Abstract: At virological failure 'de novo' selected mutations were identified in 11 of the 12 failing patients, including the K65R mutation in seven patients.
HIV-1 reverse transcriptase mutations that confer decreased in vitro susceptibility to anti-RT DNA aptamer RT1t49 confer cross resistance to other anti-RT aptamers but not to standard RT inhibitors.
Abstract: This result was tempered by the observation that NRTI-resistance mutations such as K65R can confer resistance to some anti-RT aptamers.
Result: K65R is known to cause resistance to all clinically approved
Result: However, in vitro biochemical experiments do show some resistance to AZTTP and it has been suggested this is due to K65R decreasing the rate of AZTMP excision.
Result: In contrast, mutations shown to confer resistance to multiple NRTIs, including E89G, K65R and M184V displayed low levels of resistance to RT1t49 (2-5 fold), with K65R displaying the highest level of resistance (5-fold).
A combination of decreased NRTI incorporation and decreased excision determines the resistance profile of HIV-1 K65R RT.
Abstract: For K65R, the combination of these opposing mechanisms results in decreased susceptibility to most NRTI but increased susceptibility to ZDV.
Abstract: For ABC, tenofovir, and d4T, despite having decreased excision, decreased binding or incorporation resulted in reduced susceptibilities to K65R.
Abstract: For ddI, ddC, 3TC, and FTC, decreased binding or incorporation by K65R appeared responsible for the decreased susceptibilities in cell culture.
Abstract: However, K65R also showed decreased excision of all NRTI compared to wild-type, indicating greater stability once incorporated.
Abstract: Ki/Km values were increased 2- to 13-fold for K65R compared to wild-type RT for all
K65R and Y181C are less prevalent in HAART-experienced HIV-1 subtype A patients.
Abstract: We found that HAART-experienced patients infected with subtype A had a lower prevalence of K65R and Y181C than those with subtypes B or C, despite similar exposure to antiretroviral agents that select for these mutations.
Borano-nucleotides: new analogues to circumvent HIV-1 RT-mediated nucleoside drug-resistance.
Abstract: Alpha-boranophosphates suppress RT-mediated resistance when the catalytic rate of incorporation (kpol) of the analogue 5'-triphosphate is responsable for drug resistance, such as in the case of K65R mutant and ddNTPs, and Q151M toward AZTTP and ddNTPs.
Risk of selecting K65R in antiretroviral-naive HIV-infected individuals with chronic hepatitis B treated with adefovir.
Abstract: Using bulk population sequencing and a sensitive limiting dilution analysis, the selection of K65R or other resistance mutations did not occur in HIV, suggesting that adefovir can be confidently used as hepatitis B virus (HBV) therapy in HIV/HBV-co-infected patients who do not require antiretroviral therapy.
HIV-1 genotypes related to failure of nelfinavir as the first protease inhibitor treatment.
PMID: 16270125
2005
The Brazilian journal of infectious diseases
Abstract: Nucleosides associated with mutations (NAM) were observed in 80% of the tests; no INS69, complex 151, K65R and L74V mutations, which give multi-resistance to nucleoside analogue reverse transcriptase inhibitors to tenofovir and DDI, respectively, were observed.
Short communication. Antiretroviral drug resistance among drug-naive HIV-1-infected individuals in Djibouti (Horn of Africa).
Abstract: A few strains displayed primary mutations (the non-nucleoside reverse transcriptase inhibitor [NNRTI]-associated mutations K101E, K103T, L100I and G190V; the PI-associated mutation N88D; and the NRTI-associated mutation K65R).
Early virologic failure and rescue therapy of tenofovir, abacavir, and lamivudine for initial treatment of HIV-1 infection: TONUS study.
Abstract: 14 pts with K65R and M184V/I were given a rescue therapy with a successful outcome (< 50 copies/mL; median follow-up 48 weeks).
Abstract: 76% of pts developed K65R and M184V/I mutations by W24, and 19% developed M184V/I alone.
Abstract: CONCLUSION: Convergent genetic pathway to resistance, in conjunction with lower antiretroviral potency, may explain the high rate of selection K65R and M184V mutations.
Substitutions in the Reverse Transcriptase and Protease Genes of HIV-1 Subtype B in Untreated Individuals and Patients Treated With Antiretroviral Drugs.
PMID: 19825125
2005
Journal of the International AIDS Society
HIV mutation literature information.
PMID: 
2005
AIDS (London, England)
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