Evidence map›Paper›PMID 35488894›Full record

ArticleGenetics in medicine : official journal of the American College of Medical Genetics2022

High-affinity FcγRIIIa genetic variants and potent NK cell-mediated antibody-dependent cellular cytotoxicity (ADCC) responses contributing to severe COVID-19.

Hannes Vietzen, Vera Danklmaier, Alexander Zoufaly, Elisabeth Puchhammer-Stöckl

Open access · bronzeAbstract read
In one paragraph

Article in Genetics in medicine : official journal of the American College of Medical Genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 22 citations in OpenAlex.

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  7. Targeting Decidual CD16Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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  17. Multifaceted roles of Fcγ receptors in COVID-19 and vaccine responses.American journal of translational research · 2023
    Review
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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

4 authors at 2 institutions in 1 country.

Hannes VietzenCenter for Virology, Medical University of Vienna, Vienna, Austria. Electronic address: hannes.vietzen@meduniwien.ac.at.
Vera DanklmaierCenter for Virology, Medical University of Vienna, Vienna, Austria.
Alexander ZoufalyDepartment of Medicine IV, Clinic Favoriten, Vienna, Austria; Faculty of Medicine, Sigmund Freud University, Vienna, Austria.
Elisabeth Puchhammer-StöcklCenter for Virology, Medical University of Vienna, Vienna, Austria.
Medical University of Vienna · ATSigmund Freud Privatuniversität Wien · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeHost genetic variants in activating natural killer (NK) cell receptors may contribute to differences in severity of COVID-19. NK cell-mediated antibody-mediated cellular cytotoxicity (ADCC) responses play, however, a controversial role in SARS-CoV-2 infections. It is unclear whether proinflammatory and cytotoxic SARS-CoV-2-specific ADCC responses limit disease severity or rather contribute to the immunopathogenesis of severe COVID-19.

methodsUsing a genetic association approach and subsequent in vitro antibody-dependent NK cell activation experiments, we investigated whether genetic variants in the FcγRIIIa-encoding FCGR3A gene, resulting in expression of either a low-affinity or high-affinity variant, and individual SARS-CoV-2-specific ADCC response contribute to COVID-19 severity.

resultsIn our study, we showed that the high-affinity variant of the FcγRIIIa receptor, 158-V/V, is significantly over-represented in hospitalized and deceased patients with COVID-19, whereas the low-affinity FcγRIIIa-158-F/F variant occurs more frequently in patients with mild COVID-19 (P < .0001). Furthermore, functional SARS-CoV-2 antibody-specific NK cell-mediated ADCC assays revealed that significantly higher proinflammatory ADCC responses occur in hospitalized patients with COVID-19, and are especially observed in NK cells expressing the FcγRIIIa-158-V/V variant (P < .0001).

conclusionOur study provides evidence that pronounced SARS-CoV-2-specific NK cell-mediated ADCC responses are influenced by NK cell FcγRIIIa genetic variants and are a hallmark of severe COVID-19.

Indexed as

Antineoplastic AgentsCOVID-19Antibody-Dependent Cell CytotoxicityHumansKiller Cells, NaturalSARS-CoV-2Antineoplastic AgentsADCCCOVID-19FcγRIIIaNK cellsSequence variant

Identifiers

PMID35488894
PMCPMC9055393
OpenAlexW4225135625

What OpenQuestion holds

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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.