Evidence map›Paper›PMID 35267024›Full record

ArticleThe Journal of infectious diseases2022

Contribution of Coronavirus-Specific Immunoglobulin G Responses to Complement Overactivation in Patients with Severe Coronavirus Disease 2019.

Priscila M S Castanha, Dylan J Tuttle, Georgios D Kitsios, Jana L Jacobs, Ulisses Braga-Neto, Matthew Duespohl, Sanjay Rathod, Michelle M Marti, Sarah Wheeler, Asma Naqvi and 12 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

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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

22 authors at 2 institutions in 1 country.

Priscila M S CastanhaDepartment of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.ORCID 0000-0002-1220-5308
Dylan J TuttleDepartment of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Georgios D KitsiosDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Jana L JacobsDivision of Infectious Diseases, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Ulisses Braga-NetoDepartment of Electrical and Computer Engineering, Texas A&M University, College Station, Texas, USA.
Matthew DuespohlDepartment of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Sanjay RathodCenter for Pharmacogenetics, Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Michelle M MartiDepartment of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Sarah WheelerDepartment of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.ORCID 0000-0002-7851-9836
Asma NaqviDivision of Infectious Diseases, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Brittany StainesDivision of Infectious Diseases, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
John MellorsDivision of Infectious Diseases, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Alison MorrisDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Bryan J McVerryDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Faraaz ShahAcute Lung Injury Center of Excellence, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Caitlin SchaeferDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Bernard J C MacatangayDivision of Infectious Diseases, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Barbara MetheDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Christian A FernandezCenter for Pharmacogenetics, Department of Pharmaceutical Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Simon M Barratt-BoyesDepartment of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Donald BurkeDepartment of Epidemiology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Ernesto T A MarquesDepartment of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
University of Pittsburgh · USTexas A&M University · US

Funding

Improving the disposition of antileukemic asparaginase after drug-induced immunotoxicityR01CA216815 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FERNANDEZ, CHRISTIAN ANTONIO · 2017 to 2021
$1.6M
NCI NIH HHS R01 CA216815
6 · The paper itself

Abstract

backgroundExcessive complement activation has been implicated in the pathogenesis of coronavirus disease 2019 (COVID-19), but the mechanisms leading to this response remain unclear.

methodsWe measured plasma levels of key complement markers, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA and antibodies against SARS-CoV-2 and seasonal human common cold coronaviruses (CCCs) in hospitalized patients with COVID-19 of moderate (n = 18) and critical severity (n = 37) and in healthy controls (n = 10).

resultsWe confirmed that complement activation is systemically increased in patients with COVID-19 and is associated with a worse disease outcome. We showed that plasma levels of C1q and circulating immune complexes were markedly increased in patients with severe COVID-19 and correlated with higher immunoglobulin (Ig) G titers, greater complement activation, and higher disease severity score. Additional analyses showed that the classical pathway was the main arm responsible for augmented complement activation in severe patients. In addition, we demonstrated that a rapid IgG response to SARS-CoV-2 and an anamnestic IgG response to the nucleoprotein of the CCCs were strongly correlated with circulating immune complex levels, complement activation, and disease severity.

conclusionsThese findings indicate that early, nonneutralizing IgG responses may play a key role in complement overactivation in severe COVID-19. Our work underscores the urgent need to develop therapeutic strategies to modify complement overactivation in patients with COVID-19.

Indexed as

COVID-19Antibodies, ViralCoronavirus Nucleocapsid ProteinsHumansImmunoglobulin GSARS-CoV-2Antibodies, ViralCoronavirus Nucleocapsid ProteinsImmunoglobulin Gand antibodiesclassical pathwaycommon cold coronavirusescomplement systemCOVID-19SARS-CoV-2

Identifiers

PMID35267024
PMCPMC8992249
OpenAlexW4220974536

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.