A prospective comparison of the two main indications of efavirenz in 2001 highly active antiretroviral therapy (HAART) regimens: first-line versus salvage use.
PMID: 12003964
2002
The Journal of antimicrobial chemotherapy
Abstract: Viral genotyping detected at least the K103N mutation in 41% of the 78 evaluable patients, despite lack of exposure to efavirenz and related compounds.
A mutation in the 3' region of the human immunodeficiency virus type 1 reverse transcriptase (Y318F) associated with nonnucleoside reverse transcriptase inhibitor resistance.
Abstract: Combinations of Y318F with K103N, Y181C, or both resulted in decreased efavirenz susceptibility of 43-, 3.3-, and 84-fold, respectively, as well as >100- and >60-fold decreases in delavirdine and nevirapine susceptibility, respectively.
Discordant Human Immunodeficiency Virus Type 1 drug resistance mutations, including K103N, observed in cerebrospinal fluid and plasma.
Abstract: To our knowledge, this is the first report of HIV-1 isolated from CSF harboring the K103N mutation, which confers resistance to the nonnucleoside reverse-transcriptase inhibitors, and this finding may indicate that virus in the CSF replicates independently from virus in the blood compartment.
Genetic divergence of human immunodeficiency virus type 1 Ethiopian clade C reverse transcriptase (RT) and rapid development of resistance against nonnucleoside inhibitors of RT.
PMID: 12069959
2002
Antimicrobial agents and chemotherapy
Abstract: In the case of subtype C, selection with NVP and/or EFV led to the appearance of several previously unseen mutations in RT, i.e., V106M and S98I, as well as other mutations that have been previously reported (e.g., K103N, V106A, V108I, and Y181C).
Genetic variation of the protease and reverse transcriptase genes in HIV-1 CRF04_cpx strains.
PMID: 12079565
2002
AIDS research and human retroviruses
Abstract: Substitutions classically associated with resistance to antiretroviral drugs were observed in six of seven samples, including G48V, V82A, L90M, M46I in the protease protein, and K70R, D69D/N, M184V, T215F, K103N in the reverse transcriptase protein.
Development of resistance mutations in women receiving standard antiretroviral therapy who received intrapartum nevirapine to prevent perinatal human immunodeficiency virus type 1 transmission: a substudy of pediatric AIDS clinical trials group protocol 316.
PMID: 12134253
2002
The Journal of infectious diseases
Abstract: The most common mutation was K103N, which was present in 10 women.
Extent and importance of cross-resistance to efavirenz after nevirapine failure.
PMID: 12167268
2002
AIDS research and human retroviruses
Abstract: All the strains with the K103N mutation showed high-level resistance to efavirenz, in contrast with 20% of those carrying exclusively the Y181C mutation.
Abstract: _Virological failure was observed in patients with phenotypic resistance to efavirenz (67 vs. 11%; relative risk [RR], 4; 95% confidence interval [CI], 1.07-14.89; p = 0.04), or in presence of the K103N mutation (52 vs. 17%; RR, 1.77; 95% CI, 1.12-2.79; p = 0.02), and these results remained unchanged after adjusting for HIV load, or by resistance to the accompanying drugs in the salvage regimen.
Polymorphisms of cytotoxic T-lymphocyte (CTL) and T-helper epitopes within reverse transcriptase (RT) of HIV-1 subtype C from Ethiopia and Botswana following selection of antiretroviral drug resistance.
Abstract: Mutations within immunogenic regions of clade C RT were noted during drug selection of subtype C isolates with nevirapine (S98I, Y181C, V108I and K103N), delavirdine, (A62V, V75E, L100I, K103T, V108I, Y181C), efavirenz (K103E, V106M, V179D, Y188C/H, G190A), lamivudine (M184I, M184V), and zidovudine (K70R), respectively.
Development of drug resistance in HIV-1 patients receiving a combination of stavudine, lamivudine and efavirenz.
PMID: 12385703
2002
International journal of antimicrobial agents
Abstract: Results showed that viruses carrying primary mutations, usually K103N, T215Y and M41L, presented higher levels of HIV-1 RNA, suggesting an association between a precise mutation pattern and treatment failure.
Emergence of drug-resistant HIV-1 variants in patients undergoing structured treatment interruptions.
HIV mutation literature information.
PMID: 
2002
The Journal of antimicrobial chemotherapy
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