Evidence map›Paper›PMID 33610751›Full record

ReviewAutoimmunity reviews2021

The SARS-CoV-2 as an instrumental trigger of autoimmunity.

Arad Dotan, Sylviane Muller, Darja Kanduc, Paula David, Gilad Halpert, Yehuda Shoenfeld

Open access · greenAbstract readReview
In one paragraph

Review in Autoimmunity reviews, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 275 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
275citing papers in PubMed, 9 pooled it
47.8field-weighted citation impact, top 1% 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

275 citing papers in PubMed, 9 syntheses or guidelines pooled it, 495 citations in OpenAlex.

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215 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

6 authors at 4 institutions in 4 countries.

Arad DotanZabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Ramat-Gan 52621, Israel. Affiliated to Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Sylviane MullerCNRS-Strasbourg University Unit Biotechnology and cell signaling/Strasbourg Drug Discovery and Development Institute (IMS), Strasbourg, France; Federation Hospital-University (FHU) OMICARE, Federation of Translational Medicine of Strasbourg (FMTS), Strasbourg University, Strasbourg, France; University of Strasbourg Institute for Advanced Study, Strasbourg, France.
Darja KanducDepartment of Biosciences, Biotechnologies, and Biopharmaceutics, University of Bari, Italy.
Paula DavidZabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Ramat-Gan 52621, Israel. Affiliated to Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Gilad HalpertZabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Ramat-Gan 52621, Israel. Affiliated to Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel; Laboratory of the Mosaic of Autoimmunity, Saint Petersburg State University, Saint-Petersburg 199034, Russian Federation.
Yehuda ShoenfeldZabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Ramat-Gan 52621, Israel. Affiliated to Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel; Laboratory of the Mosaic of Autoimmunity, Saint Petersburg State University, Saint-Petersburg 199034, Russian Federation. Electronic address: Yehuda.Shoenfeld@sheba.health.gov.il.
Tel Aviv University · ILInternational Drug Development · FRSt Petersburg University · RUUniversity of Bari Aldo Moro · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmunity may be generated by a variety of factors by creating a hyper-stimulated state of the immune system. It had been established long ago that viruses are a substantial component of environmental factors that contribute to the production of autoimmune antibodies, as well as autoimmune diseases. Epstein-Barr virus (EBV), cytomegalovirus (CMV) and human immunodeficiency virus (HIV) are viruses that withhold these autoimmune abilities. In a similar manner, SARS-CoV-2 may be counted to similar manifestations, as numerous records demonstrating the likelihood of COVID-19 patients to develop multiple types of autoantibodies and autoimmune diseases. In this review, we focused on the association between COVID-19 and the immune system concerning the tendency of patients to develop over 15 separate types of autoantibodies and above 10 distinct autoimmune diseases. An additional autoimmunity manifestation may be one of the common initial symptoms in COVID-19 patients, anosmia, the complete loss of the ability to sense smell, and other olfactory alterations. We summarize current knowledge on principal mechanisms that may contribute to the development of autoimmunity in the disease: the ability of SARS-CoV-2 to hyper-stimulate the immune system, induce excessive neutrophil extracellular traps formation with neutrophil-associated cytokine responses and the molecular resemblance between self-components of the host and the virus. Additionally, we will examine COVID-19 potential risk on the new-onsets of autoimmune diseases, such as antiphospholipid syndrome, Guillain-Barré syndrome, Kawasaki disease and numerous others. It is of great importance to recognize those autoimmune manifestations of COVID-19 in order to properly cope with their outcomes in the ongoing pandemic and the long-term post-pandemic period. Lastly, an effective vaccine against SARS-CoV-2 may be the best solution in dealing with the ongoing pandemic. We will discuss the new messenger RNA vaccination strategy with an emphasis on autoimmunity implications.

Indexed as

Autoimmune DiseasesCOVID-19Epstein-Barr Virus InfectionsAutoimmunityCOVID-19 VaccinesHerpesvirus 4, HumanHumansSARS-CoV-2COVID-19 VaccinesAutoantibodiesAutoimmune diseasesCOVID-19Molecular mimicryNETosisSARS-CoV-2

Identifiers

PMID33610751
PMCPMC7892316
OpenAlexW3132728920

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.