Evidence map›Paper›PMID 22593154›Full record

ArticleJournal of virology2012

Expression of human endogenous retrovirus type K (HML-2) is activated by the Tat protein of HIV-1.

Marta J Gonzalez-Hernandez, Michael D Swanson, Rafael Contreras-Galindo, Sarah Cookinham, Steven R King, Richard J Noel, Mark H Kaplan, David M Markovitz

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
11.3field-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.

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

87 citing papers in PubMed, 121 citations in OpenAlex.

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  18. The Role of Human Endogenous Retrovirus (HERV)-K119International journal of molecular sciences · 2023
    Article
  19. Review
  20. TDP-43 Epigenetic Facets and Their Neurodegenerative Implications.International journal of molecular sciences · 2023
    Review

27 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

8 authors at 2 institutions in 2 countries.

Marta J Gonzalez-HernandezDepartment of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Michael D Swanson
Rafael Contreras-Galindo
Sarah Cookinham
Steven R King
Richard J Noel
Mark H Kaplan
David M Markovitz
University of Michigan–Ann Arbor · USPonce Health Sciences University · PR

Funding

VIRAL SEQUENCES IN PEDIATRIC HIV INFECTION IN PRG12RR003050 · NCRR · PONCE SCHOOL OF MEDICINE · PI ARMSTRONG, RAUL A · 1985 to 2011
$28.1M
VIRAL SEQUENCES IN PEDIATRIC HIV INFECTION IN PRG12MD007579 · NIMHD · PONCE SCHOOL OF MEDICINE · PI PORTER, JAMES T. · 2012 to 2018
$15.9M
Replication of Human Endogenous Retroviruses in Modern HumansR01CA144043 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MARKOVITZ, DAVID MICHAEL · 2009 to 2013
$6.4M
CXC Chemokines and HIV PathogenesisR01AI062248 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MARKOVITZ, DAVID MICHAEL · 2005 to 2009
$1.6M
Role of HIV-1 Tat in the activation of HERV-K and development of HIV-1-lymphomaF31CA150523 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GONZALEZ-HERNANDEZ, MARTA JEANNETTE · 2010 to 2011
$65k
NCI NIH HHS 1F31CA150523-01NCI NIH HHS F31 CA150523NCI NIH HHS R01 CA144043NCI NIH HHS R01CA144043NCRR NIH HHS G12 RR003050NIAID NIH HHS R01 AI062248NIAID NIH HHS R01AI062248NIMHD NIH HHS G12 MD007579
6 · The paper itself

Abstract

Human endogenous retroviruses (HERVs) make up 8% of the human genome. The expression of HERV-K (HML-2), the family of HERVs that most recently entered the genome, is tightly regulated but becomes markedly increased after infection with HIV-1. To better understand the mechanisms involved in this activation, we explored the role of the HIV-1 Tat protein in inducing the expression of these endogenous retroviral genes. Administration of recombinant HIV-1 Tat protein caused a 13-fold increase in HERV-K (HML-2) gag RNA transcripts in Jurkat T cells and a 10-fold increase in primary lymphocytes, and the expression of the HERV-K (HML-2) rec and np9 oncogenes was also markedly increased. This activation was seen especially in lymphocytes and monocytic cells, the natural hosts for HIV-1 infection. Luciferase reporter gene assays demonstrated that the effect of Tat on HERV-K (HML-2) expression occurred at the level of the transcriptional promoter. The transcription factors NF-κB and NF-AT contribute to the Tat-induced activation of the promoter, as shown by chromatin immunoprecipitation assays, mutational analysis of the HERV-K (HML-2) long terminal repeat, and treatments with agents that inhibit NF-κB or NF-AT activation. These studies demonstrate that HIV-1 Tat plays an important role in activating expression of HERV-K (HML-2) in the setting of HIV-1 infection.

Indexed as

Gene Expression Regulation, ViralVirus ActivationEndogenous RetrovirusesGene Products, envHIV-1HIV InfectionsHumansJurkat CellsRecombinant Proteinstat Gene Products, Human Immunodeficiency VirusViral Envelope ProteinsERVK-6 protein, human endogenous retrovirusGene Products, envNp9 protein, HERV-K, humanRecombinant Proteinstat Gene Products, Human Immunodeficiency VirusViral Envelope Proteins

Identifiers

PMID22593154
PMCPMC3421662
OpenAlexW2037629038

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.