Evidence map›Paper›PMID 11333879›Full record

ArticleJournal of virology2001

Genotypic correlates of phenotypic resistance to efavirenz in virus isolates from patients failing nonnucleoside reverse transcriptase inhibitor therapy.

L Bacheler, S Jeffrey, G Hanna, R D'Aquila, L Wallace, K Logue, B Cordova, K Hertogs, B Larder, R Buckery and 5 more

Open access · greenAbstract readComparative Study
In one paragraph

Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 1 pooled it
7.3field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

94 citing papers in PubMed, 1 synthesis or guideline pooled it, 239 citations in OpenAlex.

  1. Pooled it
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  7. Patterns of HIV-1 Viral Load Suppression and Drug Resistance During the Dolutegravir Transition: A Population-based Longitudinal Study.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2026
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  15. Pretreatment and Acquired Antiretroviral Drug Resistance Among Persons Living With HIV in Four African Countries.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2021
    Article
  16. Article
  17. Pharmacogenomics of Antiretroviral Drug Metabolism and Transport.Annual review of pharmacology and toxicology · 2021
    Review
  18. Article
  19. Article
  20. Review

34 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 2 countries.

L BachelerDuPont Pharmaceuticals Company, Wilmington, Delaware 19880-0336, USA. lee.bacheler@dupontpharma.com
S Jeffrey
G Hanna
R D'Aquila
L Wallace
K Logue
B Cordova
K Hertogs
B Larder
R Buckery
D Baker
K Gallagher
H Scarnati
R Tritch
C Rizzo
DuPont (United States) · USWilmington University · USMassachusetts General Hospital · USHealth Economics and Outcomes Research (United Kingdom) · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Efavirenz (also known as DMP 266 or SUSTIVA) is a potent nonnucleoside inhibitor of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) activity and of HIV-1 replication in vitro and in vivo. Most patients on efavirenz-containing regimens have sustained antiviral responses; however, rebounds in plasma viral load have been observed in some patients in association with the emergence of mutant strains of HIV-1. Virus isolates from the peripheral blood mononuclear cells (PBMCs) of patients with such treatment failures, as well as recombinant viruses incorporating viral sequences derived from patient plasma, show reduced in vitro susceptibility to efavirenz in association with mutations in the RT gene encoding K103N, Y188L, or G190S/E substitutions. Patterns of RT gene mutations and in vitro susceptibility were similar in plasma virus and in viruses isolated from PBMCs. Variant strains of HIV-1 constructed by site-directed mutagenesis confirmed the role of K103N, G190S, and Y188L substitutions in reduced susceptibility to efavirenz. Further, certain secondary mutations (V106I, V108I, Y181C, Y188H, P225H, and F227L) conferred little resistance to efavirenz as single mutations but enhanced the level of resistance of viruses carrying these mutations in combination with K103N or Y188L. Viruses with K103N or Y188L mutations, regardless of the initial selecting nonnucleoside RT inhibitor (NNRTI), exhibited cross-resistance to all of the presently available NNRTIs (efavirenz, nevirapine, and delavirdine). Some virus isolates from nevirapine or delavirdine treatment failures that lacked K103N or Y188L mutations remained susceptible to efavirenz in vitro, although the clinical significance of this finding is presently unclear.

Indexed as

AlkynesAmino Acid SubstitutionAnti-HIV AgentsBenzoxazinesCells, CulturedClinical Trials, Phase II as TopicCohort StudiesCyclopropanesDelavirdineDrug Resistance, MicrobialDrug Resistance, MultipleGenotypeHIV-1HIV InfectionsHIV Reverse TranscriptaseHumansAlkynesAnti-HIV AgentsBenzoxazinesCyclopropanesDelavirdineefavirenzHIV Reverse TranscriptaseNevirapineOxazinesReverse Transcriptase Inhibitors

Identifiers

PMID11333879
PMCPMC114903
OpenAlexW2073157159

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.