ReviewiScience2020
Mitochondria: In the Cross Fire of SARS-CoV-2 and Immunity.
Review in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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.
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.
Who cites it
70 citing papers in PubMed.
- 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 · 2026Article
- Mitochondria in SARS-CoV-2 infection: Immune interactions and molecular approaches in the Post COVID-19 condition.Genetics and molecular biology · 2026Article
- Mitochondrial function is impaired in long COVID patients.Annals of medicine · 2025Observational
- Special Issue "Viral Infections and Host Immune Responses".International journal of molecular sciences · 2025Article
- Article
- Deep Learning-Based Automatic Segmentation and Analysis of Mitochondrial Damage by Zika Virus and SARS-CoV-2.Viruses · 2025Article
- Exploring DNA methylation, telomere length, mitochondrial DNA, and immune function in patients with Long-COVID.BMC medicine · 2025Article
- Review
- Long-term mitochondrial and metabolic impairment in lymphocytes of subjects who recovered after severe COVID-19.Cell biology and toxicology · 2025Article
- Peripheral blood, lung and brain gene signatures in recovered and deceased patients with COVID-19.In silico pharmacology · 2025Article
- Nanobody against SARS-CoV-2 non-structural protein Nsp9 inhibits viral replication in human airway epithelia.Molecular therapy. Nucleic acids · 2024Article
- Immune consequences of exercise in hypoxia: A narrative review.Journal of sport and health science · 2024Review
- Differential Mitochondrial, Oxidative Stress and Inflammatory Responses to SARS-CoV-2 Spike Protein Receptor Binding Domain in Human Lung Microvascular, Coronary Artery Endothelial and Bronchial Epithelial Cells.International journal of molecular sciences · 2024Article
- Tumor Necrosis Factor-α Receptor 1 Mediates Borna Disease Virus 1-Induced Changes in Peroxisomal and Mitochondrial Dynamics in Neurons.International journal of molecular sciences · 2024Article
- Mitochondria in COVID-19: from cellular and molecular perspective.Frontiers in physiology · 2024Review
- Differential effects of SARS-CoV-2 variants on central nervous system cells and blood-brain barrier functions.Journal of neuroinflammation · 2023Article
- Impact of peripheral mitochondrial DNA level on immune response after COVID-19 vaccination.iScience · 2023Article
- Pathophysiological involvement of host mitochondria in SARS-CoV-2 infection that causes COVID-19: a comprehensive evidential insight.Molecular and cellular biochemistry · 2023Review
- A Post-Pandemic Enigma: The Cardiovascular Impact of Post-Acute Sequelae of SARS-CoV-2.Circulation research · 2023Review
- Possible Pathogenesis and Prevention of Long COVID: SARS-CoV-2-Induced Mitochondrial Disorder.International journal of molecular sciences · 2023Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathophysiology, immune reaction, and differential vulnerability of different population groups and viral host immune system evasion strategies of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are not yet well understood. Here, we reviewed the multitude of known strategies of coronaviruses and other viruses to usurp mitochondria-associated mechanisms involved in the host innate immune response and put them in context with the current knowledge on SARS-CoV-2. We argue that maintenance of mitochondrial integrity is essential for adequate innate immune system responses and to blunt mitochondrial modulation by SARS-CoV-2. Mitochondrial health thus may determine differential vulnerabilities to SARS-CoV-2 infection rendering markers of mitochondrial functions promising potential biomarkers for SARS-CoV-2 infection risk and severity of outcome. Current knowledge gaps on our understanding of mitochondrial involvement in SARS-CoV-2 infection, lifestyle, and pharmacological strategies to improve mitochondrial integrity and potential reciprocal interactions with chronic and age-related diseases, e.g., Parkinson disease, are pointed out.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.