Evidence map›Paper›PMID 23375003›Full record

ReviewRetrovirology2013

Cellular and molecular mechanisms involved in the establishment of HIV-1 latency.

Daniel A Donahue, Mark A Wainberg

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Retrovirology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03980665 (The Effect of Arsenic Trioxide on Eliminating HIV-1 Reservoir Combined With cART), which is not on this map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
7.0field-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.

NCT03980665 phase1unknown statusnot on this mapstarted 2019, after this paper: background citation

The Effect of Arsenic Trioxide on Eliminating HIV-1 Reservoir Combined With cART

TypeinterventionalSponsorGuangzhou 8th People's HospitalRan2019 to 2025Enrolled20ConditionsHIV/AIDSArmsArsenic Trioxide
3 · Its place in the literature

Who cites it

61 citing papers in PubMed, 108 citations in OpenAlex.

  1. HIV-1 DNA decay dynamics in blood during more than a decade of suppressive antiretroviral therapy.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2014
    Trial
  2. Review
  3. Article
  4. CD8Immunity · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Toward Personalized Medicine for HIV/AIDS.Journal of AIDS and HIV treatment · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

1 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

2 authors at 2 institutions in 1 country.

Daniel A DonahueMcGill University AIDS Centre, Lady Davis Institute, Jewish General Hospital, Montreal, Québec, Canada. mark.wainberg@mail.mcgill.ca.
Mark A Wainberg
Jewish General Hospital · CAMcGill University · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Latently infected cells represent the major barrier to either a sterilizing or a functional HIV-1 cure. Multiple approaches to reactivation and depletion of the latent reservoir have been attempted clinically, but full depletion of this compartment remains a long-term goal. Compared to the mechanisms involved in the maintenance of HIV-1 latency and the pathways leading to viral reactivation, less is known about the establishment of latent infection. This review focuses on how HIV-1 latency is established at the cellular and molecular levels. We first discuss how latent infection can be established following infection of an activated CD4 T-cell that undergoes a transition to a resting memory state and also how direct infection of a resting CD4 T-cell can lead to latency. Various animal, primary cell, and cell line models also provide insights into this process and are discussed with respect to the routes of infection that result in latency. A number of molecular mechanisms that are active at both transcriptional and post-transcriptional levels have been associated with HIV-1 latency. Many, but not all of these, help to drive the establishment of latent infection, and we review the evidence in favor of or against each mechanism specifically with regard to the establishment of latency. We also discuss the role of immediate silent integration of viral DNA versus silencing of initially active infections. Finally, we discuss potential approaches aimed at limiting the establishment of latent infection.

Indexed as

Host-Pathogen InteractionsVirus LatencyCD4-Positive T-LymphocytesEpigenesis, GeneticHIV-1HumansModels, BiologicalTranscription, Genetic

Identifiers

PMID23375003
PMCPMC3571915
OpenAlexW2152129968

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.