Evidence map›Paper›PMID 27494508›Full record

ArticlePLoS pathogens2016

Evaluating Clonal Expansion of HIV-Infected Cells: Optimization of PCR Strategies to Predict Clonality.

Sarah B Laskey, Christopher W Pohlmeyer, Katherine M Bruner, Robert F Siliciano

Abstract read
In one paragraph

Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
–field-weighted citation impact
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

44 citing papers in PubMed.

  1. Trial
  2. Article
  3. Proviruses in CD4Science translational medicine · 2025
    Article
  4. Article
  5. Article
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  7. Article
  8. Article
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  15. Article
  16. Article
  17. Article
  18. Autologous IgG antibodies block outgrowth of a substantial but variable fraction of viruses in the latent reservoir for HIV-1.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Observational
  19. Observational
  20. Article
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

4 authors.

Sarah B LaskeyDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Christopher W PohlmeyerDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Katherine M BrunerDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Robert F SilicianoDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.

Funding

Vaccine Response and Immunotherapeutics SWGP30AI094189 · NIAID · JOHNS HOPKINS UNIVERSITY · PI Bryan Lau · 2012 to 2026
$67.0M
Using NK Cells to eliminate the latent HIV reservoirU19AI096113 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SPINA, CELSA A · 2011 to 2015
$39.5M
Viral reservoirs and sanctuaries in HAART - treated patients: role and mechanismsU19AI096109 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PALMER, SARAH ELIZABETH · 2011 to 2015
$29.5M
BIOCHEMISTRY, CELLULAR AND MOLECULAR BIOLOGY PROGRAMT32GM007445 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI GREEN, RACHEL · 1985 to 2021
$24.1M
Howard Hughes Medical InstituteNIAID NIH HHS P30 AI094189NIAID NIH HHS U19 AI096109NIAID NIH HHS U19 AI096113NIGMS NIH HHS T32 GM007445
6 · The paper itself

Abstract

In HIV-infected individuals receiving suppressive antiretroviral therapy, the virus persists indefinitely in a reservoir of latently infected cells. The proliferation of these cells may contribute to the stability of the reservoir and thus to the lifelong persistence of HIV-1 in infected individuals. Because the HIV-1 replication process is highly error-prone, the detection of identical viral genomes in distinct host cells provides evidence for the clonal expansion of infected cells. We evaluated alignments of unique, near-full-length HIV-1 sequences to determine the relationship between clonality in a short region and clonality in the full genome. Although it is common to amplify and sequence short, subgenomic regions of the viral genome for phylogenetic analysis, we show that sequence identity of these amplicons does not guarantee clonality across the full viral genome. We show that although longer amplicons capture more diversity, no subgenomic region can recapitulate the diversity of full viral genomes. Consequently, some identical subgenomic amplicons should be expected even from the analysis of completely unique viral genomes, and the presence of identical amplicons alone is not proof of clonally expanded HIV-1. We present a method for evaluating evidence of clonal expansion in the context of these findings.

Indexed as

PhylogenyCell LineHIV-1HIV InfectionsHumansPolymerase Chain Reaction

Identifiers

PMID27494508
PMCPMC4975415

What OpenQuestion holds

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LicenceCC BY
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.