Introduction: By contrast, the mutations M41L, D67N, K70R, L210W, T215F/Y and K219Q/E - typically referred to as thymidine analog mutations (TAMs) - augment the ability of HIV-1 RT to excise the chain-terminating NRTI-monophosphate from a prematurely terminated DNA chain.
Method: D67N/K70R/T215F/K219Q (TAM67) and TAM67/K65R HIV-1 RT were generated by site-directed mutagenesis of WT HIV-1LAI RT.
Result: To address a possible mechanism by which the si
Transmission networks of drug resistance acquired in primary/early stage HIV infection.
Abstract: The transmission of nucleoside analogue mutations and 215 resistant variants (T215C/D/I/F/N/S/Y) declined with clustering (7.9 vs.
Mechanism by which a glutamine to leucine substitution at residue 509 in the ribonuclease H domain of HIV-1 reverse transcriptase confers zidovudine resistance.
Abstract: In the current study, we have defined the mechanism by which Q509L confers AZT resistance by performing in-depth biochemical analyses of wild type, D67N/K70R/T215F and D67N/K70R/T215F/Q509L HIV-1 RT.
Abstract: We recently reported that zidovudine (AZT) selected for the Q509L mutation in the ribonuclease H (RNase H) domain of HIV-1 reverse transcriptase (RT), which increases resistance to AZT in combination with the thymidine analogue mutations D67N, K70R, and T215F
Genotypic resistance in plasma and peripheral blood lymphocytes in a group of naive HIV-1 patients.
Abstract: RESULTS: Direct sequencing of DNA provirus disclosed key mutations (such as G190A/S, V106A, K103N and T215F) to RT inhibitors more frequently (7 patients out 31) than in plasma RNA (2 out of 31).
[Prevalence of mutations of resistance to HIV-I reverse transcriptase inhibitors among HIV-infected patients in the Southern Federal District].
Abstract: The group of patients receiving antiviral treatment was found to have different drug resistance mutations in the HIV-1 pol gene: K70R, M184V, K219Q, T215Y/F, L74V, etc.
Lamivudine/abacavir maintains virological superiority over zidovudine/lamivudine and zidovudine/abacavir beyond 5 years in children.
Abstract: Different patterns of covariation were frequently observed for different mutations at the same position including the RT mutations T69D versus T69N, L74V versus L74I, V75I versus V75M, T215F versus T215Y, and K219Q/E versus K219N/R, and the protease mutations M46I versus M46L, I54V versus I54M/L, and N88D versus N88S.
Method: These mutations inc
Selection of mutations in the connection and RNase H domains of human immunodeficiency virus type 1 reverse transcriptase that increase resistance to 3'-azido-3'-dideoxythymidine.
Abstract: The roles of A371V and Q509L in AZT resistance were confirmed by site-directed mutagenesis: A371V and Q509L together increased AZT resistance approximately 10- to 50-fold in combination with TAMs (M41L/L210W/T215Y or D67N/K70R/T215F) but had a minimal effect without TAMs (1.7-fold).
Abstract: Thereafter, the T215I mutation appeared but was later replaced by T215F, resulting in a large increase in AZT resistance ( approximately 16,000-fold).
Molecular mechanisms of bidirectional antagonism between K65R and thymidine analog mutations in HIV-1 reverse transcriptase.
Abstract: In addition, the TAMs combination D67N/K70R/T215F/K219Q decreased susceptibility to the L-nucleotide lamivudine by a discrimination mechanism, whereas the M41L/L210W/T215Y combination had little effect on susceptibility to lamivudine.
Abstract: RESULTS: The addition of K65R to two clinically relevant combinations of TAMs (M41L/L210W/T215Y or D67N/K70R/T215F/K219Q) significantly reduced the recombinant enzymes' ability to excise all chain-terminating PMID: 17678470
2007
AIDS research and human retroviruses
Abstract: Mutations T215Y/F, M184V, and M41L were the most frequent for NRTI.
HIV mutation literature information.
PMID: 
2008
AIDS (London, England)
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