Evidence map›Paper›PMID 31430946›Full record

ReviewViruses2019

Viruses and Autoimmunity: A Review on the Potential Interaction and Molecular Mechanisms.

Maria K Smatti, Farhan S Cyprian, Gheyath K Nasrallah, Asmaa A Al Thani, Ruba O Almishal, Hadi M Yassine

Registry-linked trialOpen access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Viruses, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04846010 (Treating Sequalae Caused by Post-acute Sequelae of SARS), which is not on this map. Cited by 314 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
314citing papers in PubMed, 4 pooled it
35.6field-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.

NCT04846010 phase1 / phase2unknown statusnot on this mapstarted 2021, after this paper: background citation

Treating Sequalae Caused by Post-acute Sequelae of SARS (Severe Acute Respiratory Syndrome)-CoV-2 Infection

TypeinterventionalSponsorAll Natural Medicine Clinic, LLCRan2021 to 2022Enrolled2,000ConditionsSequelae of, Infection, Post Infection Glomerulonephritis, Post-Infectious Peripheral NeuralgiaArmsPurWet, FurFat, PurApo, PurPhl, PurClo
3 · Its place in the literature

Who cites it

314 citing papers in PubMed, 4 syntheses or guidelines pooled it, 546 citations in OpenAlex.

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254 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 1 institution in 1 country.

Maria K SmattiBiomedical Research Center, Qatar University, Doha 2713, Qatar.ORCID 0000-0002-7621-0130
Farhan S CyprianBasic Medical Science Department, College of Medicine-QU Health, Qatar University, Doha 2713, Qatar.
Gheyath K NasrallahBiomedical Research Center, Qatar University, Doha 2713, Qatar.ORCID 0000-0001-9252-1038
Asmaa A Al ThaniBiomedical Research Center, Qatar University, Doha 2713, Qatar.
Ruba O AlmishalBasic Medical Science Department, College of Medicine-QU Health, Qatar University, Doha 2713, Qatar.
Hadi M YassineBiomedical Research Center, Qatar University, Doha 2713, Qatar. Hyassine@qu.edu.qa.ORCID 0000-0001-7592-2788
Qatar University · QA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

For a long time, viruses have been shown to modify the clinical picture of several autoimmune diseases, including type 1 diabetes (T1D), systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Sjögren's syndrome (SS), herpetic stromal keratitis (HSK), celiac disease (CD), and multiple sclerosis (MS). Best examples of viral infections that have been proposed to modulate the induction and development of autoimmune diseases are the infections with enteric viruses such as Coxsackie B virus (CVB) and rotavirus, as well as influenza A viruses (IAV), and herpesviruses. Other viruses that have been studied in this context include, measles, mumps, and rubella. Epidemiological studies in humans and experimental studies in animal have shown that viral infections can induce or protect from autoimmunopathologies depending on several factors including genetic background, host-elicited immune responses, type of virus strain, viral load, and the onset time of infection. Still, data delineating the clear mechanistic interaction between the virus and the immune system to induce autoreactivity are scarce. Available data indicate that viral-induced autoimmunity can be activated through multiple mechanisms including molecular mimicry, epitope spreading, bystander activation, and immortalization of infected B cells. Contrarily, the protective effects can be achieved via regulatory immune responses which lead to the suppression of autoimmune phenomena. Therefore, a better understanding of the immune-related molecular processes in virus-induced autoimmunity is warranted. Here we provide an overview of the current understanding of viral-induced autoimmunity and the mechanisms that are associated with this phenomenon.

Indexed as

AnimalsAutoimmune DiseasesAutoimmunityHumansVirus DiseasesVirusesVirus Physiological Phenomenaautoimmunitymolecular mechanismsmolecular mimicryviral infections

Identifiers

PMID31430946
PMCPMC6723519
OpenAlexW2967488951

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.