Evidence map›Paper›PMID 20644481›Full record

ReviewCurrent opinion in rheumatology2010

Endogenous retroviral pathogenesis in lupus.

Andras Perl, David Fernandez, Tiffany Telarico, Paul E Phillips

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in rheumatology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.3field-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

34 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Overview of Oxidative Stress in Systemic Lupus Erythematosus.Antioxidants (Basel, Switzerland) · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Posttranscriptional regulation of human endogenous retroviruses by RNA-binding motif protein 4, RBM4.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article
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

4 authors at 1 institution in 1 country.

Andras PerlDivision of Rheumatology, Department of Medicine and Microbiology and Immunology, State University of New York Upstate Medical University, Syracuse, New York, USA. perla@upstate.edu
David Fernandez
Tiffany Telarico
Paul E Phillips
SUNY Upstate Medical University · US

Funding

Metabolic Control of T-cell Lineage Specification in SLER01AI072648 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 2008 to 2024
$6.1M
IMPACT OF HRES-1 ENDOGENOUS RETROVIRUS IN SLER01AI048079 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 2000 to 2013
$2.7M
Endocytic Control of Autophagosome Formation in Lupus T cellsR01AI122176 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 2016 to 2020
$2.0M
NIAID NIH HHS R01 AI048079NIAID NIH HHS R01 AI072648NIAID NIH HHS R01 AI122176NIAID NIH HHS R01 AI 48079
6 · The paper itself

Abstract

purpose of reviewGenetic and environmental factors influence the development of systemic lupus erythematosus (SLE). Endogenous retroviruses (ERVs) are proposed as a molecular link between the human genome and environmental factors, such as viruses, in lupus pathogenesis. RECENT

findingsThe HRES-1 human ERV encodes a 28-kD nuclear autoantigen and a 24-kD small GTP-ase, termed HRES-1/Rab4. HRES-1/p28 is a target of cross-reactive antiviral antibodies, whereas HRES-1/Rab4 regulates the surface expression of CD4 via endosome recycling. The tat gene of HIV-1 induces the expression of HRES-1/Rab4, which in turn downregulates expression of CD4 and susceptibility to reinfection by HIV-1. HRES-1/Rab4 is overexpressed in lupus T cells where it correlates with increased recycling of CD4 and CD3 and contributes to downregulation of CD3/TCRzeta via lysosomal degradation. Chilblain lupus has been linked to the deficiency of 3'-5' repair exonuclease Trex1 that metabolizes DNA reverse-transcribed from ERV. Trex1 deficiency or blocked integration of ERV-encoded DNA also promotes lupus in murine models. SUMMARY: ERV proteins may trigger lupus through structural and functional molecular mimicry, whereas the accumulation of ERV-derived nucleic acids stimulates interferon and anti-DNA antibody production in SLE.

Indexed as

AutoimmunityEndogenous RetrovirusesHumansLupus Erythematosus, SystemicMolecular Mimicry

Identifiers

PMID20644481
PMCPMC5314925
OpenAlexW2078912949

What OpenQuestion holds

Textmetadata
LicenceTDM
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.