Evidence map›Paper›PMID 32909007›Full record

ArticlemedRxiv : the preprint server for health sciences2020

Determinants of SARS-CoV-2 receptor gene expression in upper and lower airways.

H Aliee, F Massip, C Qi, M Stella de Biase, J van Nijnatten, E T G Kersten, N Z Kermani, B Khuder, J M Vonk, R C H Vermeulen and 28 more

Open access · greenAbstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in medRxiv : the preprint server for health sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed, 20 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

38 authors at 12 institutions in 8 countries.

H AlieeInstitute of Computational Biology, Helmholtz Centre, Munich, Germany.
F MassipBerlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine, Robert-Rössle-Str. 10, 13125 Berlin, Germany.
C QiUniversity of Groningen, University Medical Center Groningen, Groningen Research Institute for Asthma and COPD, Groningen, the Netherlands.
M Stella de BiaseBerlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine, Robert-Rössle-Str. 10, 13125 Berlin, Germany.
J van NijnattenUniversity of Groningen, University Medical Center Groningen, Groningen Research Institute for Asthma and COPD, Groningen, the Netherlands.
E T G KerstenUniversity of Groningen, University Medical Center Groningen, Groningen Research Institute for Asthma and COPD, Groningen, the Netherlands.
N Z KermaniDepartment of computing, Data Science Institute, Imperial College London, London, UK.
B KhuderNorthwestern University Feinberg School of Medicine, Division of Pulmonary and Critical Care Medicine, Chicago, IL, USA.
J M VonkUniversity of Groningen, University Medical Center Groningen, Groningen Research Institute for Asthma and COPD, Groningen, the Netherlands.
R C H VermeulenJulius Global Health, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
U-BIOPRED study group
Cambridge Lung Cancer Early Detection Programme
INER-Ciencias Mexican Lung Program
NHLBI LungMAP Consortium
M NeighborsOMNI Biomarker Development, Genentech Inc. South San Francisco. CA, USA.
G W TewProduct Development Immunology, Infectious Disease & Opthalmology, Genentech Inc. South San Francisco. CA, USA.
M GrimbaldestonOMNI Biomarker Development, Genentech Inc. South San Francisco. CA, USA.
N H T Ten HackenUniversity of Groningen, University Medical Center Groningen, Department of Pulmonary Diseases, Groningen, the Netherlands.
S HuDepartment of statistics, university of Oxford, Oxford, UK.
Y GuoDepartment of computing, Data Science Institute, Imperial College London, London, UK.
X ZhangDepartment of computing, Data Science Institute, Imperial College London, London, UK.
K SunDepartment of computing, Data Science Institute, Imperial College London, London, UK.
P S HiemstraDepartment of Pulmonology, Leiden University Medical Center, Leiden, The Netherlands.
B A PonderCancer Research UK Cambridge Institute, University of Cambridge, Robinson Way, Cambridge CB2 0RE, UK.
M J MäkeläDept. of Allergy, University of Helsinki and Helsinki University Hospital, PO Box 160, FI-00029, Helsinki, Finland.
K MalmströmDept. of Allergy, University of Helsinki and Helsinki University Hospital, PO Box 160, FI-00029, Helsinki, Finland.
R C RintoulDepartment of Oncology, University of Cambridge, Hutchison/MRC Research Centre, Box 197, Cambridge Biomedical Campus, CB2 0XZ, UK.
P A ReyfmanNorthwestern University Feinberg School of Medicine, Division of Pulmonary and Critical Care Medicine, Chicago, IL, USA.
F J TheisInstitute of Computational Biology, Helmholtz Centre, Munich, Germany.
C A BrandsmaUniversity of Groningen, University Medical Center Groningen, Groningen Research Institute for Asthma and COPD, Groningen, the Netherlands.
I M AdcockNational Heart and Lung Institute, London, UK.
W TimensUniversity of Groningen, University Medical Center Groningen, Groningen Research Institute for Asthma and COPD, Groningen, the Netherlands.
C J XuResearch group Bioinformatics and Computational Genomics, Centre for Individualised Infection Medicine, CiiM, a joint venture between the Hannover Medical School and the Helmholtz Centre for Infection Research, Hannover, Germany.
M van den BergeUniversity of Groningen, University Medical Center Groningen, Groningen Research Institute for Asthma and COPD, Groningen, the Netherlands.
R F SchwarzBerlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine, Robert-Rössle-Str. 10, 13125 Berlin, Germany.
G H KoppelmanUniversity of Groningen, University Medical Center Groningen, Groningen Research Institute for Asthma and COPD, Groningen, the Netherlands.
M C NawijnUniversity of Groningen, University Medical Center Groningen, Groningen Research Institute for Asthma and COPD, Groningen, the Netherlands.
A FaizUniversity of Groningen, University Medical Center Groningen, Groningen Research Institute for Asthma and COPD, Groningen, the Netherlands.
University Medical Center Groningen · NLUtrecht University · NLNorthwestern University · USUniversity of Technology Sydney · AUMax Delbrück Center · DEUniversity of Helsinki · FIBiomarker Technologies (China) · CNGene Therapy Laboratory · FRHelmholtz Zentrum München · DEImperial College London · GBLeiden University Medical Center · NLUniversity of Cambridge · GB

Funding

Single-Cell Transcriptomic Analysis to Identify Drivers of Pulmonary FibrosisK08HL146943 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI REYFMAN, PAUL A · 2020 to 2021
$326k
NHLBI NIH HHS K08 HL146943
6 · The paper itself

Abstract

The recent outbreak of the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), has led to a worldwide pandemic. One week after initial symptoms develop, a subset of patients progresses to severe disease, with high mortality and limited treatment options. To design novel interventions aimed at preventing spread of the virus and reducing progression to severe disease, detailed knowledge of the cell types and regulating factors driving cellular entry is urgently needed. Here we assess the expression patterns in genes required for COVID-19 entry into cells and replication, and their regulation by genetic, epigenetic and environmental factors, throughout the respiratory tract using samples collected from the upper (nasal) and lower airways (bronchi). Matched samples from the upper and lower airways show a clear increased expression of these genes in the nose compared to the bronchi and parenchyma. Cellular deconvolution indicates a clear association of these genes with the proportion of secretory epithelial cells. Smoking status was found to increase the majority of COVID-19 related genes including ACE2 and TMPRSS2 but only in the lower airways, which was associated with a significant increase in the predicted proportion of goblet cells in bronchial samples of current smokers. Both acute and second hand smoke were found to increase ACE2 expression in the bronchus. Inhaled corticosteroids decrease ACE2 expression in the lower airways. No significant effect of genetics on ACE2 expression was observed, but a strong association of DNA- methylation with ACE2 and TMPRSS2- mRNA expression was identified in the bronchus.

Identifiers

PMID32909007
PMCPMC7480059
OpenAlexW3081793946

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.