HIV mutation literature information.


  HIV Drug Resistance in Antiretroviral Treatment-Naive Individuals in the Largest Public Hospital in Nicaragua, 2011-2015.
 PMID: 27736898       2016       PloS one
Discussion: Only four of the patients with M41L (all with long-standing infection) also presented other low-abundance DR variants (<5%): K103N, Y181C, K65R, and PR G73S.


  HIV-1 Epidemiology, Genetic Diversity, and Primary Drug Resistance in the Tyumen Oblast, Russia.
 PMID: 27957489       2016       BioMed research international
Result: The mutation A62V is an accessory mutation that often occurs in combination with the multinucleoside resistance mutations K65R or Q151M.
Discussion: Mutations K103N, M184I, T215Y, G190S, Y181C, K65R, and V108I with prevalences of 0.3 to 7% depending on the region are most frequently detected in the naive HIV-infected individuals.


  From antiretroviral therapy access to provision of third line regimens: evidence of HIV Drug resistance mutations to first and second line regimens among Ugandan adults.
 PMID: 28010730       2016       BMC research notes
Abstract: The commonest clinically significant major resistance mutations associated with the highest levels of reduced susceptibility or virological response to the relevant
Conclusion: The M184V and K65R DRMs might be due to the Tenofovir and Lamivudine ART backbone and the triple nucleoside regimen of Abacavir-Zidovudine-Lamivudine that most of our patients were initiated on.
Result: In our cohort, the commonest clinically significant major NRTI resistance mutations associated with highest levels of reduced susceptibility or virological response were the Non-thymidine analogue mutations (Non-TAMs): M184V:20.7% and K65R:8.0%, while M41L and K70R (both 8.0%) were the commonest TAMs.


  Week 144 resistance analysis of elvitegravir/cobicistat/emtricitabine/tenofovir DF versus efavirenz/emtricitabine/tenofovir DF in antiretroviral-naive patients.
 PMID: 25321623       2015       Antiviral therapy
Abstract: Emergent substitutions were E92Q (n=7), N155H (n=3), Q148R (n=1) and T66I (n=1) in IN, and M184V/I (n=10) and K65R (n=4) in RT.
Abstract: In the EFV/FTC/TDF group, virus from 14 patients (4.0%; 14/352 treated patients; 4 during weeks 96-144) developed a resistance substitution to EFV (n=14; K103N: n=13), FTC (M184V/I: n=4) or TDF (K65R: n=3).


  Derivatives of mesoxalic acid block translocation of HIV-1 reverse transcriptase.
 PMID: 25355312       2015       The Journal of biological chemistry
Abstract: The K65R mutation in HIV-1 RT, which reduces affinity to PFA, increases affinity to CPHM.


  Prevalence of M184V and K65R in proviral DNA from PBMCs in HIV-infected youths with lamivudine/emtricitabine exposure.
 PMID: 25355888       2015       Journal of virology
Abstract: Besides the key resistance mutations K65R, Q151M, and M184V, we identified a novel mutation, V111I, in the polymerase domain.
Abstract: Biochemical assays demonstrate that V111I restores the polymerization defects of the K65R and Q151M viruses but negatively affects the fidelity of the HIV-2 RT enzyme.
Abstract: This mutation was significantly associated with mutations K65R and Q151M.


  Next generation sequencing improves detection of drug resistance mutations in infants after PMTCT failure.
 PMID: 25542470       2015       Journal of clinical virology
Result: K65R was detected at a low frequency in all patients.
Discussion: A major limitation of 454 and PGM sequencing is homopolymer read error, which has been associated with false positive detection of K65R in HIV-1 subtype C using the 454 platform.
Discussion: Interestingly, NVP-containing regimens have been associated with an increased risk of K65R detection, but the mechanism has not yet been described.


  Risk of drug resistance among persons acquiring HIV within a randomized clinical trial of single- or dual-agent preexposure prophylaxis.
 PMID: 25587020       2015       The Journal of infectious diseases
Abstract: METHODS: Within the largest randomized trial of FTC/TDF versus TDF as PrEP, plasma samples were tested for HIV with resistance mutations associated with FTC (K65R and M184IV) and TDF (K65R and K70E), using 454 sequencing.


  Prevalence of M184V and K65R in proviral DNA from PBMCs in HIV-infected youths with lamivudine/emtricitabine exposure.
 PMID: 25659108       2015       PloS one
Abstract: CONCLUSION: The frequency of the TDF induced K65R mutation was higher in our setting compared to non-subtype C dominated countries.
Abstract: RESULTS: Compared to d4T-exposed patients (n = 7), patients failing on a TDF-containing regimen (n = 43) were almost 5 times more likely to present with a K65R mutation (aRR 4.86 95% CI 2.29 - 10.34).
Abstract: Virus from 9 of the 11 patients (82.0%) who developed the Y115F mutation also developed K65R.


  Global HIV-1 transmitted drug resistance in the INSIGHT Strategic Timing of AntiRetroviral Treatment (START) trial.
 PMID: 25711326       2015       HIV medicine
Result: The M184VI (associated with lamivudine and emtricitabine exposure) and K65R (associated with didanosine, abacavir, and tenofovir exposure) mutations were not detected in any samples.



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