Evidence map›Paper›PMID 23143309›Full record

ArticleThe Journal of clinical investigation2012

HERV-K-specific T cells eliminate diverse HIV-1/2 and SIV primary isolates.

R Brad Jones, Keith E Garrison, Shariq Mujib, Vesna Mihajlovic, Nasra Aidarus, Diana V Hunter, Eric Martin, Vivek M John, Wei Zhan, Nabil F Faruk and 23 more

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing 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

66 citing papers in PubMed.

  1. Trial
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  11. Article
  12. Review
  13. Human endogenous retroviruses and exogenous viral infections.Frontiers in cellular and infection microbiology · 2024
    Review
  14. Article
  15. Article
  16. Deletion of Vβ3Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  17. Review
  18. Article
  19. Review
  20. Article

6 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

33 authors.

R Brad JonesDepartment of Immunology, University of Toronto, and Li Ka Shing Knowledge Institute, St. Michael’s Hospital, Toronto, Ontario, Canada. bjones.ut@gmail.com
Keith E Garrison
Shariq Mujib
Vesna Mihajlovic
Nasra Aidarus
Diana V Hunter
Eric Martin
Vivek M John
Wei Zhan
Nabil F Faruk
Gabor Gyenes
Neil C Sheppard
Ingrid M Priumboom-Brees
David A Goodwin
Lianchun Chen
Melanie Rieger
Sophie Muscat-King
Peter T Loudon
Cole Stanley
Sara J Holditch
Jessica C Wong
Kiera Clayton
Erick Duan
Haihan Song
Yang Xu
Devi SenGupta
Ravi Tandon
Jonah B Sacha
Mark A Brockman
Erika Benko
Colin Kovacs
Douglas F Nixon
Mario A Ostrowski

Funding

Virology CoreP30AI027763 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI STEVEN Grant DEEKS · 1988 to 2026
$93.6M
Human Endogenous Retroelements in HIV ImmunopathogenesisR01AI076059 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI NIXON, DOUGLAS F · 2009 to 2017
$3.9M
An endogenous retroelement vaccine against HIV-1R56AI084113 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NIXON, DOUGLAS F · 2009 to 2009
$425k
NIAID NIH HHS AI076059NIAID NIH HHS AI084113NIAID NIH HHS P30 AI027763NIAID NIH HHS R01 AI076059NIAID NIH HHS R56 AI084113
6 · The paper itself

Abstract

The genetic diversity of HIV-1 represents a major challenge in vaccine development. In this study, we establish a rationale for eliminating HIV-1-infected cells by targeting cellular immune responses against stable human endogenous retroviral (HERV) antigens. HERV DNA sequences in the human genome represent the remnants of ancient infectious retroviruses. We show that the infection of CD4+ T cells with HIV-1 resulted in transcription of the HML-2 lineage of HERV type K [HERV-K(HML-2)] and the expression of Gag and Env proteins. HERV-K(HML-2)-specific CD8+ T cells obtained from HIV-1-infected human subjects responded to HIV-1-infected cells in a Vif-dependent manner in vitro. Consistent with the proposed mode of action, a HERV-K(HML-2)-specific CD8+ T cell clone exhibited comprehensive elimination of cells infected with a panel of globally diverse HIV-1, HIV-2, and SIV isolates in vitro. We identified a second T cell response that exhibited cross-reactivity between homologous HIV-1-Pol and HERV-K(HML-2)-Pol determinants, raising the possibility that homology between HIV-1 and HERVs plays a role in shaping, and perhaps enhancing, the T cell response to HIV-1. This justifies the consideration of HERV-K(HML-2)-specific and cross-reactive T cell responses in the natural control of HIV-1 infection and for exploring HERV-K(HML-2)-targeted HIV-1 vaccines and immunotherapeutics.

Indexed as

Immunity, CellularAmino Acid SequenceAnimalsAntigens, ViralCD4-Positive T-LymphocytesCells, CulturedEndogenous RetrovirusesGene Expression Regulation, ViralGene Products, gagHIV-1HIV-2HIV InfectionsHost-Pathogen InteractionsHumansMolecular Sequence DataSimian Immunodeficiency VirusAntigens, ViralGene Products, gagvif Gene Products, Human Immunodeficiency Virusvif protein, Human immunodeficiency virus 1Viral Envelope Proteins

Identifiers

PMID23143309
PMCPMC3533554

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.