Evidence map›Paper›PMID 35592107›Full record

ArticlebioRxiv : the preprint server for biology2022

Immediate myeloid depot for SARS-CoV-2 in the human lung.

Mélia Magnen, Ran You, Arjun A Rao, Ryan T Davis, Lauren Rodriguez, Camille R Simoneau, Lisiena Hysenaj, Kenneth H Hu, UCSF COMET Consortium, Christina Love and 11 more

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

Article in bioRxiv : the preprint server for biology, 2022. 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, 3 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 2 institutions in 1 country.

Mélia MagnenDepartment of Medicine, University of California, San Francisco, San Francisco, CA 94143, USA.
Ran YouDepartment of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.
Arjun A RaoDepartment of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.
Ryan T DavisDepartment of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.
Lauren RodriguezCoLabs Initiative, University of California, San Francisco, San Francisco, CA 94143, USA.
Camille R SimoneauDepartment of Medicine, University of California, San Francisco, San Francisco, CA 94143, USA.
Lisiena HysenajDepartment of Anatomy, University of California, San Francisco, San Francisco, CA 94143, USA.
Kenneth H HuDepartment of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.
UCSF COMET Consortium
Christina LoveDepartment of Medicine, University of California, San Francisco, San Francisco, CA 94143, USA.
Prescott G WoodruffDepartment of Medicine, University of California, San Francisco, San Francisco, CA 94143, USA.
David J ErleDepartment of Medicine, University of California, San Francisco, San Francisco, CA 94143, USA.
Carolyn M HendricksonDepartment of Medicine, University of California, San Francisco, San Francisco, CA 94143, USA.
Carolyn S CalfeeDepartment of Medicine, University of California, San Francisco, San Francisco, CA 94143, USA.
Michael A MatthayDepartment of Medicine, University of California, San Francisco, San Francisco, CA 94143, USA.
Jeroen P RooseDepartment of Anatomy, University of California, San Francisco, San Francisco, CA 94143, USA.
Anita SilDepartment of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143, USA.
Melanie OttDepartment of Medicine, University of California, San Francisco, San Francisco, CA 94143, USA.
Charles R LangelierDepartment of Medicine, University of California, San Francisco, San Francisco, CA 94143, USA.
Matthew F KrummelDepartment of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.
Mark R LooneyDepartment of Medicine, University of California, San Francisco, San Francisco, CA 94143, USA.
University of California, San Francisco · USGladstone Institutes · US

Funding

Understand the metabolic fitness of naïve T cellsP01AI091580 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JEROEN ROOSE · 2011 to 2026
$31.1M
Research BaseP30DK063720 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GERMAN, MICHAEL S · 2003 to 2019
$21.8M
Spatiotemporal Control of T cell Synapse Stabilization and SignalingR01AI052116 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KRUMMEL, MATTHEW F · 2002 to 2022
$8.3M
Precision Medicine in the Acute Respiratory Distress SyndromeR35HL140026 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CALFEE, CAROLYN · 2018 to 2024
$6.8M
Microbial Pathogenesis and Host DefenseT32AI060537 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Joanne N. Engel · 2004 to 2026
$6.5M
Immunobiology of the normal and injured lungR35HL161241 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MARK ROBERTS LOONEY · 2022 to 2026
$4.2M
Mechanisms and pathogenicity of SARS-CoV-2-induced neutrophil extracellular trapsR01AI160167 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOONEY, MARK ROBERTS · 2021 to 2025
$3.1M
BD FACSAria Fusion Cell SorterS10OD021822 · OD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LEE, MICHAEL R. · 2016 to 2016
$573k
NHLBI NIH HHS R35 HL140026NHLBI NIH HHS R35 HL161241NIAID NIH HHS P01 AI091580NIAID NIH HHS R01 AI052116NIAID NIH HHS R01 AI160167NIAID NIH HHS T32 AI060537NIDDK NIH HHS P30 DK063720NIH HHS S10 OD021822
6 · The paper itself

Abstract

In the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, considerable focus has been placed on a model of viral entry into host epithelial populations, with a separate focus upon the responding immune system dysfunction that exacerbates or causes disease. We developed a precision-cut lung slice model to investigate very early host-viral pathogenesis and found that SARS-CoV-2 had a rapid and specific tropism for myeloid populations in the human lung. Infection of alveolar macrophages was partially dependent upon their expression of ACE2, and the infections were productive for amplifying virus, both findings which were in contrast with their neutralization of another pandemic virus, Influenza A virus (IAV). Compared to IAV, SARS-CoV-2 was extremely poor at inducing interferon-stimulated genes in infected myeloid cells, providing a window of opportunity for modest titers to amplify within these cells. Endotracheal aspirate samples from humans with the acute respiratory distress syndrome (ARDS) from COVID-19 confirmed the lung slice findings, revealing a persistent myeloid depot. In the early phase of SARS-CoV-2 infection, myeloid cells may provide a safe harbor for the virus with minimal immune stimulatory cues being generated, resulting in effective viral colonization and quenching of the immune system.

Identifiers

PMID35592107
PMCPMC9119017
OpenAlexW4225291718

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

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.