literature

HIV mutation literature information.

High incidence of non-B and recombinant HIV-1 strains in newly diagnosed patients in Galicia, Spain: study of genotypic resistance.

PMID: 14518705 2003 Antiviral therapy

Abstract: Several polymorphisms in RT: D123S, Q174K, D177E, T200A, V245Q, and PR: I13V, K20I, M36I, R41K, H69K, L89M were detected more frequently in non-B and recombinants than in B strains (P<0.01 to P<0.001).

Prevalence of drug-resistance-associated mutations in antiretroviral drug-naive Zambians infected with subtype C HIV-1.

PMID: 12643279 2003 AIDS research and human retroviruses

Abstract: The generated sequences revealed only secondary associated, but no primary, drug-resistance mutations The most frequent secondary mutations in the protease and RT genes were, respectively, I93L(91.7%), L89M (79.2%), M3611V (79%, 4.2%), and R211K (70.8%), S48T (62.5%).

In vitro hypersusceptibility of human immunodeficiency virus type 1 subtype C protease to lopinavir.

PMID: 12936979 2003 Antimicrobial agents and chemotherapy

Abstract: In order to characterize the impact of genetic polymorphisms on the susceptibility of subtype C strains of human immunodeficiency virus type 1 to protease inhibitors (PIs), a subtype B protease that originated from an infectious clone was modified through site-directed mutagenesis to include the amino acid residue signatures of subtype C viruses (I15V, M36I, R41K, H69K, L89 M) with (clone C6) or without (clone C5) an I93L polymorphism present as a molecular signature of the worldwide subtype C protease.

Computational studies of the resistance patterns of mutant HIV-1 aspartic proteases towards ABT-538 (ritonavir) and design of new derivatives.

PMID: 12463635 2002 Journal of molecular graphics & modelling

Abstract: We have performed a computational study of the binding of ABT-538 (ritonavir) with wild type (wt) PR and 12 model mutant structures (R8Q, V321, M461, V82A, V82F, V821, I84V, M46I/V82F, M46I/I84V, V32I/I84V, V82F/I84V and V32I/K45I/F53L/A71V/I84V/L89M (6X)) for which inhibition data are available.

Catalytic efficiency and vitality of HIV-1 proteases from African viral subtypes.

PMID: 11353856 2001 Proc Natl Acad Sci U S A

Abstract: Another protease containing a subset of these amino acid polymorphisms (M36I/R41K/H69K/L89M), which are found in subtype C and other HIV subtypes, also was studied.

Abstract: The A protease used in these studies differs in seven positions (I13V/E35D/M36I/R41K/R57K/H69K/L89M) in relation to the consensus B subtype protease.

Genotypic variation of HIV-1 reverse transcriptase and protease: comparative analysis of clade C and clade B.

PMID: 11504976 2001 AIDS (London, England)

Abstract: Most clade C viruses also showed significant differences from clade B consensus sequence at additional protease sites: R41K 100%, H69K/Q 85%, L89M 95% and I93L 80% (P < 0.0001).

Genetic variability of HIV-1 protease from Nigeria and correlation with protease inhibitors drug resistance.

PMID: 11324755 2001 Virus genes

Abstract: The protease amino acid consensus sequence of the Nigerian subtype A are in complete agreement with the consensus A differing from the USA subtype B consensus in 10 positions (L10V, I13V, K14R, I15V, K20I, M36I, R41K, P63L, H69K and L89M).

Abstract: The secondary substitutions associated with protease inhibitor resistance were observed in all Nigerian sequences at the positions L10V, M36I and L89M.

Genetic variation and susceptibilities to protease inhibitors among subtype B and F isolates in Brazil.

PMID: 9925514 1999 Antimicrobial agents and chemotherapy

Abstract: and Brazilian subtype B consensus in eight positions (I15V, E35D, M36I, R41K, R57K, Q61N, L63P, and L89M).

HIV-1 acquires resistance to two classes of antiviral drugs through homologous recombination.

PMID: 9477118 1997 Antiviral research

Abstract: Co-transfection of COS-7 cells with an HIV-1 plasmid (pSUM13) carrying five mutations in the reverse transcriptase (RT)-encoding region (A62V, V75I, F77L, F116Y, Q151M), conferring resistance to multiple dideoxynucleoside analogs (ddNs), and another HIV-1 plasmid (pSUM431) carrying five mutations in the protease-encoding region (V321, L33F, K451, 184V, L89M), conferring resistance to protease inhibitors such as KNI-272, readily produced HIV-1 carrying both sets of mutations when propagated in MT-2 cells in the presence of azidothymidine (AZT) and KNI-272.

Kinetic characterization and cross-resistance patterns of HIV-1 protease mutants selected under drug pressure.

PMID: 7626598 1995 Biochemistry

Abstract: Eleven different recombinant, drug-resistant HIV-1 protease (HIV PR) mutants--R8Q, V32I, M46I, V82A, V82F, V82I, I84V, V32I/I84V, M46I/V82F, M46I/I84V, and V32I/K45I/F53L/A71V/I84V/L89M--were generated on the basis of results of in vitro selection experiments using the inh

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