literature

HIV mutation literature information.

Resistance profile of the HIV-1 maturation inhibitor GSK3532795 in vitro and in a clinical study.

PMID: 31622432 2019 PloS one

Method: Participants with a history of genotypic/phenotypic drug resistance to protease inhibitors (PIs) or with HIV-1 genotypic drug resistance to PIs at baseline (including D30N, M46I/L, I47V/A, G48V, I50L, I54M/L, Q58E, T74P, L76V, V82A/F/L/T/S, N83D, I84V, N88S, or L90M) were excluded, despite any reported effects of PI resistance or resistance

Molecular Determinants of Epistasis in HIV-1 Protease: Elucidating the Interdependence of L89V and L90M Mutations in Resistance.

PMID: 31386353 2019 Biochemistry

Introduction: One such example is the A71V mutation, a secondary mutation that, when observed in conjunction with I50V/L, acts to restore a balance between catalytic efficiency and inhibitor binding.

Switching to bictegravir/emtricitabine/tenofovir alafenamide maintained HIV-1 RNA suppression in participants with archived antiretroviral resistance including M184V/I.

PMID: 31430369 2019 The Journal of antimicrobial chemotherapy

Method: Primary PI-R substitutions were D30N, V32I, M46I/L, I47V/A, G48V, I50V/L, I54M/L, Q58E, T74P, L76V, V82A/F/L/S/T, N83D, I84V, N88S and L90M in PR.

High Levels of HIV-1 Drug Resistance in Children Who Acquired HIV Infection Through Mother to Child Transmission in the Era of Option B+, Haiti, 2013 to 2014.

PMID: 30640198 2019 The Pediatric infectious disease journal

Result: One child had a major M46I PI mutation, which causes low level of resistance to all PIs except darunavir and tipranavir, and another had the I50L major PI mutation, which causes high level resistance to atazanavir (Table 1).

Trends in the Molecular Epidemiology and Genetic Mechanisms of Transmitted Human Immunodeficiency Virus Type 1 Drug Resistance in a Large US Clinic Population.

PMID: 29846534 2019 Clinical infectious diseases

Result: The next most common SDRMs, V32I, I50V/L, L76V, and I84V, each occurred in <=5 individuals.

Next generation sequencing of HIV-1 protease in the PIVOT trial of protease inhibitor monotherapy.

PMID: 29428459 2018 Journal of clinical virology

Introduction: It appears therefore that only a single PI monotherapy patient (described below, patient A) experienced a loss of drug options due to a mutation (I50L) selected by study drug.

Result: Notably, I50L was not detected as a minority variant at this time point despite its detection (as a mixture) by Sanger sequencing at week 48, and it was also absent by Sanger sequencing at week 71.

Result: Patient A, who received atazanavir as PI monotherapy, met the primary outcome due to an I50L mutation (patient 5 in Table 2 in main trial report).

A decade of viral mutations and associated drug resistance in a population of HIV-1+ Puerto Ricans: 2002-2011.

PMID: 28493944 2017 PloS one

Result: The 3 most prevalent HIV-1 resistance-associated mutations for PRO were L63P (73.9%), V77I (45.2%) and I13V (34.2%), whereas I50L, I50V and K20I were the least abundant mutations recorded during the 10-year period (Figs 2 and 4).

Comparison between next-generation and Sanger-based sequencing for the detection of transmitted drug-resistance mutations among recently infected HIV-1 patients in Israel, 2000-2014.

PMID: 28799325 2017 Journal of the International AIDS Society

Table: I50L

Week 48 resistance analysis of Elvitegravir/Cobicistat/Emtricitabine/Tenofovir DF versus Atazanavir + Ritonavir + Emtricitabine/Tenofovir DF in HIV-1 infected women (WAVES study GS-US-236-0128).

PMID: 28891788 2017 HIV clinical trials

Method: Primary PI-R substitutions assessed were D30N, V32I, L33F, M46I/L, I47A/V, G48V, I50L/V, I54L/M, Q58E, T74P, L76V, V82A/F/L/S/T, I84V, N88S, and L90M in PR.

Outcome of patients on second line antiretroviral therapy under programmatic condition in India.

PMID: 26572102 2015 BMC infectious diseases

Result: Among PI mutations, M46I (n = 5) was the commonest mutation, followed by N88S (n = 3), I50L (n = 2), I84V (n = 2), V 82A (n = 1).

Table: I50L

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