Evidence map›Paper›PMID 24339779›Full record

ArticlePLoS pathogens2013

Myeloid dendritic cells induce HIV-1 latency in non-proliferating CD4+ T cells.

Vanessa A Evans, Nitasha Kumar, Ali Filali, Francesco A Procopio, Oleg Yegorov, Jean-Philippe Goulet, Suha Saleh, Elias K Haddad, Candida da Fonseca Pereira, Paula C Ellenberg and 3 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

53 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
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  15. The multifaceted nature of HIV latency.The Journal of clinical investigation · 2020
    Review
  16. Review
  17. Combination Immune Checkpoint Blockade to Reverse HIV Latency.Journal of immunology (Baltimore, Md. : 1950) · 2020
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

13 authors at 5 institutions in 3 countries.

Vanessa A EvansDepartment of Infectious Diseases, Monash University, Melbourne, Victoria, Australia ; Centre for Biomedical Research, Burnet Institute, Melbourne, Victoria, Australia.
Nitasha Kumar
Ali Filali
Francesco A Procopio
Oleg Yegorov
Jean-Philippe Goulet
Suha Saleh
Elias K Haddad
Candida da Fonseca Pereira
Paula C Ellenberg
Rafick-Pierre Sekaly
Paul U Cameron
Sharon R Lewin
Vaccine & Gene Therapy Institute of Florida · USBurnet Institute · AUMonash University · AUCentre Hospitalier de l’Université de Montréal · CAThe Alfred Hospital · AU

Funding

Viral reservoirs and sanctuaries in HAART - treated patients: role and mechanismsU19AI096109 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SCHACKER, TIMOTHY W · 2011 to 2015
$29.5M
Delaney AIDS Research Enterprise to Cure HIVUM1AI126611 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DEEKS, STEVEN GRANT, PICKER, LOUIS J. · 2016 to 2020
$27.9M
The role of chemokines in the establishment of HIV latencyR56AI095073 · NIAID · MONASH UNIVERSITY · PI LEWIN, SHARON RUTH · 2012 to 2012
$271k
NIAID NIH HHS R56 AI095073NIAID NIH HHS U19 AI096109
6 · The paper itself

Abstract

Latently infected resting CD4(+) T cells are a major barrier to HIV cure. Understanding how latency is established, maintained and reversed is critical to identifying novel strategies to eliminate latently infected cells. We demonstrate here that co-culture of resting CD4(+) T cells and syngeneic myeloid dendritic cells (mDC) can dramatically increase the frequency of HIV DNA integration and latent HIV infection in non-proliferating memory, but not naïve, CD4(+) T cells. Latency was eliminated when cell-to-cell contact was prevented in the mDC-T cell co-cultures and reduced when clustering was minimised in the mDC-T cell co-cultures. Supernatants from infected mDC-T cell co-cultures did not facilitate the establishment of latency, consistent with cell-cell contact and not a soluble factor being critical for mediating latent infection of resting CD4(+) T cells. Gene expression in non-proliferating CD4(+) T cells, enriched for latent infection, showed significant changes in the expression of genes involved in cellular activation and interferon regulated pathways, including the down-regulation of genes controlling both NF-κB and cell cycle. We conclude that mDC play a key role in the establishment of HIV latency in resting memory CD4(+) T cells, which is predominantly mediated through signalling during DC-T cell contact.

Indexed as

Virus LatencyCD4-Positive T-LymphocytesCell Cycle CheckpointsCell ProliferationCells, CulturedDendritic CellsGene Regulatory NetworksHEK293 CellsHIV-1HumansMicroarray AnalysisMyeloid CellsTranscriptome

Identifiers

PMID24339779
PMCPMC3855553
OpenAlexW2075311313

What OpenQuestion holds

Textmetadata
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.