Abstract: One sample that was wild-type by genotyping was positive for K103N by AS-PCR.
Abstract: Samples were also tested for the K103N mutation using a highly sensitive allele-specific real-time PCR assay (AS-PCR).
Nevirapine resistance in women and infants after first versus repeated use of single-dose nevirapine for prevention of HIV-1 vertical transmission.
PMID: 18582198
2008
The Journal of infectious diseases
Abstract: The proportion of women infected with variants with resistance mutations, the types of mutations detected, and the frequency and level of K103N were similar in the two groups of women at 6 weeks and 6 months post partum.
Discussion: At 6 months, the proportion of women with K103N detected by LigAmp was also similar in SD NVP-naive versus SD NVP-experienced women.
Discussion: At 6 weeks, the proportion of SD NVP-experienced women with K103N detected by LigAmp (45.5%), was nearly identical to the proportion of SD NVP-naive women with K103N detected by the same method in this study (45.6%) and in the HIVNET 012 trial (47.1%).
Discussion: However, our retrospective study of the HIVNET 012 cohort found no difference in detection of K103N in women by 2 years after first versus subsequent SD NVP us
Transmission of HIV-1 minority-resistant variants and response to first-line antiretroviral therapy.
Abstract: Minority-resistant variants were searched by allele-specific PCR for the mutations K103N and M184V in reverse transcriptase and L90M in protease.
Analysis of near full-length genomic sequences of drug-resistant HIV-1 spreading among therapy-naive individuals in Nagoya, Japan: amino acid mutations associated with viral replication activity.
PMID: 18620491
2008
AIDS research and human retroviruses
Abstract: Genomes comprised seven protease inhibitor (PI)-resistant viruses possessing an M46I (n = 6) or L90M mutation (n = 1) and five non-nucleoside reverse transcriptase inhibitor-resistant viruses possessing a K103N mutation.
5-Alkyl-6-benzyl-2-(2-oxo-2-phenylethylsulfanyl)pyrimidin-4(3H)-ones, a series of anti-HIV-1 agents of the dihydro-alkoxy-benzyl-oxopyrimidine family with peculiar structure-activity relationship profile.
PMID: 18630898
2008
Journal of medicinal chemistry
Abstract: Against clinically relevant HIV-1 mutants (K103N, Y181C, and Y188L) as well as in enzyme (wt and K103N, Y181I, and L100I mutated RTs) assays, compounds carrying an ethyl/ iso-propyl group at C5 and a 2,6-dichloro-/2-chloro-6-fluoro-benzyl moiety at C6 were the most potent derivatives, also characterized by low fold resistance ratio.
Prevalence of drug resistance and associated mutations in HIV-positive Puerto Ricans: sex variations.
Abstract: The most prevalent mutations in the reverse transcriptase gene were M184V, K103N, T215Y, and M41L.
Etravirine for the treatment of HIV infection.
PMID: 18662109
2008
Expert review of anti-infective therapy
Abstract: This conformation confers an increased genetic barrier to resistance compared with other NNRTIs: multiple mutations are required before there is a decrease in susceptibility to etravirine; whereas, only one mutation (K103N) is typically needed to confer high-level resistance to the first-generation NNRTIs.
Mechanistic basis of zidovudine hypersusceptibility and lamivudine resistance conferred by the deletion of codon 69 in the HIV-1 reverse transcriptase coding region.
Abstract: Human immunodeficiency virus type 1 clones containing Delta 69 in a multidrug-resistant sequence background, including the Q151M complex and substitutions K103N, Y181C, M184V, and G190A, showed high-level resistance to all tested nucleoside RT inhibitors.
Structural basis for the improved drug resistance profile of new generation benzophenone non-nucleoside HIV-1 reverse transcriptase inhibitors.
PMID: 18665583
2008
Journal of medicinal chemistry
Abstract: Structures of mutant RTs (K103N, V106A/Y181C) with benzophenones showed only small rearrangements of the NNRTIs relative to wild-type.
Minority HIV-1 drug resistance mutations are present in antiretroviral treatment-naive populations and associate with reduced treatment efficacy.
Abstract: Eight validated real-time PCR-based assays were used to test for minority drug resistance mutations (protease L90M and reverse transcriptase M41L, K70R, K103N, Y181C, M184V, and T215F/Y) above naturally occurring frequencies.
Result: Of the two individuals who had resistance mutations at baseline and maintained virus suppression during the 48-wk course of the study, one person had K103N and the other Y181C; both had been treated with the ABC+3TC+EFV regimen.
Result: One participant who experienced failure within 2 mo had both the K103N and
HIV mutation literature information.
PMID: 
2008
Antiviral therapy
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