Abstract: Singleton mutations to protease-inhibitor/PI, nucleoside-reverse-transcriptase-inhibitor/NRTI or non-nucleoside-reverse-transcriptase-inhibitor/NNRTI predominated (8/10): PI mutations (M46L, V82F, L90M); NRTI mutations (M41L, D67N) and NNRTI mutations (K103N/S).
In vitro selection of HIV-1 CRF08_BC variants resistant to reverse transcriptase inhibitors.
PMID: 25482475
2015
AIDS research and human retroviruses
Abstract: As expected, M184I alone, or with V90I or D67N, decreased 3TC susceptibility by over 1,000-fold.
Abstract: Initial mutations, in combination with other previously reported substitutions (K20R, D67N, V90I, K101R/E, V106I/A, V108I, F116L, E138R, A139V, V189I, G190A, D218E, E203K, H221Y, F227L, N348I, and
Virological failure and HIV-1 drug resistance mutations among naive and antiretroviral pre-treated patients entering the ESTHER program of Calmette Hospital in Cambodia.
Result: The TAM2 pathway (D67N, K70R, T215F, and K219Q/E) was present in 5/22, 4/22, 8/22, 2/22 patients.
The case for addressing primary resistance mutations to non-nucleoside reverse transcriptase inhibitors to treat children born from mothers living with HIV in sub-Saharan Africa.
PMID: 24439027
2014
Journal of the International AIDS Society
Abstract: The D67N thymidine-analogue mutation was observed in only two children whose mothers had received chemoprophylaxis of mother-to-child transmission (MTCT).
Result: In addition, the D67N thymidine-analogue mutation (TAM) was observed in only two children whose mother had received prevention of HIV MTCT.
Table: D67N
HIV-1 virologic failure and acquired drug resistance among first-line antiretroviral experienced adults at a rural HIV clinic in coastal Kenya: a cross-sectional study.
Method: In this study, HIV-2 resistance mutations were identified using the list generated by the 'Collaborative HIV and Anti-HIV Drug Resistance Network', leading to the following mutations in reverse transcriptase - K65R, D67G/N, N69S/T, K70N/R, L74V, Result: The most prevalent resistance mutations to NRTI were the following: M184V (n = 17, 81%), Q151M (n = 5, 24%), S215F/Y (n = 5, 24%), V111I (n = 4, 19%), K65R (n = 3, 14%), M184I (n = 2, 10%), and D67N (n = 2, 10%).
Characteristics of HIV-1 natural drug resistance-associated mutations in former paid blood donors in Henan Province, China.
Result: D67N accounted for 2.8% and caused AZT and d4T resistance.
Result: HNHIV46, HNHIV74, HNHIV77, and HNHIV137 were clustered together, with HNHIV46 and HNHIV137 having A71V, D67N, K101E, and G190A mutations, HNHIV74 having A71T mutation, and HNHIV77 having A71V and K103N mutations.
Result: HNHIV97 locus mutations included D67N, T69A, K70R, T215Y, K219E, K103N, and Y181C.
Table: D67N
Discussion: Results from
Molecular basis of the association of H208Y and thymidine analogue resistance mutations M41L, L210W and T215Y in the HIV-1 reverse transcriptase of treated patients.
Abstract: Thymidine analogue resistance mutations (TAMs) in HIV-1 reverse transcriptase (RT) associate in two clusters: (i) TAM1 (M41L, L210W and T215Y) and TAM2 (D67N, K70R, K219E/Q, and sometimes T215F).
Limited evolution but increasing trends of primary non-nucleoside reverse transcriptase inhibitor resistance mutations in therapy-naive HIV-1-infected individuals in India.
Abstract: HIV-1 resistance to zidovudine [AZT (azidothymidine)] is associated with selection of the mutations M41L, D67N, K70R, L210W, T215F/Y and K219Q/E in RT (reverse transcriptase).
Introduction: HIV-1 resistance to AZT is associated with selection of the thymidine analog mutations (TAMs) M41L, D67N, K70R, L210W, T215F/Y and K219Q/E in RT.
Result: Consistent with previously published data, we found that RTs