Evidence map›Paper›PMID 33310781›Full record

ArticlemBio2020

Recombinant ACE2 Expression Is Required for SARS-CoV-2 To Infect Primary Human Endothelial Cells and Induce Inflammatory and Procoagulative Responses.

Jonas Nascimento Conde, William R Schutt, Elena E Gorbunova, Erich R Mackow

Open access · goldAbstract read
In one paragraph

Article in mBio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 2 pooled it
2.5field-weighted citation impact, top 6% 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

89 citing papers in PubMed, 2 syntheses or guidelines pooled it, 135 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Extra gene coding capacity of SARS-CoV-2 provides a virus engineering platform for in vitro and in vivo applications.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

29 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Jonas Nascimento Conde *Department of Microbiology and Immunology, Stony Brook University, Stony Brook, New York, USA.
William R Schutt *Department of Microbiology and Immunology, Stony Brook University, Stony Brook, New York, USA.
Elena E GorbunovaDepartment of Microbiology and Immunology, Stony Brook University, Stony Brook, New York, USA.
Erich R MackowDepartment of Microbiology and Immunology, Stony Brook University, Stony Brook, New York, USA Erich.Mackow@stonybrook.edu.ORCID 0000-0001-9156-1222
Stony Brook University · US

Funding

Defining ANDV Virulence and Attenuation MechanismsR01AI129010 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI MACKOW, ERICH R · 2017 to 2021
$2.8M
Role of Persistent Zika Virus Infection of Endothelial Cells in PathogenesisR21AI131729 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI MACKOW, ERICH R · 2017 to 2018
$432k
Baloxavir Derivatives As Inhibitors of Hantavirus Endonuclease ActivityR21AI152372 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI MACKOW, ERICH R · 2020 to 2021
$432k
NIAID NIH HHS R01 AI129010NIAID NIH HHS R21 AI131729NIAID NIH HHS R21 AI152372
6 · The paper itself

Abstract

SARS-CoV-2 causes COVID-19, an acute respiratory distress syndrome (ARDS) characterized by pulmonary edema, viral pneumonia, multiorgan dysfunction, coagulopathy, and inflammation. SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) receptors to infect and damage ciliated epithelial cells in the upper respiratory tract. In alveoli, gas exchange occurs across an epithelial-endothelial barrier that ties respiration to endothelial cell (EC) regulation of edema, coagulation, and inflammation. How SARS-CoV-2 dysregulates vascular functions to cause ARDS in COVID-19 patients remains an enigma focused on dysregulated EC responses. Whether SARS-CoV-2 directly or indirectly affects functions of the endothelium remains to be resolved and is critical to understanding SARS-CoV-2 pathogenesis and therapeutic targets. We demonstrate that primary human ECs lack ACE2 receptors at protein and RNA levels and that SARS-CoV-2 is incapable of directly infecting ECs derived from pulmonary, cardiac, brain, umbilical vein, or kidney tissues. In contrast, pulmonary ECs transduced with recombinant ACE2 receptors are infected by SARS-CoV-2 and result in high viral titers (∼1 × 10

Indexed as

Blood Coagulation FactorsInflammationAnimalsCells, CulturedChlorocebus aethiopsEndothelial CellsHumansPeptidyl-Dipeptidase ARecombinant ProteinsSARS-CoV-2Vero CellsACE protein, humanBlood Coagulation FactorsPeptidyl-Dipeptidase ARecombinant ProteinsACE2coagulopathyCOVID-19endothelial cellsendotheliitisinflammationpulmonarySARS-CoV-2

Identifiers

PMID33310781
PMCPMC7751258
OpenAlexW3113290471

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.