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 HIV mutation literature information.


  HIV type 1 subtype C drug resistance among pediatric and adult South African patients failing antiretroviral therapy.
 PMID: 19000027       2008       AIDS research and human retroviruses
Abstract: Ninety-one percent of patients harbored resistance mutations; the most frequent NRTI mutations were M184V/I (37%), D67N (32%), T215Y/F (25%), K70R (21%), M41L (20%), K219Q/E (14%), and K65R (14%), reflecting the frequent use of lamuvidine and zidovudine.


  Silent mutations are selected in HIV-1 reverse transcriptase and affect enzymatic efficiency.
 PMID: 19005273       2008       AIDS (London, England)
Abstract: In clade B samples, there was a very strong relationship between the silent mutations and the thymidine analogue mutations, in particular D67N.
Abstract: Steady-state kinetic experiments demonstrated that HIV-1 reverse transcriptase exhibited a strong tendency to pause and/or dissociate at codons 65 and 66 on RNA templates that contained the D67N and K70R mutations.
Introduction: By contrast, the mutations M41L, D67N, K70R, L210W, T215F/Y and K219Q/E - typically referred to as thymidine analog mutations (TAMs) - augment the ability of HIV-1 RT to excise the chain-terminating


  Mechanism by which a glutamine to leucine substitution at residue 509 in the ribonuclease H domain of HIV-1 reverse transcriptase confers zidovudine resistance.
 PMID: 19067547       2008       Biochemistry
Abstract: In the current study, we have defined the mechanism by which Q509L confers AZT resistance by performing in-depth biochemical analyses of wild type, D67N/K70R/T215F and D67N/K70R/T215F/Q509L HIV-1 RT.
Abstract: We recently reported that zidovudine (AZT) selected for the Q509L mutation in the ribonuclease H (RNase H) domain of HIV-1 reverse transcriptase (RT), which increases resistance to AZT in combination with the thymidine analogue mutations D67N, K70R, and T215F


  [Research on the selective kinetics of HIV-1 nucleoside reverse transcriptase inhibitor drug resistance-associated mutations among 4 AIDS patients receiving highly active antiretroviral therapy].
 PMID: 19103117       2008       Zhonghua liu xing bing xue za zhi
Abstract: Interestingly, in patient 'C', some clones comprising not only TAMs pattern 1 mutations (T215Y) but also TAMs pattern 2 mutations (K70R, D67N).
Abstract: TAMs pattern 2, including D67N, K70R and K219Q mutations, was discovered in patient 'B'.


  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.


  Drug-resistant HIV-1 prevalence in patients newly diagnosed with HIV/AIDS in Japan.
 PMID: 17194486       2007       Antiviral research
Abstract: Twenty-three cases, including three recently infected patients, were infected with HIV-1 having major drug-resistance mutations, including M41L, D67N, L100I, K103N, V106A, M184I, M184V, L210W, and revertant mutations at the 215 codon in reverse transcriptase and M46I in protease encoding regions.


  Emergence of the H208Y mutation in the reverse transcriptase (RT) of HIV-1 in association with nucleoside RT inhibitor therapy.
 PMID: 17356061       2007       The Journal of antimicrobial chemotherapy
Abstract: The prevalence of H208Y was highest in genotypes harbouring M184V and the thymidine analogue mutations (TAMs) M41L, D67N, L210W and T215Y.


  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/



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