literature

HIV mutation literature information.

Genotyping and antiretroviral drug resistance of human immunodeficiency Virus-1 in Jazan, Saudi Arabia.

PMID: 33285702 2020 Medicine

Abstract: Mutations associated with antiretroviral drugs include (V82A+I84IV), (L10F+

Result: Among the observed resistance mutations, 4/57 (7.0%) had conferring resistance to PI, other detected mutations were (L10F + V82Y), L10FV, L33LF, and L89LMV.

Result: Four patients had mutations in the protease region with no association to drug resistance (L33LF, L89LMV, L10FV, and [L10F + V82Y]), these patients were genotype C.

Detection of human immunodeficiency virus type 1 transmitted drug resistance among treatment-naive individuals residing in Jakarta, Indonesia.

PMID: 32874468 2020 Infectious disease reports

Result: Despite no drug resistance-related major mutations were identified, several drug resistance-related minor mutations including M36I [amino acid substitution from methionine (M) to isoleucine (I) at position 36 in the PR gene] (85.71%), H69K (85.71%), L89M (76.19%), K20R (57.14%), and G16E (47.62%), were detected in the PR genes (Table 1).

Discussion: In the present study, no TDR against PIs was detected, while minor mutations, M36I (85.71%), H69K (85.71%), L89M (76.19%), K20R (57.14%), and G16E (47.62%), were frequently detected among 85.7

HIV-1 drug resistance mutations detection and HIV-1 subtype G report by using next-generation sequencing platform.

PMID: 32360523 2020 Microbial pathogenesis

Abstract: The Protease inhibitor (PI) minor and major mutations were not reported but more than 95% of samples had polymorphisms mutation in K20R, M36I, H69K, L89 M positions.

Polymorphisms and drug resistance analysis of HIV-1 isolates from patients on first line antiretroviral therapy (ART) in South-eastern Nigeria.

PMID: 32267869 2020 PloS one

Abstract: Other polymorphisms found include; I13V/A, E35Q, M36I/L, N37D/S/E/H, R57K/G, L63T/P/S/Q, C67E/S, H69K/R, K70R, V82I and L89M in the range of 28.6% to 100% among the different subtypes.

Result: Polymorphisms at known secondary mutation sites (K20I, M36I/L, H69K/R and L89M) were found in all the samples while L63T/P/S/Q was found in 83.3% (10/12) and 31.3% (5/

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: 32057044 2020 Physical chemistry chemical physics

Abstract: Focusing on the wild type (WT) and G48T/L89M mutated forms of HIV-1 protease (HIV-1 PR) in complex with amprenavir (APV), indinavir (IDV), ritonavir (RTV), and nelfinavir (NFV), we have investigated the conformational dynamics and the resistance mechanism due to the G48T/L89M mutations by conducting a series of molecular dynamics (MD) simulations and free energy (MM-PBSA and solvated interaction energy (SIE)) analyses.

Abstract: The simulation results indicate that alterations in the side-chains of G48T/L89M mutated residues cause the inner active site to increase in volume and induce more curling of the flap tips, which provide the main contributions to weaker binding of inhibitors to the HIV-1

PMID: 32993693 2020 Retrovirology

Result: The most frequent mutations observed in the PR sequence were H69K (100%) and M36L (98%), followed by L89M (58.8%), I15V (25.5%), K20R (25.5%), T74S (17.6%) and L89I (5.88%).

Discussion: The most frequent minor mutations observed in the PR sequence were H69K (100%) and M36L (98%), followed by L89M (58.8%), I15V (25.5%), K20R (25.5%), and T74S (17.6%).

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.

Upward trends of acquired drug resistances in Ethiopian HIV-1C isolates: A decade longitudinal study.

PMID: 29049402 2017 PloS one

Result: However, in the majority of the patients at all time points, several secondary mutations that may facilitate the development of PI resistance were found at higher frequency which could be naturally occurring minor mutations/polymorphic changes (positions M36I, R41K, H69K, L89M, and I93L) but their clinical significance is uncertain.

Cross-sectional study of virological failure and multinucleoside reverse transcriptase inhibitor resistance at 12 months of antiretroviral therapy in Western India.

PMID: 27631260 2016 Medicine

Result: Only 1 individual had major PI resistance mutation L90M and 5 had minor PI resistance mutations L89M, V77I, L63P, H69K/R/Q, M36I, K20I/M/R/T, G16E, and L10V/I.

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

PMID: 25962088 2015 PloS one

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, H69K, and L89M/V/I were found in all 40 (100%) andK20R/T was detected in 37 (92.5%) samples.

Table: L89M/V

Discussion: Moreover, in agreement with previous reports we identified high frequencies of M36I, H69K, L89M/V/I and K20R/T mutations that may be considered as polymorphic signatures within the protease region of CRF35_AD

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