Biochemical characterization of a multi-drug resistant HIV-1 subtype AG reverse transcriptase: antagonism of AZT discrimination and excision pathways and sensitivity to RNase H inhibitors.
Result: Finally, in July 2008 four out of six TAMs relevant for highly efficient AZTMP excision (M41L, D67N, T215Y and K219E, missing K70R and L210W) as well as four out of five discrimination mutations (A62V, V75I, F116Y and Q151M, lacking F77I) were present.
Result: First, the K70R mutation, which is the missing fifth TAM residue promoting excision, was introduced (MR-70R).
Result: In a third variant, the pivotal discrimination substitution Q151M was reversed to WT and combined with K70R (MR-
HIV-1 Transmitted Drug Resistance Mutations in Newly Diagnosed Antiretroviral-Naive Patients in Turkey.
PMID: 26414663
2016
AIDS research and human retroviruses
Abstract: However, TAMs were divided into three categories and M41L, L210W, and T215Y mutations were found for TAM1 in 97 (7.4%) patients, D67N, K70R, K219E/Q/N/R, T215F, and T215C/D/S mutations were detected for TAM2 in 52 (3.9%) patients, and M41L + K219N and M41L + T215C/D/S mutations were detected for the TAM1 + TAM2 profile in 22 (1.7%) patients, respectively.
Patterns of HIV-1 Drug-Resistance Mutations among Patients Failing First-Line Antiretroviral Treatment in South India.
PMID: 26385878
2016
Journal of the International Association of Providers of AIDS Care
Abstract: RESULTS: Of the study patients followed up for 6 months, 23 patients failed first-line therapy and the mutation of I135R/T/V/X, L178 I/M, M184V/I, D67N, K70R, and K103N was most common.
Comparison of genotypic and virtual phenotypic drug resistance interpretations with laboratory-based phenotypes among CRF01_AE and subtype B HIV-infected individuals.
Result: Protease (PR) RAMs detected from this outlier sample were M46I, I47V and I84V, and reverse transcriptase (RT) RAMs were A62V, D67N, K70R, V75I, F116Y, Q151M and K219Q.
Discussion: Other RT RAMs found in the CRF01_AE sample were thymidine analogue-associated mutations (TAMs) which included D67N, K70R and K219Q.
Assessing transmissibility of HIV-1 drug resistance mutations from treated and from drug-naive individuals.
Discussion: We show here that D30N, N88D/S and L90 M also have high transmissibility and that other SDRMs have higher (M41L, T215Rev and K219E/N/Q/R for NRTIs and K101E/P for the NNRTIs) or lower transmissibility (K70E/R, L74I/V, and T215Y/F for NRTIs; Y181C/I/V for NNRTIs and I84 V and I54A/L/M/S/T/V for protease inhibit
Compensatory substitutions in the HIV-1 capsid reduce the fitness cost associated with resistance to a capsid-targeting small-molecule inhibitor.
Abstract: Q67H, K70R, and T107N each conferred low-level resistance to PF74 and collectively conferred strong resistance.
Abstract: In the present study, we dissected the individual and combinatorial contributions of each of the five substitutions Q67H, K70R, H87P, T107N, and L111I to PF74 resistance, PF74 binding, and HIV-1 infectivity.
Abstract: PF74 binding to HIV-1 particles was reduced by the Q67H, K70R, and T107N substitutions, consistent with the location of these positions in the inhibitor-binding pocket.
Abstract: The substitutions K70R and PMID: 25582324
2015
AIDS research and human retroviruses
Discussion: In addition, we found that mutations E35D, N37DST, R57K, and K70R in the PR and D123N and I135TV in the RT were present at high rates in this cohort.
High prevalence of the K65R mutation in HIV-1 subtype C infected patients failing tenofovir-based first-line regimens in South Africa.
Result: K70R was more frequently detected in d4T-exposed patients (15.0%, n = 12) as compared to the TDF-exposed group (8.8%, n = 7) but again, the difference was not significant.
Table: K70R
Characterization of HIV drug resistance mutations among patients failing first-line antiretroviral therapy from a tertiary referral center in Lusaka, Zambia.
Result: A wide range of mutations conferring multi-NRTI resistance were also observed, including M41L (n = 7, 10%), A62V (n = 15, 22%), D67N (n = 10, 15%), K70R (n = 10, 15%), V75I (n = 2, 3%), F77L (n = 1, 1%), Y115F (n = 6, 9%), F116Y (n = 1, 1%), Q151M (n = 1, 1%), L210W (n = 3, 4%), T215Y/F (n = 7, 10%) and (n = 5, 7%), and K219Q/E (n = 4, 6%) and (n = 7, 10%).
Silent mutations at codons 65 and 66 in reverse transcriptase alleviate indel formation and restore fitness in subtype B HIV-1 containing D67N and K70R drug resistance mutations.
Result: Accordingly, we examined whether the TAMs D67N/K70R increase errors introduced by HIV-1 RT during intracellular RTn that are alleviated by silent mutations K65K and K66K.
Result: Accordingly, we investigated whether HIV-1 harboring K65K or K66K (AAA to AAG change) in the presence of the TAMs, D67N and K70R (HIVTAMK65K and HIVTAMK66K, respectively), potentiated resistance to RT inhibitors.
Result: Based on our previous data showing that K65K and K66K alleviate pausing of recombinant HIV-1 RT during cDNA synthesis of a synthetic RN
HIV mutation literature information.
PMID: 
2016
Nucleic acids research
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