Evidence map›Paper›PMID 32510973›Full record

ArticleAmerican journal of physiology. Cell physiology2020

Decoding SARS-CoV-2 hijacking of host mitochondria in COVID-19 pathogenesis.

Keshav K Singh, Gyaneshwer Chaubey, Jake Y Chen, Prashanth Suravajhala

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 238 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
238citing papers in PubMed, 2 pooled it
7.3field-weighted citation impact, top 2% 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

238 citing papers in PubMed, 2 syntheses or guidelines pooled it, 373 citations in OpenAlex.

  1. Pooled it
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  9. Defective RNA Polymerase III sensing of mitochondrial DNA in pulmonary epithelial cells impairs type I IFN immunity to SARS-CoV-2.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  10. Impact of nutrition on long COVID.Sports medicine and health science · 2026
    Review
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178 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 3 institutions in 2 countries.

Keshav K SinghDepartment of Genetics, School of Medicine, University of Alabama at Birmingham, Kaul Genetics Building, Birmingham, Alabama.
Gyaneshwer ChaubeyCytogenetics Laboratory, Department of Zoology, Banaras Hindu University, Varanasi, Uttar Pradesh, India.
Jake Y ChenDepartment of Genetics, Computer Science, and Biomedical Engineering, University of Alabama at Birmingham, Birmingham, Alabama.
Prashanth SuravajhalaDepartment of Biotechnology and Bioinformatics, Birla Institute of Scientific Research Statue Circle, Jaipur, Rajasthan, India.
University of Alabama at Birmingham · USBanaras Hindu University · INBirla Institute of Scientific Research · IN

Funding

Mitochondria in Prostate Cancer DiversityR01CA204430 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SINGH, KESHAV K · 2016 to 2020
$1.7M
HHS | NIH | National Cancer Institute (NCI) R01CA204430NCI NIH HHS R01 CA204430
6 · The paper itself

Abstract

Because of the ongoing pandemic around the world, the mechanisms underlying the SARS-CoV-2-induced COVID-19 are subject to intense investigation. Based on available data for the SARS-CoV-1 virus, we suggest how CoV-2 localization of RNA transcripts in mitochondria hijacks the host cell's mitochondrial function to viral advantage. Besides viral RNA transcripts, RNA also localizes to mitochondria. SARS-CoV-2 may manipulate mitochondrial function indirectly, first by ACE2 regulation of mitochondrial function, and once it enters the host cell, open-reading frames (ORFs) such as ORF-9b can directly manipulate mitochondrial function to evade host cell immunity and facilitate virus replication and COVID-19 disease. Manipulations of host mitochondria by viral ORFs can release mitochondrial DNA (mtDNA) in the cytoplasm and activate mtDNA-induced inflammasome and suppress innate and adaptive immunity. We argue that a decline in ACE2 function in aged individuals, coupled with the age-associated decline in mitochondrial functions resulting in chronic metabolic disorders like diabetes or cancer, may make the host more vulnerable to infection and health complications to mortality. These observations suggest that distinct localization of viral RNA and proteins in mitochondria must play essential roles in SARS-CoV-2 pathogenesis. Understanding the mechanisms underlying virus communication with host mitochondria may provide critical insights into COVID-19 pathologies. An investigation into the SARS-CoV-2 hijacking of mitochondria should lead to novel approaches to prevent and treat COVID-19.

Indexed as

Adaptive ImmunityAngiotensin-Converting Enzyme 2AnimalsBetacoronavirusCoronavirus InfectionsCOVID-19DNA, MitochondrialGene Expression Regulation, ViralHost Microbial InteractionsHumansImmunity, InnateMitochondriaPandemicsPeptidyl-Dipeptidase APneumonia, ViralRNA, ViralACE2 protein, humanAngiotensin-Converting Enzyme 2DNA, MitochondrialPeptidyl-Dipeptidase ARNA, ViralagingcoronavirusCOVID-19mitochondriamitochondrial DNASARS-CoV

Identifiers

PMID32510973
PMCPMC7381712
OpenAlexW3033090821

What OpenQuestion holds

Textmetadata
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.