Abstract: CONCLUSION: Different combinations of V118I, H208Y, and T215Y produce NNRTI hypersusceptibility.
Abstract: In addition, H208Y/T215Y, V118I/T215Y, and V118I/H208Y/T215Y were hypersusceptible to delavirdine and nevirapine.
Abstract: RESULTS: The single mutations V118I, H208Y, and T215Y did not show hypersusceptibility to efavirenz with mean fold-change of 0.58, 0.55, and 0.70, respectively (P < 0.01 and P = 0.12).
Abstract: The genetic basis for PMID: 16632914
2006
Japanese journal of infectious diseases
Abstract: In plasma HIV-1 RNA, D67N, K70R, T215Y, and Y188L were present in the reverse transcriptase (RT) region, and two primary mutations, I84V and L90M, were noted in the protease (Pro) region.
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.
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.
Insertions and deletions in HIV-1 reverse transcriptase: consequences for drug resistance and viral fitness.
Abstract: T215Y) in the viral RT confers an ATP-dependent phosphorolytic activity that facilitates the removal of the inhibitor from primers terminated with zidovudine or stavudine.
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.
A dual superinfection and recombination within HIV-1 subtype B 12 years after primoinfection.
PMID: 16763489
2006
Journal of acquired immune deficiency syndromes (1999)
Abstract: This result suggests a superinfection with 2 HIV-1 strains, one of which showed the T215Y + M184V resistance mutations.
Fitness comparison of thymidine analog resistance pathways in human immunodeficiency virus type 1.
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 clustering of L210W with TAM-1 mutations and T215F with TAM-2 mutations.
Abstract: Whereas introduction of L210W improved the relative fitness of an
Involvement of novel human immunodeficiency virus type 1 reverse transcriptase mutations in the regulation of resistance to nucleoside inhibitors.
Abstract: In particular, T39A, K43E/Q, K122E, E203K, and H208Y clustered with the nucleoside analogue mutation 1 cluster (NAM1; M41L+L210W+T215Y).
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: 
2006
AIDS (London, England)
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