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 NRTI monophosphate.
Impact of the number of failed therapeutic regimes on the development of resistance mutations to HIV-1 in northeast Brazil.
PMID: 17962868
2007
The Brazilian journal of infectious diseases
Abstract: There was a significant increase in resistance mutations V82A/F/L/T, I84V, L90M, M41L, K70R, L210W, T215Y/F and K219Q/E in MF.
N348I in the connection domain of HIV-1 reverse transcriptase confers zidovudine and nevirapine resistance.
Method: The analysis was performed for N348I and for each of the TAMs: M41L, D67N, K70R, L210W, T215Y/F, and K219Q/E.
Result: N348I was highly associated with several key drug resistance mutations, including M184V/I (p = 6.6 x 10-45) the TAMs M41L (p = 1.8 x 10-14), D67N (p = 7.7 x 10-10), K70R (p = 1.4 x 10-10), T215Y/F (p = 6.0 x 10-21), K219Q/E (p = 8.0 x 10-4), and L210W (p = 0.002), and the NNRTI re
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.
Antiviral efficacy and genotypic resistance patterns of combination therapy with stavudine/tenofovir in highly active antiretroviral therapy experienced patients.
Abstract: Any single type-1 thymidine analogue mutation (TAM; M41L, L210W, T215Y) had a negative effort on the change in HIV RNA at 6 months, whereas among type-2 TAMs (D67N, K70R, K219Q), only D67N showed a trend for a negative effect.
Prevalence of M184V and K65R in proviral DNA from PBMCs in HIV-infected youths with lamivudine/emtricitabine exposure.
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.
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: Whereas T215Y occurs alone or with M41L and L210W (TAM-1 pattern), T215F rarely occurs with these mutations
Abstract: Whereas introduction of L210W improved the relative fitness of an M41L/T215Y mutant in the presence of ZDV, introduction of this mutation into a D67N/K70R/K219Q background resulted in decreased relative fitness in the presence or absence of drug.
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.
Alkoxyalkyl esters of (S)-9-[3-hydroxy-2-(phosphonomethoxy)propyl]adenine are potent inhibitors of the replication of wild-type and drug-resistant human immunodeficiency virus type 1 in vitro.
PMID: 16870786
2006
Antimicrobial agents and chemotherapy
Abstract: We synthesized several alkoxyalkyl esters of (S)-HPMPA and now report that hexadecyloxypropyl-(S)-HPMPA [HDP-(S)-HPMPA] and octadecyloxyethyl-(S)-HPMPA [ODE-(S)-HPMPA]had 50% effective concentrations of 0.4 to 7.0 nanomolar and were nearly fully active against HIV variants having reverse transcriptase mutations M184V and K103N and against a zidovudine-resistant variant with mutations D67N, K70R, T215Y, and K219Q.
HIV mutation literature information.
PMID: 
2007
AIDS (London, England)
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