literature

HIV mutation literature information.

Emergence of drug resistance-associated mutations in HIV-1 subtype C protease gene in north India.

PMID: 23888308 2013 Virus genes

Abstract: Approximately 70% polymorphisms as minor mutations were observed in protease gene, of which 14 distinct amino acids changes were linked to partial DR such as G16E, K20R, M36I, D60E, I62V, L63P, I64M, H69K, T74A/S, V77I, V82I, I85V, L89M, and I93L.

Tenofovir-based regimens associated with less drug resistance in HIV-1-infected Nigerians failing first-line antiretroviral therapy.

PMID: 23079810 2013 AIDS (London, England)

Result: Secondary mutations related to polymorphisms (I13V (95%), M36I (83%), H69K (82%), V82I (43%) and L63P (28%)) also occurred among those genotyped.

HIV-1 drug resistance-associated mutations among antiretroviral-naive Thai patients with chronic HIV-1 infection.

PMID: 23161095 2013 Journal of medical virology

Abstract: Minor DRAMs to PIs including I13V, M36I, H69K, and L89M were observed more frequently in CRF_01 AE.

Transmission patterns of HIV-subtypes A/AE versus B: inferring risk-behavior trends and treatment-efficacy limitations from viral genotypic data obtained prior to and during antiretroviral therapy.

PMID: 23469241 2013 PloS one

Result: The latter differed significantly in the frequencies of the major resistance RT mutations T215FY and K219QE (NRTI) and of several secondary/accessory mutations, including: the protease mutations I13V, M36I, I62V, L63P, A71V, V77I,

Table: M36I

Discussion: the protease mutations M36I, L89M or the RT mutation R211S, and others (Tables 5 and 6; see also Kantor et al.).

Elucidating a relationship between conformational sampling and drug resistance in HIV-1 protease.

PMID: 23566104 2013 Biochemistry

Introduction: D30N occurs specifically in response to nelfinavir treatment, whereas M36I and A71V, along with other non-active site substitutions, appear as a result of selective pressure of treatments using various protease inhibitors.

Introduction: In particular, SDSL-DEER was used to understand the effects of the accumulation of primary, D30N, and secondary mutations M36I and A71V on the flap conformational sampling of WT subtype B HIV-1 PR.

Method: Seven stabilized (Q7K, L33I, L63I) and inactive (D25N) constructs (Bsi) with engineered labeling sites (

Extreme multidrug resistant HIV-1 protease with 20 mutations is resistant to novel protease inhibitors with P1'-pyrrolidinone or P2-tris-tetrahydrofuran.

PMID: 23590295 2013 Journal of medicinal chemistry

Introduction: Recently, we characterized a clinically derived HIV-1 protease (PR20) bearing 20 mutations [Q7K, L10F, I13V, I15V, D30N, V32I, L33F, E35D, M36I, S37N, I47V, I54L, Q58E, I62V, L63P, A71V, I84V, N88D, L89T and L90M] and extremely resist

Transmitted HIV drug resistance in treatment-naive Romanian patients.

PMID: 23592112 2013 Journal of medical virology

Result: The most common accessory PI resistance mutations found were M36I (56/61 patients) and R41K (56/61 patients), followed by mutations L89M (51/61), I15V (50/61), and L63T (41/61).

Discussion: A high frequency of minor PI resistance mutations (M36I, L63P, and K20R/I) has been reported in newly diagnosed immigrants from Spain, infected with non-B subtypes.

Discussion: The most common accessory PI resistance mutation observed in this study was M36I, and this has been reported to increase viral fitness and confer resistance to ritonavir and nelfinavir.

Highly-sensitive allele-specific PCR testing identifies a greater prevalence of transmitted HIV drug resistance in Japan.

PMID: 24358257 2013 PloS one

Table: M36I

Enhanced stability of monomer fold correlates with extreme drug resistance of HIV-1 protease.

PMID: 24079831 2013 Biochemistry

Result: The DRM, ANAM-11, bears six mutations identical or similar to PR20 (L10I/F, M36I, L63P, A71V, I84V, L90M) and exhibits similar properties of increased dimer dissociation (Kd = 0.1 +- 0.04 muM) along with moderately enhanced thermal stability (Table 1A).

Trends in prevalence of HIV-1 drug resistance in Thailand 2009-2010.

PMID: 24038219 2013 Journal of clinical laboratory analysis

Abstract: CONCLUSIONS: In 2010, three mutations in PR gene, M36I, H69K, and L90M, were decreased significantly.

Abstract: Three sequences in PR gene, M36I, H69K, and L90M, were decreased significantly in 2010 when compared to 2009.

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