Evidence map›Paper›PMID 36371813›Full record

ReviewMolecular immunology2022

Antibody-Dependent Enhancement (ADE) and the role of complement system in disease pathogenesis.

Swapna Thomas, Maria K Smatti, Allal Ouhtit, Farhan S Cyprian, Muna A Almaslamani, Asmaa Al Thani, Hadi M Yassine

Open access · hybridAbstract readReview
In one paragraph

Review in Molecular immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
6.0field-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

44 citing papers in PubMed, 65 citations in OpenAlex.

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  9. Cytokine storm.Nature reviews. Disease primers · 2026
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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

7 authors at 2 institutions in 1 country.

Swapna ThomasBiomedical Research Center, Qatar University, Qatar; Biological and Environmental Sciences, College of Arts and Sciences, Qatar University, Qatar. Electronic address: swapna.thomas@qu.edu.qa.
Maria K SmattiBiomedical Research Center, Qatar University, Qatar. Electronic address: msmatti@qu.edu.qa.
Allal OuhtitBiological and Environmental Sciences, College of Arts and Sciences, Qatar University, Qatar. Electronic address: aouhtit@qu.edu.qa.
Farhan S CyprianBasic Medical Science Department, College of Medicine-QU Health, Qatar University, Qatar. Electronic address: fcyprian@qu.edu.qa.
Muna A AlmaslamaniCommunicable Disease Center, Hamad Medical Corporation, Doha, Qatar. Electronic address: malmaslamani@hamad.qa.
Asmaa Al ThaniBiomedical Research Center, Qatar University, Qatar; Department of Biomedical Sciences, College of Health Science-QU Health, Qatar University, Qatar. Electronic address: aaja@qu.edu.qa.
Hadi M YassineBiomedical Research Center, Qatar University, Qatar; Department of Biomedical Sciences, College of Health Science-QU Health, Qatar University, Qatar. Electronic address: hyassine@qu.edu.qa.
Qatar University · QAHamad Medical Corporation · QA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antibody-dependent enhancement (ADE) has been associated with severe disease outcomes in several viral infections, including respiratory infections. In vitro and in vivo studies showed that antibody-response to SARS-CoV and MERS-CoV could exacerbate infection via ADE. Recently in SARS CoV-2, the in vitro studies and structural analysis shows a risk of disease severity via ADE. This phenomenon is partially attributed to non-neutralizing antibodies or antibodies at sub-neutralizing levels. These antibodies result in antigen-antibody complexes' deposition and propagation of a chronic inflammatory process that destroys affected tissues. Further, antigen-antibody complexes may enhance the internalization of the virus into cells through the Fc gamma receptor (FcγR) and lead to further virus replication. Thus, ADE occur via two mechanisms; 1. Antibody mediated replication and 2. Enhanced immune activation. Antibody-mediated effector functions are mainly driven by complement activation, and the first complement in the cascade is complement 1q (C1q) which binds to the virus-antibody complex. Reports say that deficiency in circulating plasma levels of C1q, an independent predictor of mortality in high-risk patients, including diabetes, is associated with severe viral infections. Complement mediated ADE is reported in several viral infections such as dengue, West Nile virus, measles, RSV, Human immunodeficiency virus (HIV), and Ebola virus. This review discusses ADE in viral infections and the in vitro evidence of ADE in coronaviruses. We outline the mechanisms of ADE, emphasizing the role of complements, especially C1q in the outcome of the enhanced disease.

Indexed as

COVID-19Severe Acute Respiratory SyndromeAntibodies, ViralAntibody-Dependent EnhancementAntigen-Antibody ComplexComplement C1qHumansAntibodies, ViralAntigen-Antibody ComplexComplement C1qADEC1qComplementsCoronavirusesCOVID-19Non-neutralizing antibodies

Identifiers

PMID36371813
PMCPMC9647202
OpenAlexW4308887989

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.