Evidence map›Paper›PMID 34960687›Full record

ArticleViruses2021

Single-Cell and Bulk RNASeq Profiling of COVID-19 Patients Reveal Immune and Inflammatory Mechanisms of Infection-Induced Organ Damage.

Alexandrea Bass, Yiran Liu, Sivanesan Dakshanamurthy

Open access · goldAbstract read
In one paragraph

Article in Viruses, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

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  6. A therapy for suppressing canonical and noncanonical SARS-CoV-2 viral entry and an intrinsic intrapulmonary inflammatory response.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  19. RNA sequence analysis of nasopharyngeal swabs from asymptomatic and mildly symptomatic patients with COVID-19.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2022
    Article
  20. Rlip Protein: A Potential Target for COVID-19.Journal of community hospital internal medicine perspectives · 2022
    Article
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

3 authors at 1 institution in 1 country.

Alexandrea BassDepartment of Biochemistry and Molecular Biology, Georgetown University Medical Center, Washington, DC 20057, USA.
Yiran LiuDepartment of Biochemistry and Molecular Biology, Georgetown University Medical Center, Washington, DC 20057, USA.
Sivanesan DakshanamurthyLombardi Comprehensive Cancer Center, Molecular and Experimental Therapeutic Research in Oncology Program, Georgetown University Medical Center, Washington, DC 20057, USA.
Georgetown University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The SARS-CoV-2 virus's ability to induce hypercytokinemia and cause multiple organ failure makes it imperative to find effective treatments. To understand the mechanism of viral infection and its effects on organ tissues, we analyzed multiple single-cell and bulk RNAseq data from COVID-19 patients' organ samples. Various levels of severity of infection were accounted for, with comparative analyses between mild, moderate, and severely infected patients. Our analysis uncovered an upregulation of the innate immune response via several inflammatory genes, IL-2, IL-6, IL-8, IL-17A, and NF-κB. Consequently, we found that the upregulation of these downstream effects can lead to organ injury. The downregulated pathways such as eukaryotic initiation factor 2 (eIF2) and eIF4-mediated host translation, were found to lead to an increased viral translation. We also found that the loss of inhibitory peptides can suppress an overactive innate immune response via NF-κB and interleukin-mediated pathways. Investigation of viral-host protein mapping showed that the interaction of viral proteins with host proteins correlated with the down- and upregulation of host pathways such as decreased eIF2-mediated host translation and increased hypertrophy and fibrosis. Inflammation was increased via the stimulation of pro-inflammatory cytokines and suppression of host translation pathways that led to reduced inflammatory inhibitors. Cardiac hypertrophy and organ fibrosis were the results of increased inflammation in organs of severe and critical patients. Finally, we identified potential therapeutic targets for the treatment of COVID-19 and its deleterious effects on organs. Further experimental investigation would conclusively determine the effects of COVID-19 infection on organs other than the lungs and the effectiveness of the proposed therapeutic targets.

Indexed as

Immunity, InnateSequence Analysis, RNASingle-Cell AnalysisCOVID-19Cytokine Release SyndromeCytokinesFibrosisGene ExpressionHumansInflammationLungSARS-CoV-2Severity of Illness IndexCytokinesCOVID-19 organ damageCOVID-19 patients gene expressionimmune and inflammatory mechanisms of COVID-19single and bulk RNASeq cell profiling and analysis

Identifiers

PMID34960687
PMCPMC8706409
OpenAlexW3217582582

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.