Viral Genetic Diversity and Polymorphisms in a Cohort of HIV-1-Infected Patients Eligible for Initiation of Antiretroviral Therapy in Abuja, Nigeria.
PMID: 25582324
2015
AIDS research and human retroviruses
Abstract: Eleven polymorphic mutations (G16E, K20I, L23P, E35D, M36I, N37D/S/T, R57K, L63P, and V82I) were detected in the <
Discussion: A study has shown that the polymorphic mutation M36I in the PR region was associated with a higher rate of PI treatment failure.
Discussion: The polymorphic mutations M36I, L63P, V82I, and M89I were proportionately present in the sequences of CRF02-AG, CRF43-02G, and CRF06-cpx and subtype G.
Characterization of HIV drug resistance mutations among patients failing first-line antiretroviral therapy from a tertiary referral center in Lusaka, Zambia.
Discussion: A prior study of antiretroviral drug-nave HIV-1-infected Zambian adults (n=28) demonstrated a high frequency of pre-existing minor mutations in the protease gene:including I93L (92%), L89M (79%), and M36I (79%):which corroborates results from our current study (Handema et al., 2003).
Transmitted Drug Resistance Mutations in Antiretroviral-Naive Injection Drug Users with Chronic HIV-1 Infection in Iran.
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: M36I
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.
Effectiveness of a Treatment Switch to Nevirapine plus Tenofovir and Emtricitabine (or Lamivudine) in Adults with HIV-1 Suppressed Viremia.
Abstract: Protease substitutions I13V, E35D, M36I, R57K, H69K, and L89M, which serve as drug-resistance support mutations in subtype B, were present in the majority of subtype-A1 sequences
Discussion: Protease substitutions I13V, E35D, M36I, R57K, H69K, and L89M, which are drug-resistance support mutations in subtype B, were present in the majority of subtype-A1 sequences of the population studied, suggesting that these sequence alterations may occur as natural polymorphisms, and may serve as genetic signatures.
Gag-Protease Sequence Evolution Following Protease Inhibitor Monotherapy Treatment Failure in HIV-1 Viruses Circulating in East Africa.
PMID: 26258548
2015
AIDS research and human retroviruses
Introduction: Of note, mutations M36I and H69K were present in all subtype A and C patient viruses and I93L was present in all subtype C viruses, and were consensus residues in each subtype, respectively.
The Evolving Genotypic Profile of HIV-1 Mutations Related to Antiretroviral Treatment in the North Region of Brazil.
Result: In contrast, several secondary mutations were found to differ between B and non-B subtypes: L63P (p < 0.001) and A71T (p = 0.021) were higher in subtype B, and M36I (p < 0.001), K20R (p < 0.001), L10V (p = 0.004), L89 M (p < 0.001), and F53L (p = 0.011) were higher in non-B subtypes.
Result: With respect to accessory or secondary mutations, the most frequent were L63P (60.7%), M36I (41.1%), I93L (40.1%), I62V (39%), V77I (35.8%), A71V (24.9%), and L10I (24.7%) (Figure 1(d)).
Discussion: L63P and
Conformational variation of an extreme drug resistant mutant of HIV protease.
PMID: 26397743
2015
Journal of molecular graphics & modelling
Method: Plasmid DNA encoding PR (subtype B of group M) with 20 mutations Q7K; L10F; I13V; I15V; D30N; V32I; L33F; E35D; M36I; S37N; I47V; I54L; Q58E; I62V; L63P; A71V; I84V; N88D; L89T and L90M (termed PR20) cloned between the Nde1 and BamH1 sites
Low Incidence of HIV-1C Acquired Drug Resistance 10 Years after Roll-Out of Antiretroviral Therapy in Ethiopia: A Prospective Cohort Study.
Result: However, in all the 8 patients, naturally occurring minor mutations/polymorphic changes at PR region (positions M36I, R41K, H69K, L89M, and I93L) were observed.
HIV mutation literature information.
PMID: 
2015
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