Abstract: RT subtype B virus isolates tended to acquire different ZDV resistance mutations (Q151M and D67N or T215Y, D67D/N and F214L) compared to subtype C (D67N, K70R, T215I or T215F).
Introduction: Two distinct TAM resistance pathways can be observed: TAM-1 (M41L, T210W and T215Y) and TAM-2 (D67N, K70R, T215F and K219Q).
Result:
Table: T215Y
Screening for and verification of novel mutations associated with drug resistance in the HIV type 1 subtype B(') in China.
Result: The 9 mutations M41L, D67N, K70R, K103N, Y181C, M184V, T215Y, L283I and N348I resulted in resistance to NRTIs or NNRTIs, but the impact of 7 mutations at 6 positions (D123E, V292I, K366R, T369A, T369V, A371V and I375V) on antiviral drug response was unknown.
Virological failure rates and HIV-1 drug resistance patterns in patients on first-line antiretroviral treatment in semirural and rural Gabon.
PMID: 23199801
2012
Journal of the International AIDS Society
Result: Ten patients had viruses with the TAM-1 mutation T215Y/F associated with AZT/D4T resistance.
Figure: M41L, L210W, and T215Y mutations are indicative of the TAM-1 pathway; D67N/G, K70R, T215F, and K219Q/E/R mutations are indicative of the TAM-2 pathway.
Monitoring HIV viral load in resource limited settings: still a matter of debate?
Result: The most frequent TAMs were T215F/Y (11/12, 91.7%), M41L (10/12, 83.3%), L210W (3/12, 27,3%), D67N (3/12, 25.0%), K70R (1/12, 8.3%) and V75I (1/12, 8.3%) (Table 3).
Table: T215Y/F
Table: T215Y
Low prevalence of transmitted K65R and other tenofovir resistance mutations across different HIV-1 subtypes: implications for pre-exposure prophylaxis.
PMID: 23305651
2012
Journal of the International AIDS Society
Method: Tenofovir-associated resistance mutations included K65R, T69 insertion, K70E and >=3 thymidine-analogue mutations (TAMs; M41L, D67N, K70R, L210W, T215F/Y, K219Q/E), inclusive of either M41L or L210W.
Minority HIV mutation detection in dried blood spots indicates high specimen integrity and reveals hidden archived drug resistance.
Abstract: STUDY DESIGN: Evaluate nucleic acids from the DBS of 33 antiretroviral-experienced subtype B-infected subjects for minority M41L, K65R, K70R, K103N, Y181C, M184V, and T215Y/F mutations by real-time PCR.
"K70Q adds high-level tenofovir resistance to ""Q151M complex"" HIV reverse transcriptase through the enhanced discrimination mechanism."
Introduction: Increased excision of NRTIs is imparted by Excision Enhancement Mutations, typically M41L, D67N, K70R, T215Y/F, L210W, and K219E/Q (also known as Thymidine Associated Mutations, or TAMs).
Discussion: Mutations at position 70 of RT have been known to confer NRTI resistance by two distinct mechanisms: K70R combined with at least two excision enhancing mutations, D67N and T215Y, enhances ATP-mediated excision of AZT and d4T (excision-dependent mechanism).
Differences in reversion of resistance mutations to wild-type under structured treatment interruption and related increase in replication capacity.
Introduction: Mixtures of wild-type and variants T215Y in RT, L10F, I54V and V82A in PR appeared 6 months after the first mixture at position 184 was detected.
Introduction: The authors reported a faster rate of reversion for primary resistance mutations (K70R, M184I/V, T215Y/F in RT, and D30N, M46I/L, V82A, L90M in PR) compared to secondary mutations (M41L, D67N,
Clinical significance of HIV reverse-transcriptase inhibitor-resistance mutations.
Abstract: Several large-scale HIV-1 genotypic analyses have revealed that the most prevalent nucleos(t)ide analog RT inhibitor (NRTI)-resistance mutation is M184V/I followed by a series of thymidine analog-associated mutations: M41L, D67N, K70R, L210W, T215Y/F and K219Q/E.
Thymidine analogue excision and discrimination modulated by mutational complexes including single amino acid deletions of Asp-67 or Thr-69 in HIV-1 reverse transcriptase.
PMID: 21504903
2011
The Journal of biological chemistry
Abstract: M41L, T215Y, etc.) while the deletion of Thr-69 (Delta69) is rarely found in isolates containing TAMs.
Abstract: M41L/T215Y), while Delta69 (or the complex S68G/Delta69/K70G) antagonize the effects of TAMs in ATP-mediated excision.
HIV mutation literature information.
PMID: 
2012
PloS one
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