literature

HIV mutation literature information.

SURVEILLANCE OF HIV-1 DRUG-RESISTANCE MUTATIONS IN THAILAND FROM 1999 TO 2014.

PMID: 29641878 2017 The Southeast Asian journal of tropical medicine and public health

Abstract: PRdrug-associated mutations (M36I/L/V, H69K/R and L89I/M/V) previously consideredas CRF01_AE polymorphisms constituted > 90% prevalence in all samples.The launch of antiretroviral treatment influenced the pattern of mutations and theUniversal Coverage Scheme also impacted the rate of development of resistancemutations on a national scale.

From antiretroviral therapy access to provision of third line regimens: evidence of HIV Drug resistance mutations to first and second line regimens among Ugandan adults.

PMID: 28010730 2016 BMC research notes

Table: L89V

Structural Studies of a Rationally Selected Multi-Drug Resistant HIV-1 Protease Reveal Synergistic Effect of Distal Mutations on Flap Dynamics.

PMID: 27992544 2016 PloS one

Result: This inactive protease with active site D25N mutation has 22 other mutations (L10I, V11I, L23I, V32I, L33F, S37N, M46I, I47V, I50V, F53L, I54V, Q58E, D60E, L63P, H69R, A71V, G73S, V77I, V82F, L89V, L90M, <

Unique Flap Conformation in an HIV-1 Protease with High-Level Darunavir Resistance.

PMID: 26870021 2016 Frontiers in microbiology

Introduction: The latest International AIDS Society (IAS)-USA panel list shows 11 mutations associated with DRV resistance: V11I, V32I, L33F, I47V, I50V, I54M/L, T74P, L76V, I84V, and L89V (Wensing et al.,).

Result: The major virus (referred to as FS5929R1) had two major DRV resistance mutations (I47V and I50V), four minor mutations (V11I, V32I, L33F, and L89V), and V82F

Defective hydrophobic sliding mechanism and active site expansion in HIV-1 protease drug resistant variant Gly48Thr/Leu89Met: mechanisms for the loss of saquinavir binding potency.

PMID: 25513833 2015 Biochemistry

Introduction: Leu89Val, a secondary mutation, is an accessory mutation and is located outside the active site in the hydrophobic core of PR and occurs in response to treatment with IDV, NFV, FPV, and DRV.

The L33F darunavir resistance mutation acts as a molecular anchor reducing the flexibility of the HIV-1 protease 30s and 80s loops.

PMID: 29124158 2015 Biochemistry and biophysics reports

Introduction: Clinical isolates previously obtained from the Wayne State University Infectious Disease Clinic in Detroit, MI contain major drug resistance mutations L33F, I47V, I50V, I54M, L76V, V82I/F, and I84F as well as nonpolymorphicaccessory mutations L10V/G, V11I, I13V, K20T/R, L33I/M, K43T, F53L, A71L, T74P, and L89V.

Transmitted Drug Resistance Mutations in Antiretroviral-Naive Injection Drug Users with Chronic HIV-1 Infection in Iran.

PMID: 25962088 2015 PloS one

Abstract: Although not in the WHO SDRMs list, several minor protease inhibitor resistant mutations listed in the International Antiviral Society-USA panel were identified, of which M36I, H69K, L89M/V/I (each one 100%) and K20R/T (92.5%) can be considered as polymorphic signatures for CRF35_AD.The relatively high rate of TDR mutations in our study raises concerns about the risk of treatment failure in chronically infected IDUs of Sanandaj city.

Result: We found no SDRMs to protease inhibitors (PIs); however, based on the mutations listed in the International Antiviral Society-USA (IAS-USA) panel, 13minor mutations were detected in the PR region, of which M36I,

A uniquely prevalent nonnucleoside reverse transcriptase inhibitor resistance mutation in Russian subtype A HIV-1 viruses.

PMID: 25259833 2014 AIDS (London, England)

Result: Of the 243 patients who received one or more protease inhibitors, 32 (13%) had a study-defined protease inhibitor-resistance mutation most commonly L10F, K20T, V32I, L33F, M46I/L, I47V/A, I50L, F53L, I54V/L, Q58E, L76V, V82A/C, I84V, L89V, and L90M.

Cobicistat-boosted darunavir in HIV-1-infected adults: week 48 results of a Phase IIIb, open-label single-arm trial.

PMID: 25926858 2014 AIDS research and therapy

Method: Patients were required to have plasma VL >=1000 HIV-1 RNA copies/ml (Amplicor HIV-1 Monitor Test, version 1.5, Roche Diagnostics, Basel, Switzerland) at screening, eGFRCG >=80 ml/min, genotypic sensitivity to the two investigator-selected N[t]RTIs (GenoSure MG assay, Monogram Biosciences, South San Francisco, CA, USA), and none of the following darunavir RAMs: V11I, V32I, L33F, I47V, I50V, I54M, I54L, T74P, L76V, I84V or L89V.

Characteristics of HIV-1 natural drug resistance-associated mutations in former paid blood donors in Henan Province, China.

PMID: 24586665 2014 PloS one

Discussion: Results from the HIV-1 drug resistance mutation research by the International AIDS Society-USA (updated in March 2013) have revealed that PI resistance mutation sites are L10I, K20M, V32I, M36I, M46I/L, I47V/A, I50V, Q58E, A71V, G73S, V82A/F/T, I84V, L89V,L90M; NRTIs resistance mutations are M41L, A62V,

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