Evidence map›Paper›PMID 21628544›Full record

ArticleAntimicrobial agents and chemotherapy2011

Novel method for simultaneous quantification of phenotypic resistance to maturation, protease, reverse transcriptase, and integrase HIV inhibitors based on 3'Gag(p2/p7/p1/p6)/PR/RT/INT-recombinant viruses: a useful tool in the multitarget era of antiretroviral therapy.

Jan Weber, Ana C Vazquez, Dane Winner, Justine D Rose, Doug Wylie, Ariel M Rhea, Kenneth Henry, Jennifer Pappas, Alison Wright, Nizar Mohamed and 7 more

Open access · greenAbstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

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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

17 authors at 1 institution in 1 country.

Jan WeberDiagnostic Hybrids, Inc., Cleveland, Ohio, USA.
Ana C Vazquez
Dane Winner
Justine D Rose
Doug Wylie
Ariel M Rhea
Kenneth Henry
Jennifer Pappas
Alison Wright
Nizar Mohamed
Richard Gibson
Benigno Rodriguez
Vicente Soriano
Kevin King
Eric J Arts
Paul D Olivo
Miguel E Quiñones-Mateu
Case Western Reserve University · US

Funding

Impact of HIV-1 Fitness on Disease ProgressionR01AI049170 · NIAID · UNIVERSITY OF WESTERN ONTARIO · PI ARTS, ERIC J · 2002 to 2024
$6.8M
NIAID NIH HHS R01 AI049170
6 · The paper itself

Abstract

Twenty-six antiretroviral drugs (ARVs), targeting five different steps in the life cycle of the human immunodeficiency virus type 1 (HIV-1), have been approved for the treatment of HIV-1 infection. Accordingly, HIV-1 phenotypic assays based on common cloning technology currently employ three, or possibly four, different recombinant viruses. Here, we describe a system to assess HIV-1 resistance to all drugs targeting the three viral enzymes as well as viral assembly using a single patient-derived, chimeric virus. Patient-derived p2-INT (gag-p2/NCp7/p1/p6/pol-PR/RT/IN) products were PCR amplified as a single fragment (3,428 bp) or two overlapping fragments (1,657 bp and 2,002 bp) and then recombined into a vector containing a near-full-length HIV-1 genome with the Saccharomyces cerevisiae uracil biosynthesis gene (URA3) replacing the 3,428 bp p2-INT segment (Dudley et al., Biotechniques 46:458-467, 2009). P2-INT-recombinant viruses were employed in drug susceptibility assays to test the activity of protease (PI), nucleoside/nucleotide reverse transcriptase (NRTI), nonnucleoside reverse transcriptase (NNRTI), and integrase strand-transfer (INSTI) inhibitors. Using a single standardized test (ViralARTS HIV), this new technology permits the rapid and automated quantification of phenotypic resistance for all known and candidate antiretroviral drugs targeting all viral enzymes (PR, RT, including polymerase and RNase H activities, and IN), some of the current and potential assembly inhibitors, and any drug targeting Pol or Gag precursor cleavage sites (relevant for PI and maturation inhibitors) This novel assay may be instrumental (i) in the development and clinical assessment of novel ARV drugs and (ii) to monitor patients failing prior complex treatment regimens.

Indexed as

Drug Resistance, Multiple, ViralGenes, polAnti-HIV AgentsBase SequenceHEK293 CellsHIV-1HIV InfectionsHIV Integrase InhibitorsHIV Protease InhibitorsHIV Reverse TranscriptaseHumansPhenotypeReverse Transcriptase InhibitorsReverse Transcriptase Polymerase Chain ReactionRibonuclease HSequence Analysis, RNAAnti-HIV AgentsHIV Integrase InhibitorsHIV Protease InhibitorsHIV Reverse TranscriptaseReverse Transcriptase InhibitorsRibonuclease H

Identifiers

PMID21628544
PMCPMC3147656
OpenAlexW2122400805

What OpenQuestion holds

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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.