literature

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,

PMID: 24444369 2014 AIDS research and therapy

Table: L100I

Non-nucleoside reverse transcriptase inhibitor (NNRTI) cross-resistance: implications for preclinical evaluation of novel NNRTIs and clinical genotypic resistance testing.

PMID: 23934770 2014 The Journal of antimicrobial chemotherapy

Abstract: RESULTS: Sixteen mutations at 10 positions were significantly associated with the greatest contribution to reduced phenotypic susceptibility (>=10-fold) to one or more NNRTIs, including: 14 mutations at six positions for nevirapine (K101P, K103N/S, V106A/M, Y181C/I/V, Y188C/L and G190A/E/Q/S); 10 mutations at six positions for efavirenz (L100I, K101P, K103N, V106M, Y188C/L and G190A/E/Q/S); 5 mutations at four positions for etravirine (

PMID: 23364785 2013 Journal of medical virology

Abstract: Five NNRTI resistant mutant forms of RT were produced (L100I, K103N, L100I/K103N, Y181C, V179D) in order to validate the assay for ETR.

Increasing trends in primary NNRTI resistance among newly HIV-1-diagnosed individuals in Buenos Aires, Argentina.

PMID: 24093951 2013 Journal of the International AIDS Society

Method: Sequences were analyzed to identify mutations associated with reduced susceptibility to protease and RT inhibitors, as reported by the International AIDS Society-USA in 2010: RT-M41L, A62V, K65R, D67N, 69 insert, K70R, L74V,V75I, F77L, L100I, K101P, K103N, V106A, V106M, V108I, Y115F, F116Y,

Simultaneous detection of major drug resistance mutations in the protease and reverse transcriptase genes for HIV-1 subtype C by use of a multiplex allele-specific assay.

PMID: 23985909 2013 Journal of clinical microbiology

Abstract: All the wild-type and mutant alleles were unequivocally distinguished with plasmid templates, and the limits of detection were 1.56% for K219Q and K219E, 3.13% for L76V, 6.25% for K65R, K70R, L74V, L100I, K103N, K103R, Q151M, Y181C, and I47V, and 12.5% for M41L, K101P, K101E, V106A, V106M, Y115F, M184V,

PMID: 23959304 2013 Antimicrobial agents and chemotherapy

Abstract: Interestingly, viruses bearing the L100I RAM were hypersusceptible to AIC292.

Persistence of HIV-1 transmitted drug resistance mutations.

PMID: 23904291 2013 The Journal of infectious diseases

Table: L100I

Trends in Genotypic HIV-1 Antiretroviral Resistance between 2006 and 2012 in South African Patients Receiving First- and Second-Line Antiretroviral Treatment Regimens.

PMID: 23840622 2013 PloS one

Result: Among the patients receiving EFV, L100I occurred in a higher proportion of the 53 patients receiving ABC/3TC (23%) compared with the remaining 748 patients (3.1%; p<0.001) and Y181C occurred in a higher proportion of the 127 patients receiving TDF/3TC (18%) compared with the remaining 674 patients (2.5%; p<0.001).

Discussion: The statistical associations of Y181C with TDF and of L100I with ABC have not previously been reported.

Tenofovir-based regimens associated with less drug resistance in HIV-1-infected Nigerians failing first-line antiretroviral therapy.

PMID: 23079810 2013 AIDS (London, England)

Method: Etravirine resistance was calculated using weighted scores, where L100I, K101P, Y181C/I/V result in the greatest impaired clinical response.

Result: The L100I (36%), K103N (79%), and P225H (21%) mutations were more common in efavirenz based regimens as compared to nevirapine based regimens [Table 3].