Evidence map›Paper›PMID 33521069›Full record

ArticleFrontiers in cardiovascular medicine2020

Gene Expression Profiling Reveals the Shared and Distinct Transcriptional Signatures in Human Lung Epithelial Cells Infected With SARS-CoV-2, MERS-CoV, or SARS-CoV: Potential Implications in Cardiovascular Complications of COVID-19.

Prabhash Kumar Jha, Aatira Vijay, Arda Halu, Shizuka Uchida, Masanori Aikawa

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
2.6field-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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 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

5 authors at 4 institutions in 2 countries.

Prabhash Kumar JhaCenter for Excellence in Vascular Biology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States.
Aatira VijayDepartment of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, United States.
Arda HaluCenter for Interdisciplinary Cardiovascular Sciences, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States.
Shizuka UchidaDepartment of Clinical Medicine, Center for RNA Medicine, Aalborg University, Copenhagen, Denmark.
Masanori AikawaCenter for Excellence in Vascular Biology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States.
Brigham and Women's Hospital · USAalborg University · DKCleveland Clinic Lerner College of Medicine · USHarvard University · US

Funding

Pro-inflammatory activation of human macrophages regulated by lncRNAsR01HL149302 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI AIKAWA, MASANORI · 2019 to 2022
$2.9M
PARP9 and PARP14 in atherosclerosisR01HL126901 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI AIKAWA, MASANORI · 2016 to 2019
$2.4M
NHLBI NIH HHS R01 HL126901NHLBI NIH HHS R01 HL149302
6 · The paper itself

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative virus for the current global pandemic known as coronavirus disease 2019 (COVID-19). SARS-CoV-2 belongs to the family of single-stranded RNA viruses known as coronaviruses, including the MERS-CoV and SARS-CoV that cause Middle East respiratory syndrome (MERS) and severe acute respiratory syndrome (SARS), respectively. These coronaviruses are associated in the way that they cause mild to severe upper respiratory tract illness. This study has used an unbiased analysis of publicly available gene expression datasets from Gene Expression Omnibus to understand the shared and unique transcriptional signatures of human lung epithelial cells infected with SARS-CoV-2 relative to MERS-CoV or SARS-CoV. A major goal was to discover unique cellular responses to SARS-CoV-2 among these three coronaviruses. Analyzing differentially expressed genes (DEGs) shared by the three datasets led to a set of 17 genes, suggesting the lower expression of genes related to acute inflammatory response (TNF, IL32, IL1A, CXCL1, and CXCL3) in SARS-CoV-2. This subdued transcriptional response to SARS-CoV-2 may cause prolonged viral replication, leading to severe lung damage. Downstream analysis of unique DEGs of SARS-CoV-2 infection revealed changes in genes related to apoptosis (NRP1, FOXO1, TP53INP1, CSF2, and NLRP1), coagulation (F3, PROS1, ITGB3, and TFPI2), and vascular function (VAV3, TYMP, TCF4, and NR2F2), which may contribute to more systemic cardiovascular complications of COVID-19 than MERS and SARS. The study has uncovered a novel set of transcriptomic signatures unique to SARS-CoV-2 infection and shared by three coronaviruses, which may guide the initial efforts in the development of prognostic or therapeutic tools for COVID-19.

Indexed as

cardiovasclar diseaseCOVID-19 and transcriptome analysisMERS-CoVSARS-CoVSARS-CoV-2

Identifiers

PMID33521069
PMCPMC7844200
OpenAlexW3124269062

What OpenQuestion holds

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LicenceCC BY
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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.