Result: M36I was the second most common mutation for 2006 (164 of 707, 23.2%), while this position was occupied by V77I for the reminder of the study with prevalences of (201 of 608, 33.1%), (222 of 706, 31.4%), (125 of 340, 36.8%), and (45 of 139, 32.4%).
Result: Statistically significant differences between men and women were recorded for A71V (P = 0.05) and L90M (P = 0.04) in 2006, and M36I (P = 0.005) in 2008.
Discussion: M36I, a mutation that allows faster in vitro HIV-1 replication regardless of the presence of protease inhibitors, was the second most common mutation for 2006.
Prediction of drug-resistance in HIV-1 subtype C based on protease sequences from ART naive and first-line treatment failures in North India using genotypic and docking analysis.
Abstract: No major mutations were seen in the PR sequences in isolates from treatment-naive individuals, although isolates from two patients had T74S mutation, known to be associated with reduced susceptibility to nelfinavir (NFV) and a combination of M36I, H69K and L89M mutations found in isolates from 77 patients (59.7%), considered to be conferring resistance to tipranavir (TPV) according to ANRS algorithm.
Long-term follow-up of 11 protease inhibitor (PI)-naive and PI-treated HIV-infected patients harbouring virus with insertions in the HIV-1 protease gene.
Abstract: The insertions were mainly located between codons 33 and 39 and associated with surrounding mutations (M36I/L and R41K).
The L76V mutation in HIV-1 protease is potentially associated with hypersusceptibility to protease inhibitors Atazanavir and Saquinavir: is there a clinical advantage?
Characterization of HIV type 1 subtype C protease gene: selection of L63P mutation in protease inhibitor-naive Indian patients.
PMID: 21453185
2011
AIDS research and human retroviruses
Abstract: Selection of T12S, I15V, L19I, M36I, R41K, H69K, L89M, and I93L was observed both in global and Indian subtype C while the L63P mutation was selected in Indian PR sequences.
Drug resistance mutations in patients infected with HIV-2 living in Spain.
PMID: 21558334
2011
The Journal of antimicrobial chemotherapy
Abstract: No major mutations associated with drug resistance in HIV-1 were recognized in 29 PR, 20 RT and 5 INT sequences from antiretroviral-naive HIV-2 individuals, although natural polymorphisms with potential effects on susceptibility to PR inhibitors were recognized at 10 positions (L10V/I, V32I, M36I, M46I, I47V, Q58E, A71V/I, G73A, V82I and L89I/V) and for nucleoside reverse transcriptase inhibitors at three positions (T69N, V75I
Prevalence and resistance mutations of non-B HIV-1 subtypes among immigrants in Southern Spain along the decade 2000-2010.
Abstract: Patients infected with non-B subtypes showed a high frequency of minor protease inhibitor resistance mutations, M36I, L63P, and K20R/I.
Result: The M36I mutation in protease was observed in all patients, whilst K20I/R, L63P, V77I
Table: M36I
Discussion: Our results indicated that patients infected with HIV-1 non-B subtypes showed a high frequency of minor PR mutations (polymorphisms) as M36I, L63P, and K20R/I, in contrast to the low proportion of major resistance mutations.
Correlation between resistance profile and immunosuppression in heavily treated HIV-1 infected Romanian patients.
PMID: 22180722
2011
Romanian biotechnological letters
Result: The most commonly encountered polymorphisms that may induce early development of drug resistance, were L63T, present in 80.5% of the cases and M36I in 77.8% of the cases, followed by L89M (50%), K20R (72.3%) and L10V (63.9%) of the patients.
Does GSS still maintain relevance on HAART outcome after the introduction of newest active antiretroviral drugs? 48 weeks results.
Result: Among the more polymorphic PI mutations (nevertheless included in the IAS-USA December 2010 list as PI-resistance mutations) the most prevalent ones were E35D, M36I, L63P and V91S reaching a percentage ranging between 30% and 50%.
HIV mutation literature information.
PMID: 
2012
AIDS research and treatment
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