Efavirenz: resistance and cross-resistance. NLM AIDSLINE Important note: Information in this article was accurate in 2000. The state of the art may have changed since the publication date.

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Efavirenz: resistance and cross-resistance.

Int J Clin Pract Suppl. 1999 Jun;103:21-5. Unique Identifier : AIDSLINE MED/20087919
Clotet B; Hospital Universitari Germans Trias I Pujol, Badalona, Spain.

Abstract: Resistant strains, the major cause of treatment failure in the management of HIV infection, evolve whenever virus replication is incompletely suppressed by drug therapy. In such cases, genotypic analysis of proviral DNA or phenotypic analysis of viral isolates or recombinant molecular clones can provide useful information for the clinician. With regard to NNRTIs, a single mutation at K103N is the most predominant resistance RT mutation observed with the NNRTIs and confers cross-resistance between efavirenz, nevirapine and delavirdine. K103N is found in HIV strains isolated from patients experiencing a viral rebound in plasma HIV-RNA levels who have received an efavirenz-containing regimen. Phenotypic analysis showed that the K103N mutation alone confers an approximate 20-fold increase in the IC50 of efavirenz.

Keywords: JOURNAL ARTICLE REVIEW REVIEW, TUTORIAL Anti-HIV Agents/*THERAPEUTIC USE Delavirdine/THERAPEUTIC USE Drug Resistance, Microbial/GENETICS Genotype Human HIV Infections/DRUG THERAPY HIV-1/*DRUG EFFECTS/GENETICS *Mutation Nevirapine/THERAPEUTIC USE Oxazines/*THERAPEUTIC USE Phenotype Reverse Transcriptase Inhibitors/*THERAPEUTIC USE Treatment Failure Virus Replication

KWDjournalarticlereviewreview,tutorialanti-hivagents/KWDtherapeuticusedelavirdine/therapeuticusedrugresistance,microbial/geneticsgenotypehumanhivinfections/drugtherapyhiv-1/KWDdrugeffects/geneticsKWDmutationnevirapine/therapeuticuseoxazines/KWDtherapeuticusephenotypereversetranscriptaseinhibitors/KWDtherapeuticusetreatmentfailurevirusreplication
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A0040888

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