Abstract: N348I appeared early in therapy and was highly associated with thymidine analogue mutations (TAMs) M41L and T215Y/F (p < 0.001), the lamivudine resistance mutations M184V/I (p < 0.001), and non-nucleoside RTI (NNRTI) resistance mutations K103N and Y181C/I (p < 0.001).
Method: The analysis was performed for N348I and for each of the TAMs: M41L, D67N, K70R, L210W, T215Y/F, and K219Q/E.
Result: PMID: 16436719
2006
Antimicrobial agents and chemotherapy
Abstract: SPD754 susceptibility was reduced 1.2- to 2.2-fold against isolates resistant to zidovudine (M41L, T215Y/F, plus a median of three additional nucleoside analogue mutations [NAMs]) and/or lamivudine (M184V) and was reduced 1.3- to 2.8-fold against isolates resistant to abacavir (L74V, Y115F, and M184V plus one other NAM) or stavudine (V75T/M, M41L, T215F/Y, and four other NAMs).
An additive/subtractive genotypic score as a determinant of the virological response to didanosine in HIV-1 infected patients.
Abstract: RESULTS: Changes at three codons (M41L, L210W, T215Y/F/D/C/E) were associated with a worse VR and three mutations (K70R, M184V, K219Q) with a better VR.
Abstract: The strongest association with the VR was obtained with the score M41L+L210W+T215Y/F/D/C/E-K70R-K219Q.
The K65R mutation in human immunodeficiency virus type 1 reverse transcriptase exhibits bidirectional phenotypic antagonism with thymidine analog mutations.
Abstract: Among samples with K65R, a strong negative association was evident with the TAMs M41L, D67N, L210W, T215Y/F, and K219Q/E (P<0.005) but not with other NRTI mutations, including the Q151M complex.
Abstract: To test this possibility, we generated recombinant HIV-1 encoding K65R in two different TAM backgrounds: M41L/L210W/T215Y and D67N/K70R/T215F/K219Q.
Evidence of differential selection of HIV-1 variants carrying drug-resistant mutations in seroconverters.
Abstract: Among RT mutations present both in PTs and SCs, M1841/V and T215F/Y had the lowest relative efficiency of transmission, whereas V1181, Y181C/I and K219E/Q showed the highest relative efficiency.
Risk factors for selection of the L74I reverse transcriptase mutation in human immunodeficiency virus type 1-infected patients.
PMID: 16801444
2006
Antimicrobial agents and chemotherapy
Abstract: L74I was strongly associated with T215F, K70R, and V75M/S/T/A mutations and increased with the number of thymidine analog mutations.
Fitness comparison of thymidine analog resistance pathways in human immunodeficiency virus type 1.
Abstract: By contrast, introduction of T215F into the D67N/K70R/K219Q background increased viral fitness in the presence of ZDV.
Abstract: In addition, T215Y mutants showed greater infectivity than did wild-type HIV-1 over a range of ZDV concentrations, but T215F mutants had only a modest advantage over the wild-type virus.
Abstract: The L210W mutation most often occurs with M41L and T215Y and rarely occurs with the T215F or TAM-2 mutation.
Abstract: These results help explain why T215Y but not T215F usually emerges as the first major TAM, as well as the cl
Involvement of novel human immunodeficiency virus type 1 reverse transcriptase mutations in the regulation of resistance to nucleoside inhibitors.
Abstract: Differently, D218E clustered with the NAM2 pathway (D67N+K70R+K219Q+T215F), and its presence in this cluster determined an increase in zidovudine resistance.
Antagonism between the HIV-1 reverse-transcriptase mutation K65R and thymidine-analogue mutations at the genomic level.
PMID: 16897664
2006
The Journal of infectious diseases
Abstract: K65R was never found on the same genome with T215F/Y and >or=2 other TAMs, except in the presence of the Q151M multiple nucleoside reverse-transcriptase inhibitor (NRTI)--resistance complex.
Abstract: These results indicate that antagonism between the K65R and T215Y/F pathways of NRTI resistance occurs at the genomic level.
Abstract: We hypothesized, on the basis of this observed antagonism, that K65R and T215Y/F with multiple TAMs would not be selected on the same human immunodeficiency virus type 1 genome in vivo.
HIV mutation literature information.
PMID: 
2007
The Brazilian journal of infectious diseases
Browser Board
Co-occurred Entities
Filtrator
ViMRT