Discussion: Single mutations in reverse transcriptase (RT) confer resistance to nucleoside RT inhibitors (M184V, K65R) and nonnucleoside RT inhibitors (Y181C) without significantly compromising viral fitness, yet these drugs are used in most antiretroviral regimens.
A comparison of the phenotypic susceptibility profiles of emtricitabine and lamivudine.
Result: In comparison, mutations such as K65R, K70E, L74V, Q151M, and M184V increase the selectivity of RT for incorporation of natural deoxynucleoside triphosphate substrate versus the NRTI-triphosphate.
Prevalence of M184V and K65R in proviral DNA from PBMCs in HIV-infected youths with lamivudine/emtricitabine exposure.
Abstract: BACKGROUND: The effect of the HIV reverse transcriptase K65R mutation on virological response to salvage therapy has not been clearly defined.
Abstract: CONCLUSIONS: Development of the K65R mutation does not preclude a high rate of virological response to rescue therapy.
Abstract: METHODS: From six Italian clinical centres, all consecutive patients starting salvage antiretroviral therapy after virological failure in the presence of the K65R mutation identified by a genotypic resistance test were selected.
Prevalence of M184V and K65R in proviral DNA from PBMCs in HIV-infected youths with lamivudine/emtricitabine exposure.
Abstract: For TFV, decreased excision by K65R and K65R+M184V may partially counteract the K65R-driven decrease in incorporation relative to wild-type resulting in only low levels of TFV resistance.
Abstract: For most NRTIs, the primary mechanism of resistance by K65R, M184V and K65R+M184V mutant RTs is to disrupt the NRTI-binding/incorporation steps.
Abstract: In cell culture, the K65R+M184V virus showed slightly increased susceptibility to TFV, AZT and d4T compared with K65R alone, but showed f
Viral fitness: relation to drug resistance mutations and mechanisms involved: nucleoside reverse transcriptase inhibitor mutations.
PMID: 19372871
2007
Current opinion in HIV and AIDS
Abstract: Further studies have helped explain the antagonistic effects between amino acid substitutions, K65R, L74V, M184V, and thymidine analogue mutations, showing how viral replicative fitness influences the evolution of thymidine analogue resistance pathways.
Mechanisms of resistance associated with excision of incorporated nucleotide analogue inhibitors of HIV-1 reverse transcriptase.
PMID: 19372874
2007
Current opinion in HIV and AIDS
Abstract: M184V, L74V, and K65R that diminish the effects of thymidine analogue-associated mutations.
Abstract: SUMMARY: The non-thymidine analogue-associated mutations M184V, L74V, and K65R show incompatibilities with thymidine-analogue-associated mutations.
Tenofovir DF, emtricitabine, and efavirenz vs. zidovudine, lamivudine, and efavirenz for HIV.
PMID: 16421366
2006
The New England journal of medicine
Abstract: In none of the patients did the K65R mutation develop.
Chemical system biology based molecular interactions to identify inhibitors against Q151M mutant of HIV-1 reverse transcriptase.
Abstract: In this study, we measured the antiviral activity of FTC and 3TC against HIV-1 containing K65R, Q151M, and K65R/Q151M mutations.
Abstract: Overall, this study demonstrated that K65R and K65R/Q151M related drug resistance to FTC and 3TC was mainly due to a significant decrease in the rate of incorporation.
Abstract: The double mutation K65R/Q151M has been shown to be more resistant to many NRTIs than either of the single mutations alone.
Prevalence of M184V and K65R in proviral DNA from PBMCs in HIV-infected youths with lamivudine/emtricitabine exposure.
Abstract: Finally, we studied the incorporation of these deoxycytidine analogues into a HIV-1 genomic DNA/DNA primer/template by K65R HIV-1 RT to address certain concerns associated with DNA sequence specificity.
Abstract: The K65R mutation in the HIV reverse transcriptase (RT) confers reduced susceptibility to 3TC, ddC, ddI, abacavir, and tenofovir in vitro.
HIV mutation literature information.
PMID: 
2007
PloS one
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