HIV mutation literature information.


  Impact of HIV-1 reverse transcriptase polymorphism at codons 211 and 228 on virological response to didanosine.
 PMID: 17310813       2006       Antiviral therapy
Abstract: A mutation score (M41L+D67N+T69D-K70R +L74V-M 1 84V/I+T21 5Y/F+ K219Q/E+ R211A/D/G/K/S+ L228H/M/R), including two RT polymorphisms not previously described to be associated with ddl resistance (211 and 228) and RT mutations previously described, was associated with a continuum of virological response and increased the predictability of virological response to ddl.


  Clinically relevant genotype interpretation of resistance to didanosine.
 PMID: 15855490       2005       Antimicrobial agents and chemotherapy
Abstract: Eight mutations were associated with a reduced response to ddI, M41L, D67N, T69D, L74V, V118I, L210W, T215Y/F, and K219Q/E, and two mutations were associated with a better response, K70R and M184V/I.
Abstract: The best prediction of the virologic response to ddI was obtained with a composite score comprising mutations added and subtracted (set II, M41L + T69D + L74V+ T215Y/F + K219Q/E - K70R -


  Anti-HIV activity of (-)-(2R,4R)-1- (2-hydroxymethyl-1,3-dioxolan-4-yl)-thymine against drug-resistant HIV-1 mutants and studies of its molecular mechanism.
 PMID: 15943470       2005       Journal of medicinal chemistry
Abstract: (-)-(2R,4R)-1-(2-Hydroxymethyl-1,3-dioxolan-4-yl)thymine (DOT) is the first thymidine kinase-activated nucleoside that is significantly active against all of the clinically significant NRTI-resistant HIV-1 mutants, including AZT (D67N/K70R/T215Y/K219Q), Tenofovir (K65R), and Lamivudine (M184V).


  The 3'-azido group is not the primary determinant of 3'-azido-3'-deoxythymidine (AZT) responsible for the excision phenotype of AZT-resistant HIV-1.
 PMID: 15970587       2005       The Journal of biological chemistry
Abstract: The results indicate that mutations correlated with resistance to AZT (D67N/K70R/T215F/K219Q) confer resistance to the 3'-azidopyrimidine nucleosides (AZddC, AZT, and AZddU) but not to the 3'-azidopurine nucleosides (AZddA and AZddG).


  Lack of resistant mutation development after receiving short-course zidovudine plus lamivudine to prevent mother-to-child transmission.
 PMID: 15990579       2005       AIDS (London, England)
Abstract: One of the three infected infants carried the M184V and K219Q mutations.


  Comparison of tests and procedures to build clinically relevant genotypic scores: application to the Jaguar study.
 PMID: 16038473       2005       Antiviral therapy
Abstract: RESULTS: Eight mutations were associated with a reduced virological response to ddI: M41L, D67N, T69D, L74V, V1181, L210W, T215Y/F and K219Q/E and two mutations with a better virological response: K70R and M184V/I.


  Anti-human immunodeficiency virus type 1 activity and resistance profile of 2',3'-didehydro-3'-deoxy-4'-ethynylthymidine in vitro.
 PMID: 16048947       2005       Antimicrobial agents and chemotherapy
Abstract: Approximately 6- to 11-fold decreases in susceptibility to 4'-Ed4T were observed for HIV-1 carrying NRTI-associated mutations (D67N, K70R, T215F, and K219Q) or the lamivudine (3TC)-resistant mutation M184V.


  Structural analysis of reverse transcriptase mutations at codon 215 explains the predominance of T215Y over T215F in HIV-1 variants selected under antiretroviral therapy.
 PMID: 16200350       2005       Journal of biomedical science
Abstract: Mutation T215F was preferentially associated with K70R (>71%), D67N (>73%) and K219Q/E/N (>76%), whereas T215Y was associated with M41L (>84%) and L210W (>58%).


  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
Table: K219Q


  Mutations conferring drug resistance affect eukaryotic expression of HIV type 1 reverse transcriptase.
 PMID: 15018707       2004       AIDS research and human retroviruses
Abstract: Genes encoding AZT-resistant RTs with single or combined mutations D67N, K70R, T215F, and K219Q, and RTs derived from drug-resistant HIV-1 strains were designed and expressed in a variety of eukaryotic cells.



Browser Board

 Co-occurred Entities




   Filtrator