Result: Others 13 (65%) (E6D, Q18H, E35D, S37N, T39A, K43E, S68N, I93L, E169D, Q197K, T200V, T200E and E224D) had not been previously reported to be drug resistance mutations.
Discussion: Some studies had shown that accessory mutations at positions 39 (T39A), 43 (K43E) were more frequent in viral isolates from patients failing therapy than in naive individuals, and those mutations were previously identified as accessory mutations associated with the accumulation of TAMs (thymi
Co-evolution of compensatory mutation K43E with mutation M41L in long-term HIV antiretroviral treatment.
Abstract: CONCLUSION: We determined that a known compensatory mutation, K43E, frequently co-occurs with the drug resistance mutation M41L and may offer a significant advantage in the long-term survival of such drug resistant strains.
Abstract: In this study, we characterized the emergence and depletion dynamics of a compensatory mutation K43E that correlated with primary nucleoside reverse transcriptase inhibitor (NRTI) drug resistance mutations in Chinese HIV patients on antiretroviral treatment.
Abstract: SGA sequences were analyzed by Markov Chain Monte Carlo (MCMC) phylogenetic trees with molecular clock to identify and track compensatory mutation K43E correlated with primary DR mutation M41L.
Subtype-specific differences in the development of accessory mutations associated with high-level resistance to HIV-1 nucleoside reverse transcriptase inhibitors.
PMID: 23386260
2013
The Journal of antimicrobial chemotherapy
Abstract: Codon changes K43E, E44D and V118I were found to have no effect on susceptibility to three NRTIs with or without TAMs in either subtype; however, some accessory mutations had subtype-specific effects on viral infectivity.
Potential elucidation of a novel CTL epitope in HIV-1 protease by the protease inhibitor resistance mutation L90M.
Result: It was concluded that RT K43E could have caused false assignment of HLA subtype C*03 in Pol sequences obtained from drug exposed patients exhibiting other RT inhibitor resistance related mutations.
Polymorphic mutations associated with the emergence of the multinucleoside/tide resistance mutations 69 insertion and Q151M.
PMID: 22027876
2012
Journal of acquired immune deficiency syndromes (1999)
Abstract: Frequencies of 8 polymorphic mutations (K43E, V60I, S68G, S162C, T165I, I202V, R211K, F214L) were significantly different between groups.
Transmitted antiretroviral drug resistance and thumb subdomain polymorphisms among newly HIV type 1 diagnosed patients infected with CRF01_AE and CRF07_BC virus in Guangdong Province, China.
PMID: 22587343
2012
AIDS research and human retroviruses
Abstract: Until now, this is the first observation of the five newly identified accessory mutations, V35T, K43E, V60I, K122E, and E203D, and seven thumb subdomain polymorphisms, A272P, K277R, K281R, T286A, E291D, V292I, and I293V, in the RT gene in China.
Mechanism of dissociative inhibition of HIV protease and its autoprocessing from a precursor.
Result: 8A, lane 4) binds to PRM1, one of our constructs of TFR-PR, bearing a fortuitous K43E substitution mutation which does not affect autoprocessing or resultant catalytic activity, failed to bind (lane 3).
Prolonged tenofovir treatment of macaques infected with K65R reverse transcriptase mutants of SIV results in the development of antiviral immune responses that control virus replication after drug withdrawal.
Result: For animal 33091, plasma collected at the time of tenofovir withdrawal and at the time of euthanasia (41 weeks after tenofovir withdrawal) had pure K65R populations; most other RT mutations were found in both samples (N69S, Y115F, I118V, D121H, V201A, S211N), while some mutations were found in only 1 sample (K40E and R82R/K at time of tenofovir withdrawal; K43E at time of euthanasia).
Clinical, virological and biochemical evidence supporting the association of HIV-1 reverse transcriptase polymorphism R284K and thymidine analogue resistance mutations M41L, L210W and T215Y in patients failing tenofovir/emtricitabine therapy.
Introduction: Studies with recombinant HIV-1 have shown that the amino acid substitutions K43E, Q207D and F214L influence the viral replication capacity in the presence of TAMs.
Discussion: It has been suggested that secondary mutations such as E40F and K43E or L214F that associate with amino acid substitutions of the TAM1 resistance pathway could increase viral fitness by influencing the catalytic efficiency of the RT.
Differential in vitro kinetics of drug resistance mutation acquisition in HIV-1 RT of subtypes B and C.
Discussion: This change, alongside with other mutations (K43E/N/Q, H208Y, and D218E), have already been associated with NRTI resistance; however, its actual impact in NRTI resistance has not been yet characterized.
HIV mutation literature information.
PMID: 
2017
PloS one
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