Evidence map›Paper›PMID 33281822›Full record

ReviewFrontiers in immunology2020

How Retroviruses and Retrotransposons in Our Genome May Contribute to Autoimmunity in Rheumatological Conditions.

Tomas Mustelin, Kennedy C Ukadike

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Viruses: Friends or foes.Microbial biotechnology · 2022
    Article
  17. Review
  18. Article
  19. Human endogenous retroviruses and ageing.Immunity & ageing : I & A · 2021
    Article
  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

2 authors at 1 institution in 1 country.

Tomas MustelinDivision of Rheumatology, Department of Medicine, University of Washington, Seattle, WA, United States.
Kennedy C UkadikeDivision of Rheumatology, Department of Medicine, University of Washington, Seattle, WA, United States.
University of Washington · US

Funding

RESEARCH TRAINING IN RHEUMATOLOGYT32AR007108 · NIAMS · UNIVERSITY OF WASHINGTON · PI Shaun Jackson, Tomas M Mustelin · 1986 to 2026
$6.6M
Role of protein citrullination in rheumatoid arthritisR01AR074939 · NIAMS · UNIVERSITY OF WASHINGTON · PI MUSTELIN, TOMAS M · 2020 to 2024
$1.9M
The roots of SLE: Can we cure it with a reverse transcriptase inhibitor?R21AR075134 · NIAMS · UNIVERSITY OF WASHINGTON · PI MUSTELIN, TOMAS M · 2019 to 2020
$427k
HERV-K immunity, a trigger of citrullination in rheumatoid arthritis?R21AR077266 · NIAMS · UNIVERSITY OF WASHINGTON · PI MUSTELIN, TOMAS M · 2021 to 2022
$425k
Stem cell therapy for fracture nonunion under inflammatory diseasesR21AR077226 · NIAMS · WASHINGTON UNIVERSITY · PI GUILAK, FARSHID, SHEN, JIE · 2020 to 2021
$376k
NIAMS NIH HHS R01 AR074939NIAMS NIH HHS R21 AR075134NIAMS NIH HHS R21 AR077226NIAMS NIH HHS R21 AR077266NIAMS NIH HHS T32 AR007108
6 · The paper itself

Abstract

More than 200 human disorders include various manifestations of autoimmunity. The molecular events that lead to these diseases are still incompletely understood and their causes remain largely unknown. Numerous potential triggers of autoimmunity have been proposed over the years, but very few of them have been conclusively confirmed or firmly refuted. Viruses have topped the lists of suspects for decades, and it seems that many viruses, including those of the Herpesviridae family, indeed can influence disease initiation and/or promote exacerbations by a number of mechanisms that include prolonged anti-viral immunity, immune subverting factors, and mechanisms, and perhaps "molecular mimicry". However, no specific virus has yet been established as being truly causative. Here, we discuss a different, but perhaps mechanistically related possibility, namely that retrotransposons or retroviruses that infected us in the past and left a lasting copy of themselves in our genome still can provoke an escalating immune response that leads to autoimmune disease. Many of these loci still encode for retroviral proteins that have retained some, or all, of their original functions. Importantly, these endogenous proviruses cannot be eliminated by the immune system the way it can eliminate exogenous viruses. Hence, if not properly controlled, they may drive a frustrated and escalating chronic, or episodic, immune response to the point of a frank autoimmune disorder. Here, we discuss the evidence and the proposed mechanisms, and assess the therapeutic options that emerge from the current understanding of this field.

Indexed as

Disease SusceptibilityEndogenous RetrovirusesRetroelementsAlu ElementsAnimalsAutoimmune DiseasesAutoimmunityGenome, HumanHumansImmunityLong Interspersed Nucleotide ElementsProvirusesRheumatic DiseasesRetroelementsautoimmunityendogenous retrovirusesnucleic acid sensorsretroelementsretrotransposonsreverse transcriptasetype I interferon

Identifiers

PMID33281822
PMCPMC7691656
OpenAlexW3100454418

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.