literature

HIV mutation literature information.

Novel human immunodeficiency virus type 1 protease mutations potentially involved in resistance to protease inhibitors.

PMID: 15855527 2005 Antimicrobial agents and chemotherapy

Abstract: In particular, E34Q, K43T, and K55R, which were associated with lopinavir treatment, correlated with mutations associated with lopinavir resistance (E34Q with either L33F or F53L, or K43T with I54A) or clustered with multi-PI resistance mutations (K43T with V82A and I54V or V82A, V32I, and I47V, or K55R with V82A, I54V, and M46I).

Tipranavir: a ritonavir-boosted protease inhibitor.

PMID: 16060700 2005 Drugs

Abstract: Analysis of clinical isolates from treatment-experienced patients identified the following tipranavir resistance-associated HIV protease mutations: L10V, I13V, K20M/R/V, L33F, E35G, M36I, K43T, M46L, I47V, I54A/M/V, Q58E, H69K, T74P, V82L/T, N83D, I84V.

Treatment response and drug resistance in patients infected with HIV type 1 group O viruses.

PMID: 16060830 2005 AIDS research and human retroviruses

Abstract: One selected changes M41L, E44D, D67N, V75M, M184V, and T215Y at the RT, and G48M, F53L, I54V, V82A, and L90M at the protease.

Selection and characterization of HIV-1 showing reduced susceptibility to the non-peptidic protease inhibitor tipranavir.

PMID: 16122817 2005 Antiviral research

Abstract: At the end of the selection experiments, viruses harbouring 10 mutations in the protease (L10F, I13V, V32I, L33F, M36I, K45I, I54V, A71V, V82L, I84V) as well as a mutation in the CA/SP1 gag cleavage site were selected and showed 87-fold decreased susceptibility to tipranavir.

Mutations at codons 54 and 82 of HIV protease predict virological response of HIV-infected children on salvage lopinavir/ritonavir therapy.

PMID: 16195257 2005 The Journal of antimicrobial chemotherapy

Abstract: Children with I54V and V82A/F had higher prevalence of lopinavir-associated resistance mutations and showed RP of 0.36 (CI95%: 0.17; 0.76; P = 0.007) for achieving uVL.

Abstract: Moreover, I54V and V82A/F led to the poorest virological response.

Abstract: The relative proportion (RP) to uVL was 0.32 (CI95%: 0.16; 0.33; P = 0.002) in children with I54V (46% of total) and 0.48 (CI95%: 0.24; 0.97; P = 0.041) in children with V82A/F (52% of total).

Substitutions in the Reverse Transcriptase and Protease Genes of HIV-1 Subtype B in Untreated Individuals and Patients Treated With Antiretroviral Drugs.

PMID: 19825125 2005 Journal of the International AIDS Society

Table: I54V

Persistence of mutations during replication of an HIV library containing combinations of selected protease mutations.

PMID: 15168798 2004 Antiviral research

Abstract: Other amino acid substitutions, i.e., L10I, I54V, L63P, A71V and V82A, were well retained (t(1/2) > 36 days).

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

Comparing the accumulation of active- and nonactive-site mutations in the HIV-1 protease.

PMID: 15379553 2004 Biochemistry

Abstract: The M46I and I54V were just as effective at decreasing inhibitor binding as the I84V mutation when compared to V6 and LAI.

Abstract: The decrease in catalytic efficiency was partially recovered by the addition of mutations M46I and I54V.

Abstract: We have engineered a series of variants containing the nonactive-site mutations M46I and I54V and the active-site mutation I84V.

Genotypic inhibitory quotient as predictor of virological response to ritonavir-amprenavir in human immunodeficiency virus type 1 protease inhibitor-experienced patients.

PMID: 12543665 2003 Antimicrobial agents and chemotherapy

Abstract: Baseline PI resistance mutations (L10F/I/V, K20M/R, E35D, R41K, I54V, L63P, V82A/F/T/S, I84V) identified by univariate analysis and included in a genotypic score and APV C(min) at week 8 were predictive of the virological response at week 12.

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