HIV mutation literature information.


  Clinically validated mutation scores for HIV-1 resistance to fosamprenavir/ritonavir.
 PMID: 18390885       2008       The Journal of antimicrobial chemotherapy
Abstract: Two fosamprenavir/ritonavir mutation scores were constructed: score A (L10F/I/V + L33F + M36I + I54L/M/V/A/T/S + I62V + V82A/F/C/G + I84V + L90M) was based only on mutations associated with a worse VR, whereas score B (L10FIV + L33F + M36I + I54L/M/V/A/T/S + A71V - V77I - N88S + L90M) also took into account favourable mutations.


  Effect of flap mutations on structure of HIV-1 protease and inhibition by saquinavir and darunavir.
 PMID: 18597780       2008       Journal of molecular biology
Abstract: The crystal structures of flap mutants PR(I50V) (PR with I50V mutation), PR(I54V) (PR with I54V mutation), and PR(I54M) (PR with I54M mutation) complexed with saquinavir (SQV) as well as PR(G48V) (PR with G48V mutation), PR(I54V), and PR(I54M) complexed with darunavir (DRV) were determined at resolutions of 1.05-1.40 A.|m


  Pattern and impact of emerging resistance mutations in treatment experienced patients failing darunavir-containing regimen.
 PMID: 18690163       2008       AIDS (London, England)
Abstract: Emergence of DRV-associated-resistance mutations was observed in 72% (18/25) of patients, at codons L89I/M/V (32%), V32I (28%), V11I (20%), I47V/A (20%), I54L/M (20%), L33F/I (16%) and I50V (16%).


  Genotypic resistance analysis of the virological response to fosamprenavir-ritonavir in protease inhibitor-experienced patients in CONTEXT and TRIAD clinical trials.
 PMID: 18852278       2008       Antimicrobial agents and chemotherapy
Abstract: The JT procedure led to selecting the CONTEXT/TRIAD genotypic set of mutations, I15V, M46I/L, I54L/M/V, D60E, L63P/T, and I84V, as providing the strongest association with the VR (P = 1.45 x 10(-11)).


  Combating HIV resistance - focus on darunavir.
 PMID: 19209258       2008       Therapeutics and clinical risk management
Abstract: Darunavir resistance-associated mutations have been defined as V11I, V32I, L33F, I47V, I50V, I54L/M, G73S, L76V, I84V, and L89V.


  Prevalence of darunavir resistance mutations in HIV-1-infected patients failing other protease inhibitors.
 PMID: 17646201       2007       The Journal of antimicrobial chemotherapy
Abstract: The prevalence of major darunavir resistance mutations was I50V 2.1%, I54M 1.3%, L76V 2.7% and I84V 14.5%.


  HIV-1 subtype B protease and reverse transcriptase amino acid covariation.
 PMID: 17500586       2007       PLoS computational biology
Abstract: Different patterns of covariation were frequently observed for different mutations at the same position including the RT mutations T69D versus T69N, L74V versus L74I, V75I versus V75M, T215F versus T215Y, and K219Q/E versus K219N/R, and the protease mutations M46I versus M46L, I54V versus I54M/L, and N88D versus N88S.
Method:


  Tipranavir: a new protease inhibitor for the treatment of antiretroviral-experienced HIV-infected patients.
 PMID: 17425479       2007       Expert opinion on pharmacotherapy
Abstract: The TPV mutation score includes L10V, I13V, K20M/R/V, L33F, E35G, M36I, K43T, M46L, I47V, I54A/M/V, Q58E, H69K, T74P, V82L/T, N83D and I84V.


  Interpretation of genotype and pharmacokinetics for resistance to fosamprenavir-ritonavir-based regimens in antiretroviral-experienced patients.
 PMID: 17296739       2007       Antimicrobial agents and chemotherapy
Abstract: The Zephir mutation score included 12 IAS protease mutations associated with poorer virological response: L10I/F/R/V, L33F, M36I, M46I/L, I54L/M/T/V, I62V, L63P, A71I/L/V/T, G73A/C/F/T, V82A/F/S/T, I84V, L90M, and polymorphism mutations I13V, L19I, K55R, and L89M.


  Natural polymorphisms in the human immunodeficiency virus type 2 protease can accelerate time to development of resistance to protease inhibitors.
 PMID: 17116674       2007       Antimicrobial agents and chemotherapy
Abstract: The acquisition of the I54M, I84V, L90M, and L99F mutations resulted in multi-PI-resistant viruses, conferring 10-fold to more than 100-fold resistance.
Abstract: Within 10 to 15 weeks of serial passage, three major mutations--I54M, I82F, and L90M--arose in HIV-2 viral cultures exposed to APV, NFV, and IDV, whereas I82L was selected with TPV.



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