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 HIV mutation literature information.


  Polymorphism and drug-selected mutations in the protease gene of human immunodeficiency virus type 2 from patients living in Southern France.
 PMID: 14766818       2004       Journal of clinical microbiology
Abstract: In addition, at six positions (positions 7, 46, 62, 71, 90, and 99), the amino acid variability or the amino acid frequencies or both differed significantly in PI-treated and untreated patients, suggesting that mutations 7K-->R, 46V-->I, 62V-->A/T, 71V-->I, 90L-->M and 99L-->F were occurring under PI-selective pressure.


  Crystal structures of HIV protease V82A and L90M mutants reveal changes in the indinavir-binding site.
 PMID: 15066177       2004       European journal of biochemistry
Abstract: PR(V82A) showed local changes in residues 81-82 at the site of the mutation, while PR(L90M) showed local changes near Met90 and an additional interaction with indinavir.
Abstract: The crystal structures of the wild-type HIV-1 protease (PR) and the two resistant variants, PR(V82A) and PR(L90M), have been determined in complex with the antiviral drug, indinavir, to gain insight into the molecular basis of drug resistance.
Abstract: The inhibition (K(i)) of PR(V82A) and PR(L90M) was 3.3- and


  GW433908/ritonavir once daily in antiretroviral therapy-naive HIV-infected patients: absence of protease resistance at 48 weeks.
 PMID: 15090770       2004       AIDS (London, England)
Abstract: In the nelfinavir arm the key protease mutations D30N and/or L90M were frequently observed.


  Mutation D30N is not preferentially selected by human immunodeficiency virus type 1 subtype C in the development of resistance to nelfinavir.
 PMID: 15155216       2004       Antimicrobial agents and chemotherapy
Abstract: Following nelfinavir treatment, the unique nelfinavir mutation D30N was substantially less frequent in C (7%) than in B (23%; P = 0.03) while L90M was similar (P < 0.5).


  Persistence of mutations during replication of an HIV library containing combinations of selected protease mutations.
 PMID: 15168798       2004       Antiviral research
Abstract: The frequency of the amino acid substitutions V82T/I and L90M decreased rapidly with a short half life (t(1/2) < 10 days).


  Primary drug-resistance in HIV-positive patients on initiation of first-line antiretroviral therapy in Germany.
 PMID: 15257882       2004       European journal of medical research
Abstract: 10.5% showed mutations indicating nucleoside reverse transcriptase inhibitor- (NRTI) resistance (M41L, E44D, D67N, T69D/N, L74V, V118I, M184V, L210W, K219Q), 2.8% showed non-nucleoside reverse transcriptase inhibitor (NNRTI) resistance (K103N, V108I, Y181C), and 2.1% showed protease-inhibitor- (PI) associated resistance (


  Resistance profiles observed in virological failures after 24 weeks of amprenavir/ritonavir containing regimen in protease inhibitor experienced patients.
 PMID: 15258963       2004       Journal of medical virology
Abstract: However, in some cases, mutations classically described after the use of other PIs (V82F and L90M) were selected but always with APV-specific mutations.


  The influence of protease inhibitor resistance profiles on selection of HIV therapy in treatment-naive patients.
 PMID: 15259893       2004       Antiviral therapy
Abstract: HIV variants resistant to saquinavir and ritonavir usually contain L90M and V82A substitutions, respectively.
Abstract: Resistance to nelfinavir is primarily associated with D30N but may alternatively be found with L90M.


  2004: which HIV-1 drug resistance mutations are common in clinical practice?
 PMID: 15332433       2004       AIDS reviews
Abstract: For example, only the nucleoside reverse transcriptase inhibitor (NRTI) mutations M184V, M41L T215Y, D67N, K70R and L210W, non-nucleoside reverse transcriptase inhibitor (NNRTI) mutations K103N and Y181C, and protease inhibitor (PI) mutation L90M, occur in more than 10% of samples tested for resistance in this population.


  Crystallization of a non-B and a B mutant HIV protease.
 PMID: 15333937       2004       Acta crystallographica. Section D, Biological crystallography
Abstract: the subtype B mutant, with mutations Q7K, S37N, R41K, K45R, I54V, L63P, A71V, V82A and L90M, and the subtype F (wild type), naturally carrying mutations Q7K, I15V, E35D, M36I, S37N, R41K, R57K, D60E, Q61N, I62V, L63S, I64L and L89M, with res



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