HIV mutation literature information.


  HIV-1 subtype B protease and reverse transcriptase amino acid covariation.
 PMID: 17500586       2007       PLoS computational biology
Method: NRTI-selected mutations included T39A, M41L, K43E/Q/N, E44D/A, A62V, K65R, D67N/G/E, T69D/N/S/insertion, K70R, L74V/I, V75I/M/T/A, F77L, V90I, K104N, Y115F, F116Y, V118I, Q151M, M184V/I, E203K,
 PMID: 17507476       2007       Journal of virology
Abstract: The first resistance mutations to appear in HIV-1(LAI) were two polymerase domain thymidine analog mutations (TAMs), D67N and K70R, and two novel mutations, A371V in the connection domain and Q509L in the RNase H domain, that together conferred up to 90-fold AZT resistance.
Abstract: The roles of A371V and Q509L in AZT resistance were confirmed by site-directed mutagenesis: A371V and Q509L together increased AZT resistance approximately 10- to 50-fold in combination with TAMs (M41L/L210W/T215Y or D67N/


  Anti-retroviral drug resistance-associated mutations among non-subtype B HIV-1-infected Kenyan children with treatment failure.
 PMID: 17516531       2007       Journal of medical virology
Abstract: In 7 of 12 children, M184V appeared with one thymidine-analogue-associated mutation (TAM) as the first mutation, while the remaining 5 children had only TAMs appearing either individually (n = 2), or as TAMs 1 (M41L, L210W, and T215Y) and 2 (D67N, K70R, and K219Q/E/R) appearing together (n = 3).


  Mechanism of action of (-)-(2R,4R)-1-(2-hydroxymethyl-1,3-dioxolan-4-yl) thymine as an anti-HIV agent.
 PMID: 17542153       2007       Antiviral chemistry & chemotherapy
Abstract: RTs containing the D67N/K70R/T215Y/K219Q or T695-SS/T215Y mutations show enhanced removal of DOT-MP from terminated primer as well as approximately four-fold decreased binding/incorporation.


  Molecular mechanisms of bidirectional antagonism between K65R and thymidine analog mutations in HIV-1 reverse transcriptase.
 PMID: 17589186       2007       AIDS (London, England)
Abstract: In addition, the TAMs combination D67N/K70R/T215F/K219Q decreased susceptibility to the L-nucleotide lamivudine by a discrimination mechanism, whereas the M41L/L210W/T215Y combination had little effect on susceptibility to lamivudine.
Abstract: RESULTS: The addition of K65R to two clinically relevant combinations of TAMs (M41L/L210W/T215Y or D67N/K70R/T215F/K219Q) significantly reduced the recombinant enzymes' ability to excise all chain-terminating  PMID: 17678469       2007       AIDS research and human retroviruses
Abstract: The mutation T215Y was the first step in the evolution of the 67N 70R 215Y genotype and was followed by mutations K70R and D67N.


  N348I in the connection domain of HIV-1 reverse transcriptase confers zidovudine and nevirapine resistance.
 PMID: 18052601       2007       PLoS medicine
Method: The analysis was performed for N348I and for each of the TAMs: M41L, D67N, K70R, L210W, T215Y/F, and K219Q/E.
Result: N348I was highly associated with several key drug resistance mutations, including M184V/I (p = 6.6 x 10-45) the TAMs M41L (p = 1.8 x 10-14), D67N (p = 7.7 x 10-10), K70R (p = 1.4 x 10-10), T215Y/F (p = 6.0 x 10-21), K219Q/E (p = 8.0 x 10-4), and L210W (p = 0.002), and the NNRTI re


  [Study on genotypic resistance mutations to antiretroviral drugs on HIV strains of treated and treatment-naive HIV-1 infectious patients in Hubei province].
 PMID: 18396668       2007       Zhonghua liu xing bing xue za zhi
Abstract: Some protease (PR) drug-resistant mutations were found in these samples, such as D30N (2.27%), D30G (2.27%), M46I (4.55%), M46N (2.27%), I47V (4.55%), I84V (4.55%), I84L (2.27%), N88S (2.27%) and L90S (2.27%) that all belonged to major drug-resistant but A71T (29.55%) belonged to minor resistance mutations Five treated patients were detected having mutations associated RT drug resistance: M41L (5.26%), A62V (5.26%),D67N (5.26%),  PMID: 16632914       2006       Japanese journal of infectious diseases
Abstract: In plasma HIV-1 RNA, D67N, K70R, T215Y, and Y188L were present in the reverse transcriptase (RT) region, and two primary mutations, I84V and L90M, were noted in the protease (Pro) region.


  Antiviral efficacy and genotypic resistance patterns of combination therapy with stavudine/tenofovir in highly active antiretroviral therapy experienced patients.
 PMID: 16640104       2006       Antiviral therapy
Abstract: Any single type-1 thymidine analogue mutation (TAM; M41L, L210W, T215Y) had a negative effort on the change in HIV RNA at 6 months, whereas among type-2 TAMs (D67N, K70R, K219Q), only D67N showed a trend for a negative effect.



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