literature

HIV mutation literature information.

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%).

Tipranavir-ritonavir genotypic resistance score in protease inhibitor-experienced patients.

PMID: 18625773 2008 Antimicrobial agents and chemotherapy

Abstract: Mutations at six residues were associated with a lower VR (E35D/G/K/N, M36I/L/V, Q58E, Q61D/E/G/H/N/R, H69I/K/N/Q/R/Y, and L89I/M/R/T/V), and one mutation was associated with a higher VR (F53L/W/Y).

Abstract: The genotypic score M36I/L/V-53L/W/Y + Q58E + H69I/K/N/Q/R/Y + L89I/M/R/T/V was selected as providing a strong association with VR.

Drug resistance-associated genotypic alterations in the pol gene of HIV type 1 isolates in ART-naive individuals in North India.

PMID: 18240959 2008 AIDS research and human retroviruses

Abstract: Forty-nine percent had mutations in the hinge (M36I, R41K, H69K) and alpha-helix (L89M) regions of the C-virus protease, which has been linked to increased catalytic activity.

Polymorphisms and drug resistance analysis of HIV-1 CRF01_AE strains circulating in Fujian Province, China.

PMID: 17619115 2007 Archives of virology

Abstract: RESULTS: In comparison with the consensus sequence of B strains, the most common protease polymorphisms in HIV-1 CRF01_AE strains prevailing in Fujian Province, China, were I13V (76.9%), E35D (76.9%), M36I (100%), R41K (98.1%), H69K (90.4%), and L89M (96.2%).

Structural characterization of B and non-B subtypes of HIV-protease: insights into the natural susceptibility to drug resistance development.

PMID: 17467738 2007 Journal of molecular biology

Abstract: Our results further indicate that two naturally occurring polymorphic substitutions in subtype F and other non-B HIV proteases, M36I and L89M, may lead to early development of drug resistance in patients infected with non-B HIV subtypes.

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.

Association of Gag cleavage sites to protease mutations and to virological response in HIV-1 treated patients.

PMID: 16875739 2007 The Journal of infection

Abstract: Two patterns of mutations in the protease were identified: (M46I/L, I54V, V82A/T/F) was associated to the A431V and (K20I/R/M, L89M/I) to the S373Q and L449P.

Update on primary HIV-1 resistance in Argentina: emergence of mutations conferring high-level resistance to nonnucleoside reverse transcriptase inhibitors in drug-naive patients.

PMID: 16773027 2006 Journal of acquired immune deficiency syndromes (1999)

Abstract: The substitution L89M, recently suggested as a resistance-related mutation in some subtype F viruses, was observed in 1 RecBF.

Revealing the binding and drug resistance mechanism of amprenavir, indinavir, ritonavir, and nelfinavir complexed with HIV-1 protease due to double mutations G48T/L89M by molecular dynamics simulations and free energy analyses.

PMID: 15871131 2005 The Journal of infectious diseases

Abstract: BACKGROUND: This work evaluates the role of subtype F human immunodeficiency virus type 1 (HIV-1) protease (PR) substitutions L89M and L90M in viral replication and resistance to PR inhibitors (PIs).

Abstract: CONCLUSION: The L89M mutation in subtype F viruses is a high genetic barrier to the accumulation of the L90M resistance mutation and can function as a resistance mutation, depending on the presence of other polymorphisms in the subtype F PR backbone.

Abstract: RESULTS: The subtype F clone (89M90L) showed a replicative capacity comparable to that of the PI-susceptible subtype B clone (89<

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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