literature

HIV mutation literature information.

Low frequency of genotypic resistance in HIV-1-infected patients failing an atazanavir-containing regimen: a clinical cohort study.

PMID: 23711895 2013 The Journal of antimicrobial chemotherapy

Result: The remaining 43 minor atazanavir mutations were either not detected in this dataset (L10C, K20V, E34Q, F53Y, I54L/M/T/A, A71L, G73C/T, V82F and I93M) or were not significantly associated with atazanavir exposure (L10I/F/V, G16E, K20R/M/I/T, L24I, V32I, L33I/F/V, M36L/V, M46L, G48V, I54V

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

Table: G73S

Low prevalence of transmitted drug resistance in patients newly diagnosed with HIV-1 infection in Sweden 2003-2010.

PMID: 22448246 2012 PloS one

Method: The following resistance mutations were scored: to nucleoside reverse transcriptase inhibitors (NRTIs): M41L, K65R, D67N/G/E, T69D/insertion, K70R/E, L74V/I, V75M/T/A/S, F77L, Y115F, F116Y, Q151M, M184V/I, L210W, T215Y/F/I/S/C/D/V/E, K219Q/EN/R; to non-nucleoside revers

Virologic failures on initial boosted-PI regimen infrequently possess low-level variants with major PI resistance mutations by ultra-deep sequencing.

PMID: 22355307 2012 PloS one

Abstract: The remaining 12 subjects, all with VLs<10,000, had protease gene UDS, and 4 had low-level PI DRMs: F53L(2), L76V(1), I54S(1), G73S(1).

Result: Of the 12 specimens that had ultra deep sequencing of only the protease gene, 4/12 (33.3%) had low level PI mutations: F53L(2), L76V(1), I54S(1) and G73S(1) (Figure 1b).

TMC310911, a novel human immunodeficiency virus type 1 protease inhibitor, shows in vitro an improved resistance profile and higher genetic barrier to resistance compared with current protease inhibitors.

PMID: 21896904 2011 Antimicrobial agents and chemotherapy

Abstract: IVRS performed with r13025 in the presence of DRV required less time and resulted in more PI resistance-associated mutations (V32I, I50V, G73S, L76V, and V82I; FC in DRV EC(50) = 258).

Lopinavir/ritonavir resistance in patients infected with HIV-1: two divergent resistance pathways?

PMID: 21755502 2011 Journal of medical virology

Abstract: In contrast, I54V, G73S and L90M were less prevalent in viruses L76V positive than L76V negative (I54V, 42% vs. 83%, P = 0.01; G73S, 0% vs. 33%, P = 0.02; L90M, 25% vs. 83%, P = 0.0006).

The L76V mutation in HIV-1 protease is potentially associated with hypersusceptibility to protease inhibitors Atazanavir and Saquinavir: is there a clinical advantage?

PMID: 21314993 2011 AIDS research and therapy

Table: G73S

Indinavir resistance evolution in one human immunodeficiency virus type 1 infected patient revealed by single-genome amplification.

PMID: 20960178 2010 Virologica Sinica

Abstract: 97.9% of variants had the M46I/G73S/L90M pattern at XLF6.

Abstract: After the patient began Indinavir treatment, the variants carrying polymorphisms declined while variants carrying the secondary mutation G73S gained the advantage.

Abstract: As therapy was prolonged, G73S was combined with M46I/L90M to form a resistance pattern M46I/G73S/L90M, which then became the dominant population.