Evidence map›Paper›PMID 17065321›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

Genotypic predictors of human immunodeficiency virus type 1 drug resistance.

Soo-Yon Rhee, Jonathan Taylor, Gauhar Wadhera, Asa Ben-Hur, Douglas L Brutlag, Robert W Shafer

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
6.8field-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

84 citing papers in PubMed, 1 synthesis or guideline pooled it, 256 citations in OpenAlex.

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  18. Assessing Tuning Parameter Selection Variability in Penalized Regression.Technometrics : a journal of statistics for the physical, chemical, and engineering sciences · 2019
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24 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

6 authors at 5 institutions in 2 countries.

Soo-Yon RheeDivision of Infectious Diseases, Department of Medicine, Stanford University, Stanford, CA 94305, USA.
Jonathan Taylor
Gauhar Wadhera
Asa Ben-Hur
Douglas L Brutlag
Robert W Shafer
Office of Infectious Diseases · USBradley University · USColorado State University · USStanford University · USStatistical Service · CY

Funding

Targeting ensembles of Drug Resistant HIV ProteasesP01GM066524 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI RANA, TARIQ M · 2002 to 2011
$16.3M
IDENTIFICATION OF MULTIDRUG RESISTANT HIV1 ISOLATESR01AI046148 · NIAID · STANFORD UNIVERSITY · PI SHAFER, ROBERT WILLIAM · 1999 to 2008
$2.4M
NIAID NIH HHS AI46148-01NIAID NIH HHS R01 AI046148NIGMS NIH HHS 5P01GM066524-03NIGMS NIH HHS P01 GM066524
6 · The paper itself

Abstract

Understanding the genetic basis of HIV-1 drug resistance is essential to developing new antiretroviral drugs and optimizing the use of existing drugs. This understanding, however, is hampered by the large numbers of mutation patterns associated with cross-resistance within each antiretroviral drug class. We used five statistical learning methods (decision trees, neural networks, support vector regression, least-squares regression, and least angle regression) to relate HIV-1 protease and reverse transcriptase mutations to in vitro susceptibility to 16 antiretroviral drugs. Learning methods were trained and tested on a public data set of genotype-phenotype correlations by 5-fold cross-validation. For each learning method, four mutation sets were used as input features: a complete set of all mutations in > or =2 sequences in the data set, the 30 most common data set mutations, an expert panel mutation set, and a set of nonpolymorphic treatment-selected mutations from a public database linking protease and reverse transcriptase sequences to antiretroviral drug exposure. The nonpolymorphic treatment-selected mutations led to the best predictions: 80.1% accuracy at classifying sequences as susceptible, low/intermediate resistant, or highly resistant. Least angle regression predicted susceptibility significantly better than other methods when using the complete set of mutations. The three regression methods provided consistent estimates of the quantitative effect of mutations on drug susceptibility, identifying nearly all previously reported genotype-phenotype associations and providing strong statistical support for many new associations. Mutation regression coefficients showed that, within a drug class, cross-resistance patterns differ for different mutation subsets and that cross-resistance has been underestimated.

Indexed as

Drug Resistance, ViralGenotypeHIV-1MutationPhenotypeReverse Transcriptase InhibitorsReverse Transcriptase Inhibitors

Identifiers

PMID17065321
PMCPMC1622926
OpenAlexW2128685318

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.