Evidence map›Paper›PMID 32654992›Full record

ArticleEBioMedicine2020

A targeted reactivation of latent HIV-1 using an activator vector in patient samples from acute infection.

Jamie F S Mann, Joshua Pankrac, Katja Klein, Paul F McKay, Deborah F L King, Richard Gibson, Chanuka N Wijewardhana, Rahul Pawa, Jodi Meyerowitz, Yong Gao and 7 more

Abstract read
In one paragraph

Article in EBioMedicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Proviruses in CD4Science translational medicine · 2025
    Article
  2. Effective and targeted latency reversal in CD4Emerging microbes & infections · 2024
    Article
  3. Article
  4. Review
  5. Article
  6. Addressing an HIV cure in LMIC.Retrovirology · 2021
    Review
  7. Review
  8. Article
  9. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors.

Jamie F S MannDepartment of Microbiology and Immunology, University of Western Ontario, London, Ontario N6A 5C1, Canada; Division of Infectious Diseases, Department of Medicine, Case Western Reserve University, Cleveland, OH 44106, United States.
Joshua PankracDepartment of Microbiology and Immunology, University of Western Ontario, London, Ontario N6A 5C1, Canada.
Katja KleinDepartment of Microbiology and Immunology, University of Western Ontario, London, Ontario N6A 5C1, Canada; Division of Infectious Diseases, Department of Medicine, Case Western Reserve University, Cleveland, OH 44106, United States.
Paul F McKayImperial College London, Department of Infectious Diseases, Division of Medicine, Norfolk Place, London W2 1PG, UK.
Deborah F L KingImperial College London, Department of Infectious Diseases, Division of Medicine, Norfolk Place, London W2 1PG, UK.
Richard GibsonDepartment of Microbiology and Immunology, University of Western Ontario, London, Ontario N6A 5C1, Canada.
Chanuka N WijewardhanaDepartment of Microbiology and Immunology, University of Western Ontario, London, Ontario N6A 5C1, Canada.
Rahul PawaDepartment of Microbiology and Immunology, University of Western Ontario, London, Ontario N6A 5C1, Canada.
Jodi MeyerowitzNuffield Department of Clinical Medicine, Peter Medawar Building for Pathogen Research, John Radcliffe Hospital, Oxford OX1 3SY, UK.
Yong GaoDepartment of Microbiology and Immunology, University of Western Ontario, London, Ontario N6A 5C1, Canada; Division of Infectious Diseases, Department of Medicine, Case Western Reserve University, Cleveland, OH 44106, United States.
David H CanadayDivision of Infectious Diseases, Department of Medicine, Case Western Reserve University, Cleveland, OH 44106, United States.
Mariano AvinoDepartment of Pathology and Laboratory Medicine, University of Western Ontario, London, Ontario N6A 5C1, Canada.
Art F Y PoonDepartment of Pathology and Laboratory Medicine, University of Western Ontario, London, Ontario N6A 5C1, Canada.
Caroline FosterThe 900 Clinic, Jefferies Wing, Imperial College Healthcare NHS Trust, London W2 1NY, UK.
Sarah FidlerDepartment of Medicine, Imperial College London, London, UK.
Robin J ShattockImperial College London, Department of Infectious Diseases, Division of Medicine, Norfolk Place, London W2 1PG, UK.
Eric J ArtsDepartment of Microbiology and Immunology, University of Western Ontario, London, Ontario N6A 5C1, Canada; Division of Infectious Diseases, Department of Medicine, Case Western Reserve University, Cleveland, OH 44106, United States. Electronic address: earts@uwo.ca.

Funding

Impact of HIV-1 Fitness on Disease ProgressionR01AI049170 · NIAID · UNIVERSITY OF WESTERN ONTARIO · PI ARTS, ERIC J · 2002 to 2024
$6.8M
HIV-1 Fitness and RecombinationR56AI049170 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI ARTS, ERIC J · 2012 to 2012
$400k
Impact of HIV-1 Fitness on Disease ProgressionR21AI049170 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI ARTS, ERIC J · 2001 to 2001
$265k
Medical Research Council MR/L00528X/1NIAID NIH HHS R01 AI049170NIAID NIH HHS R21 AI049170NIAID NIH HHS R56 AI049170
6 · The paper itself

Abstract

backgroundDuring combined anti-retroviral treatment, a latent HIV reservoir persists within resting memory CD4 T cells that initiates viral recrudescence upon treatment interruption. Strategies for HIV-1 cure have largely focused on latency reversing agents (LRAs) capable of reactivating and eliminating this viral reservoir. Previously investigated LRAs have largely failed to achieve a robust latency reversal sufficient for reduction of latent HIV pool or the potential of virus-free remission in the absence of treatment.

methodsWe utilize a polyvalent virus-like particle (VLP) formulation called Activator Vector (ACT-VEC) to 'shock' provirus into transcriptional activity. Ex vivo co-culture experiments were used to evaluate the efficacy of ACT-VEC in relation to other LRAs in individuals diagnosed and treated during the acute stage of infection. IFN-γ ELISpot, qRT-PCR and Illumina MiSeq were used to evaluate antigenicity, latency reversal, and diversity of induced virus respectively.

findingsUsing samples from HIV

interpretationTaken together, these results show that ACT-VEC can induce HIV reactivation from latently infected CD4 T cells collected from participants on first line combined antiretroviral therapy for at least two years after being diagnosed and treated at acute/early stage of infection. These findings could provide guidance to possible targeted cure strategies and treatments.

fundingNIH and CIHR.

Indexed as

Genetic VectorsVirus ActivationVirus LatencyAdultAntiretroviral Therapy, Highly ActiveBiomarkersCD4 Lymphocyte CountCD4-Positive T-LymphocytesFemaleGene Expression Regulation, ViralGene OrderHigh-Throughput Nucleotide SequencingHIV-1HIV InfectionsHumansImmunophenotypingBiomarkersRNA, ViralActivator vector (ACT-VEC)HIV-1 CureHIV-1 LatencyImmunotherapyTranscriptional reactivationVirus-Like Particles

Identifiers

PMID32654992
PMCPMC7502668

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.