Evidence map›Paper›PMID 39435487›Full record

ArticleEmerging microbes & infections2024

SARS-CoV-2 hijacks host CD55, CD59 and factor H to impair antibody-dependent complement-mediated lysis.

Laura Gebetsberger, Zahra Malekshahi, Aron Teutsch, Gabor Tajti, Frédéric Fontaine, Nara Marella, André Mueller, Lena Prantl, Hannes Stockinger, Heribert Stoiber and 1 more

Abstract read
In one paragraph

Article in Emerging microbes & infections, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
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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

11 authors.

Laura GebetsbergerMedical University of Vienna, Center for Pathophysiology, Infectiology and Immunology, Institute for Hygiene and Applied Immunology, Vienna, Austria.ORCID 0000-0002-6480-6228
Zahra MalekshahiMedical University of Innsbruck, Institute of Virology, Innsbruck, Austria.
Aron TeutschMedical University of Innsbruck, Institute of Virology, Innsbruck, Austria.
Gabor TajtiMedical University of Vienna, Center for Pathophysiology, Infectiology and Immunology, Institute for Hygiene and Applied Immunology, Vienna, Austria.
Frédéric FontaineCeMM - Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
Nara MarellaCeMM - Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
André MuellerCeMM - Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
Lena PrantlMedical University of Innsbruck, Institute of Virology, Innsbruck, Austria.
Hannes StockingerMedical University of Vienna, Center for Pathophysiology, Infectiology and Immunology, Institute for Hygiene and Applied Immunology, Vienna, Austria.ORCID 0000-0001-6404-4430
Heribert StoiberMedical University of Innsbruck, Institute of Virology, Innsbruck, Austria.
Anna Ohradanova-RepicMedical University of Vienna, Center for Pathophysiology, Infectiology and Immunology, Institute for Hygiene and Applied Immunology, Vienna, Austria.ORCID 0000-0002-8005-8522

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The complement system is a vital anti-microbial defence mechanism against circulating pathogens. Excessive complement activation can have deleterious outcomes for the host and is consequently tightly modulated by a set of membrane-associated and fluid-phase regulators of complement activation (RCAs). Here, we demonstrate that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) hijacks host cellular RCA members CD55 and CD59 and serum-derived Factor H (FH) to resist antibody-dependent complement-mediated lysis triggered by immunized human sera. Blockage of the biological functions of virion-associated CD55 and CD59 and competition of FH recruitment with functionally inactive recombinant FH-derived short consensus repeats SCR18-20 restore SARS-CoV-2 complement sensitivity in a synergistic manner. Moreover, complement-mediated virolysis is dependent on classical pathway activation and does not occur in the absence of virus-specific antibodies. Altogether, our findings present an intriguing immune escape mechanism that provides novel insights into the immunopathology observed in severe coronavirus disease 2019 (COVID-19).

Indexed as

CD55 AntigensCD59 AntigensComplement ActivationComplement Factor HCOVID-19SARS-CoV-2Antibodies, ViralHumansImmune EvasionAntibodies, ViralCD55 AntigensCD55 protein, humanCD59 AntigensCD59 protein, humanCFH protein, humanComplement Factor Hantiviral immunitycomplementimmune evasionregulators of complement activationSARS-CoV-2

Identifiers

PMID39435487
PMCPMC11520101

What OpenQuestion holds

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Registered trials

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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.