Evidence map›Paper›PMID 34108966›Full record

ArticleFrontiers in immunology2021

Transcriptional Changes in CD16+ Monocytes May Contribute to the Pathogenesis of COVID-19.

Vanessa Chilunda, Pablo Martinez-Aguado, Li C Xia, Laura Cheney, Aniella Murphy, Veronica Veksler, Vanessa Ruiz, Tina M Calderon, Joan W Berman

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  16. CD16Frontiers in immunology · 2023
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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

9 authors at 1 institution in 1 country.

Vanessa ChilundaDepartment of Pathology, Albert Einstein College of Medicine, Bronx, NY, United States.
Pablo Martinez-AguadoDepartment of Pathology, Albert Einstein College of Medicine, Bronx, NY, United States.
Li C XiaDepartment of Epidemiology and Public Health, Division of Biostatistics, Albert Einstein College of Medicine, Bronx, NY, United States.
Laura CheneyDepartment of Pathology, Albert Einstein College of Medicine, Bronx, NY, United States.
Aniella MurphyDepartment of Pathology, Albert Einstein College of Medicine, Bronx, NY, United States.
Veronica VekslerDepartment of Pathology, Albert Einstein College of Medicine, Bronx, NY, United States.
Vanessa RuizDepartment of Pathology, Albert Einstein College of Medicine, Bronx, NY, United States.
Tina M CalderonDepartment of Pathology, Albert Einstein College of Medicine, Bronx, NY, United States.
Joan W BermanDepartment of Pathology, Albert Einstein College of Medicine, Bronx, NY, United States.
Albert Einstein College of Medicine · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007288 · NIGMS · YESHIVA UNIVERSITY · PI AKABAS, MYLES H. · 1985 to 2022
$35.6M
Patient and Population Health Outcomes Research SWGP30AI124414 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI Kathryn M. Anastos · 2017 to 2026
$28.3M
Effect of buprenorphine on monocytes in the context of neuroAids and opioid abuseR01DA041931 · NIDA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI Joan Weinberger Berman, JENNIFER L KELSCHENBACH · 2017 to 2026
$7.4M
Training in HIV/AIDS Pathogenesis; Basic and Translational ResearchT32AI007501 · NIAID · YESHIVA UNIVERSITY · PI PRASAD, VINAYAKA R. · 1995 to 2024
$6.6M
Geographic Medicine and Emerging InfectionsT32AI070117 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI WEISS, LOUIS M. · 2008 to 2023
$5.1M
Mechanisms of opioid- mediated HIV neuropathogenesisR01DA048609 · NIDA · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI BERMAN, JOAN WEINBERGER, GOLDSTEIN, HARRIS · 2019 to 2023
$4.2M
Impact of illicit drugs, HIV, and ART on neuroinflammation and BBB disruptionR01DA044584 · NIDA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI BERMAN, JOAN WEINBERGER, GOLDSTEIN, HARRIS · 2017 to 2021
$4.0M
Monocyte CNS HIV entry & neurodegeneration: Translational studies in the CART eraR01MH112391 · NIMH · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI BERMAN, JOAN WEINBERGER, MORGELLO, SUSAN · 2017 to 2021
$3.7M
NRSA Training CoreTL1TR002557 · NCATS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI MARANTZ, PAUL R · 2018 to 2022
$1.0M
NCATS NIH HHS TL1 TR002557NIAID NIH HHS P30 AI124414NIAID NIH HHS T32 AI007501NIAID NIH HHS T32 AI070117NIDA NIH HHS R01 DA041931NIDA NIH HHS R01 DA044584NIDA NIH HHS R01 DA048609NIGMS NIH HHS T32 GM007288NIMH NIH HHS R01 MH112391
6 · The paper itself

Abstract

The COVID-19 pandemic has caused more than three million deaths globally. The severity of the disease is characterized, in part, by a dysregulated immune response. CD16+ monocytes are innate immune cells involved in inflammatory responses to viral infections, and tissue repair, among other functions. We characterized the transcriptional changes in CD16+ monocytes from PBMC of people with COVID-19, and from healthy individuals using publicly available single cell RNA sequencing data. CD16+ monocytes from people with COVID-19 compared to those from healthy individuals expressed transcriptional changes indicative of increased cell activation, and induction of a migratory phenotype. We also analyzed COVID-19 cases based on severity of the disease and found that mild cases were characterized by upregulation of interferon response and MHC class II related genes, whereas the severe cases had dysregulated expression of mitochondrial and antigen presentation genes, and upregulated inflammatory, cell movement, and apoptotic gene signatures. These results suggest that CD16+ monocytes in people with COVID-19 contribute to a dysregulated host response characterized by decreased antigen presentation, and an elevated inflammatory response with increased monocytic infiltration into tissues. Our results show that there are transcriptomic changes in CD16+ monocytes that may impact the functions of these cells, contributing to the pathogenesis and severity of COVID-19.

Indexed as

Transcription, GeneticTranscriptomeAdultAgedApoptosis Regulatory ProteinsCase-Control StudiesCOVID-19CytokinesFemaleGene Expression ProfilingGPI-Linked ProteinsHost-Pathogen InteractionsHumansInflammation MediatorsInterferon Regulatory FactorsMaleApoptosis Regulatory ProteinsCytokinesFCGR3B protein, humanGPI-Linked ProteinsInflammation MediatorsInterferon Regulatory FactorsMitochondrial ProteinsReceptors, IgGcell movementinflammationnon-classical monocytesSARS-CoV-2single-cell transcriptomics

Identifiers

PMID34108966
PMCPMC8181441
OpenAlexW3165544177

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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.