Evidence map›Paper›PMID 29618654›Full record

ArticleJCI insight2018

Exosomal Tat protein activates latent HIV-1 in primary, resting CD4+ T lymphocytes.

Xiaoli Tang, Huafei Lu, Mark Dooner, Stacey Chapman, Peter J Quesenberry, Bharat Ramratnam

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

40 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Searching for a HIV-1 Cure.Theranostics · 2026
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. The reservoir of latent HIV.Frontiers in cellular and infection microbiology · 2022
    Review
  19. Review
  20. Review
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

6 authors at 1 institution in 1 country.

Xiaoli TangDivision of Infectious Diseases and.
Huafei LuDivision of Infectious Diseases and.
Mark DoonerDivision of Hematology and Oncology, Department of Medicine, Rhode Island Hospital and Warren Alpert Medical School of Brown University, Providence, Rhode Island, USA.
Stacey ChapmanCenter for AIDS Research, The Miriam Hospital, Providence, Rhode Island, USA.
Peter J QuesenberryDivision of Hematology and Oncology, Department of Medicine, Rhode Island Hospital and Warren Alpert Medical School of Brown University, Providence, Rhode Island, USA.
Bharat RamratnamDivision of Infectious Diseases and.
Office of Infectious Diseases · US

Funding

Translational ScienceP30AI042853 · NIAID · MIRIAM HOSPITAL · PI CURT G BECKWITH · 1998 to 2026
$51.7M
Tracking and Evaluation CoreU54GM115677 · NIGMS · BROWN UNIVERSITY · PI ROUNDS, SHARON IRENE SMITH · 2016 to 2025
$45.0M
Virology CoreP01AA019072 · NIAAA · BROWN UNIVERSITY · PI WRAY, TYLER BLAKE · 2010 to 2024
$19.7M
Stem Cells and AgingP20GM119943 · NIGMS · RHODE ISLAND HOSPITAL · PI QUESENBERRY, PETER J. · 2017 to 2021
$10.6M
TYORISINE PHOSPHATASE SHP2 IN HEMATOPOIETIC STEM CELL PROPERTY MAINTENANCEP20RR025179 · NCRR · RHODE ISLAND HOSPITAL · PI YANG, WENTIAN · 2009 to 2011
$6.4M
COBRE Center for Cancer Research DevelopmentP30GM110759 · NIGMS · RHODE ISLAND HOSPITAL · PI RAMRATNAM, BHARAT · 2015 to 2019
$6.3M
Reproductive Hormones and their impact on HIV-1 acquisitionR01HD072693 · NICHD · RHODE ISLAND HOSPITAL · PI CU-UVIN, SUSAN, GUPTA, PHALGUNI · 2012 to 2016
$2.3M
Studies in HIV-1 Pathogenesis and TransmissionK24HD080539 · NICHD · RHODE ISLAND HOSPITAL · PI RAMRATNAM, BHARAT · 2014 to 2018
$807k
NCRR NIH HHS P20 RR025179NIAAA NIH HHS P01 AA019072NIAID NIH HHS P30 AI042853NICHD NIH HHS K24 HD080539NICHD NIH HHS R01 HD072693NIGMS NIH HHS P20 GM119943NIGMS NIH HHS P30 GM110759NIGMS NIH HHS U54 GM115677
6 · The paper itself

Abstract

Replication competent HIV-1 persists in a subpopulation of CD4+ T lymphocytes despite prolonged antiretroviral treatment. This residual reservoir of infected cells harbors transcriptionally silent provirus capable of reigniting productive infection upon discontinuation of antiretroviral therapy. Certain classes of drugs can activate latent virus but not at levels that lead to reductions in HIV-1 reservoir size in vivo. Here, we show the utility of CD4+ receptor targeting exosomes as an HIV-1 latency reversal agent (LRA). We engineered human cellular exosomes to express HIV-1 Tat, a protein that is a potent transactivator of viral transcription. Preparations of exosomal Tat-activated HIV-1 in primary, resting CD4+ T lymphocytes isolated from antiretroviral-treated individuals with prolonged periods of viral suppression and led to the production of replication competent HIV-1. Furthermore, exosomal Tat increased the potency of selected LRA by over 30-fold in terms of HIV-1 mRNA expression, thereby establishing it as a potentially new class of biologic product with possible combinatorial utility in targeting latent HIV-1.

Indexed as

Drug CarriersAdultAgedAnti-HIV AgentsAntiretroviral Therapy, Highly ActiveCD4-Positive T-LymphocytesCell EngineeringCloning, MolecularExosomesFemaleHEK293 CellsHIV-1HIV InfectionsHumansMaleMiddle AgedAnti-HIV AgentsDrug CarriersMYC protein, humanProto-Oncogene Proteins c-mycRecombinant Fusion Proteinstat Gene Products, Human Immunodeficiency VirusAIDS/HIVDrug therapyInfectious diseaseMolecular biologyT cells

Identifiers

PMID29618654
PMCPMC5928859
OpenAlexW2796080021

What OpenQuestion holds

Textmetadata
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.