIV-infected persons, most of whom have been exposed to sequential therapies for long periods of time.
Abstract: No differences were found when patients with Q151M and codon 67-69 rearrangements were compared.
Abstract: Twelve of them carried the Q151M complex and 9 harbored different codon 67-69 inserts.
HIV mutation literature information.
PMID: 
2003
The Journal of biological chemistry
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