Evidence map›Paper›PMID 26067822›Full record

ArticlePLoS pathogens2015

HIV Latency Is Established Directly and Early in Both Resting and Activated Primary CD4 T Cells.

Leonard Chavez, Vincenzo Calvanese, Eric Verdin

Abstract read
In one paragraph

Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers.

0numbers the graph read from it
0cells of the map it votes in
147citing 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

147 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. HIV reservoirs in lymphomagenesis: hidden driver in the era of viral suppression?Microbiology and molecular biology reviews : MMBR · 2025
    Review
  9. Article
  10. HIV Virion Capturing Liposomes for Therapeutic Vaccination.bioRxiv : the preprint server for biology · 2025
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

87 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

3 authors.

Leonard ChavezGladstone Institute of Virology and Immunology, San Francisco, California, United States of America; Biomedical Sciences Program, University of California, San Francisco, San Francisco, California, United States of America.
Vincenzo CalvaneseGladstone Institute of Virology and Immunology, San Francisco, California, United States of America.
Eric VerdinGladstone Institute of Virology and Immunology, San Francisco, California, United States of America; Department of Medicine, University of California, San Francisco, San Francisco, California, United States of America.

Funding

Virology CoreP30AI027763 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI STEVEN Grant DEEKS · 1988 to 2026
$93.6M
Using NK Cells to eliminate the latent HIV reservoirU19AI096113 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KARN, JONATHAN · 2011 to 2015
$39.5M
Novel Model for HIV Latency in Primary Memory T CellsDP1DA031126 · NIDA · J. DAVID GLADSTONE INSTITUTES · PI VERDIN, ERIC M. · 2010 to 2014
$4.7M
Epigenetic regulation of HIV latencyR01DA030216 · NIDA · J. DAVID GLADSTONE INSTITUTES · PI VERDIN, ERIC M. · 2010 to 2014
$2.6M
NIAID NIH HHS P30 AI027763NIAID NIH HHS U19 AI096113NIDA NIH HHS 1DP1 DA031126NIDA NIH HHS 1R01 DA030216NIDA NIH HHS DP1 DA031126NIDA NIH HHS R01 DA030216
6 · The paper itself

Abstract

Highly active antiretroviral therapy (HAART) suppresses human immunodeficiency virus (HIV) replication to undetectable levels but cannot fully eradicate the virus because a small reservoir of CD4+ T cells remains latently infected. Since HIV efficiently infects only activated CD4+ T cells and since latent HIV primarily resides in resting CD4+ T cells, it is generally assumed that latency is established when a productively infected cell recycles to a resting state, trapping the virus in a latent state. In this study, we use a dual reporter virus--HIV Duo-Fluo I, which identifies latently infected cells immediately after infection--to investigate how T cell activation affects the establishment of HIV latency. We show that HIV latency can arise from the direct infection of both resting and activated CD4+ T cells. Importantly, returning productively infected cells to a resting state is not associated with a significant silencing of the integrated HIV. We further show that resting CD4+ T cells from human lymphoid tissue (tonsil, spleen) show increased latency after infection when compared to peripheral blood. Our findings raise significant questions regarding the most commonly accepted model for the establishment of latent HIV and suggest that infection of both resting and activated primary CD4+ T cells produce latency.

Indexed as

CD4-Positive T-LymphocytesCells, CulturedCell SeparationFlow CytometryHIV-1HIV InfectionsHumansLymphocyte ActivationVirus LatencyVirus Replication

Identifiers

PMID26067822
PMCPMC4466167

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.