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 HIV mutation literature information.


  Emergence of antiretroviral drug resistance in therapy-naive HIV infected patients in Hungary.
 PMID: 19130746       2008       Acta microbiologica et immunologica Hungarica
Abstract: Viral variants harbouring resistance mutations such as: M41, T69R, K70R, M184V, T215Y in the pol gene were detected in 14% of the subjects.


  Mutational patterns associated with the 69 insertion complex in multi-drug-resistant HIV-1 reverse transcriptase that confer increased excision activity and high-level resistance to zidovudine.
 PMID: 17070543       2007       Journal of molecular biology
Abstract: Further studies, using recombinant RTs obtained by site-directed mutagenesis, revealed that M41L, A62V and in a lesser extent K70R, were the key mutations that together with T69S, T215Y and the dipeptide insertion conferred high levels of ATP-dependent phosphorolytic activity on AZT and d4T-terminated primers.


  The fitness cost of mutations associated with human immunodeficiency virus type 1 drug resistance is modulated by mutational interactions.
 PMID: 17192300       2007       Journal of virology
Abstract: We also demonstrate that the fitness cost of M184V and K70R can be decreased or enhanced by other resistance mutations such as D67N and K219Q.


  [Prevalence of mutations of resistance to HIV-I reverse transcriptase inhibitors among HIV-infected patients in the Southern Federal District].
 PMID: 17385442       2007       Klinicheskaia laboratornaia diagnostika
Abstract: The group of patients receiving antiviral treatment was found to have different drug resistance mutations in the HIV-1 pol gene: K70R, M184V, K219Q, T215Y/F, L74V, etc.


  Characterization of an HIV-1 group M variant that is distinct from the known subtypes.
 PMID: 17411380       2007       AIDS research and human retroviruses
Abstract: Surprisingly, the only regular RT mutation acquired during this period was K70R, which suggests that the genetic background of this variant is perhaps not suitable for the generation of the standard 41L, 67N, and 215Y/F mutations that typically arise during prolonged, nonsuccessful, zidovudine treatment.


  Lamivudine/abacavir maintains virological superiority over zidovudine/lamivudine and zidovudine/abacavir beyond 5 years in children.
 PMID: 17457088       2007       AIDS (London, England)
Abstract: Reverse transcriptase resistance mutations emerging on therapy differed between the groups: zidovudinelamivudine (M41L, D67N, K70R, M184V, L210W, T215Y); zidovudineabacavir (M41L, D67N, K70R, L210W, T215F/Y, K219Q); lamivudineabacavir (K65R, L74V, Y115F, M184V).


  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.



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