Evidence map›Paper›PMID 33670195›Full record

ReviewViruses2021

Viral Infections and Systemic Lupus Erythematosus: New Players in an Old Story.

Marco Quaglia, Guido Merlotti, Marco De Andrea, Cinzia Borgogna, Vincenzo Cantaluppi

Open access · goldAbstract readReview
In one paragraph

Review in Viruses, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 116 citations in OpenAlex.

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  19. Syk inhibitor attenuates lupus in FcγRIIbCell death discovery · 2025
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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

5 authors at 2 institutions in 1 country.

Marco QuagliaNephrology and Kidney Transplantation Unit, Department of Translational Medicine, University of Piemonte Orientale (UPO), "Maggiore della Carità" University Hospital, Via P. Solaroli 17, 28100 Novara, Italy.
Guido MerlottiNephrology and Kidney Transplantation Unit, Department of Translational Medicine, University of Piemonte Orientale (UPO), "Maggiore della Carità" University Hospital, Via P. Solaroli 17, 28100 Novara, Italy.ORCID 0000-0001-9069-6192
Marco De AndreaCenter for Translational Research on Autoimmune and Allergic Disease-CAAD, 28100 Novara, Italy.ORCID 0000-0002-3188-5783
Cinzia BorgognaCenter for Translational Research on Autoimmune and Allergic Disease-CAAD, 28100 Novara, Italy.
Vincenzo CantaluppiNephrology and Kidney Transplantation Unit, Department of Translational Medicine, University of Piemonte Orientale (UPO), "Maggiore della Carità" University Hospital, Via P. Solaroli 17, 28100 Novara, Italy.ORCID 0000-0002-4120-3555
Università degli Studi del Piemonte Orientale “Amedeo Avogadro” · ITUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A causal link between viral infections and autoimmunity has been studied for a long time and the role of some viruses in the induction or exacerbation of systemic lupus erythematosus (SLE) in genetically predisposed patients has been proved. The strength of the association between different viral agents and SLE is variable. Epstein-Barr virus (EBV), parvovirus B19 (B19V), and human endogenous retroviruses (HERVs) are involved in SLE pathogenesis, whereas other viruses such as Cytomegalovirus (CMV) probably play a less prominent role. However, the mechanisms of viral-host interactions and the impact of viruses on disease course have yet to be elucidated. In addition to classical mechanisms of viral-triggered autoimmunity, such as molecular mimicry and epitope spreading, there has been a growing appreciation of the role of direct activation of innate response by viral nucleic acids and epigenetic modulation of interferon-related immune response. The latter is especially important for HERVs, which may represent the molecular link between environmental triggers and critical immune genes. Virus-specific proteins modulating interaction with the host immune system have been characterized especially for Epstein-Barr virus and explain immune evasion, persistent infection and self-reactive B-cell "immortalization". Knowledge has also been expanding on key viral proteins of B19-V and CMV and their possible association with specific phenotypes such as antiphospholipid syndrome. This progress may pave the way to new therapeutic perspectives, including the use of known or new antiviral drugs, postviral immune response modulation and innate immunity inhibition. We herein describe the state-of-the-art knowledge on the role of viral infections in SLE, with a focus on their mechanisms of action and potential therapeutic targets.

Indexed as

Antiphospholipid SyndromeAutoimmunityCytomegalovirusCytomegalovirus InfectionsEndogenous RetrovirusesEpstein-Barr Virus InfectionsHerpesvirus 4, HumanHost-Pathogen InteractionsHumansImmunity, InnateLupus Erythematosus, SystemicParvoviridae InfectionsParvovirus B19, Humanantiphospholipid syndromeautoimmunitycytomegalovirusEpstein–Barr virushuman endogenous retroviruseshuman immunodeficiency virusparvovirus B19retrovirusessystemic lupus erythematosustransfusion-transmitted virus

Identifiers

PMID33670195
PMCPMC7916951
OpenAlexW3127303346

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.