ReviewThe Journal of general virology2023
SARS-CoV-2 and the DNA damage response.
Review in The Journal of general virology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 20 citations in OpenAlex.
- hnRNPC facilitates coronavirus replication by directly binding the frameshift-stimulatory element of viral genomic RNA.PLoS pathogens · 2026Article
- Integrative Multidimensional Profiling of Individuals Recovered from Mild COVID-19 Reveals Immune-Metabolic-Oxidative Network Interactions.International journal of molecular sciences · 2026Article
- Interactomics of SARS-CoV-2 Macrodomain 1 Reveals Putative Clients of ADP-Ribosyl Hydrolase Activity.Viruses · 2026Article
- Plasma Ceramides Levels in Severe COVID-19 Disease: Correlations with Survival.Open forum infectious diseases · 2026Article
- COVID vaccination and post-infection cancer signals: Evaluating patterns and potential biological mechanisms.Oncotarget · 2026Review
- SARS-CoV-2-induced damage to rat cortical neuronal networks ex vivo is mediated by the pro-inflammatory activation of the cGAS-STING pathway.Journal of neurovirology · 2025Article
- Identification and mechanism analysis of biomarkers related to butyrate metabolism in COVID-19 patients.Annals of medicine · 2025Article
- Presence of SARS-CoV-2 in fetal organs via intraamniotic infection.Nature communications · 2025Article
- Minimalistic transcriptomic signatures permit accurate early prediction of COVID-19 mortality.JCI insight · 2025Article
- Interactomics of SARS-CoV-2 Macrodomain 1 Reveals Putative Clients of ADP-ribosyl Hydrolase Activity.bioRxiv : the preprint server for biology · 2025Article
- Human protein interaction networks of ancestral and variant SARS-CoV-2 in organ-specific cells and bodily fluids.Nature communications · 2025Article
- Article
- Genetic and Epigenetic Intersections in COVID-19-Associated Cardiovascular Disease: Emerging Insights and Future Directions.Biomedicines · 2025Review
- Equivocating and Deliberating on the Probability of COVID-19 Infection Serving as a Risk Factor for Lung Cancer and Common Molecular Pathways Serving as a Link.Pathogens (Basel, Switzerland) · 2024Review
- Exploring the Relationship between Telomere Length and Cognitive Changes in Post-COVID-19 Subjects.Biomedicines · 2024Article
- DNA Damage in Moderate and Severe COVID-19 Cases: Relation to Demographic, Clinical, and Laboratory Parameters.International journal of molecular sciences · 2024Article
- P53-Independent G1-Cell Cycle Arrest Increases SARS-CoV-2 RNA Replication.Microorganisms · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The recent coronavirus disease 2019 (COVID-19) pandemic was caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is characterized by respiratory distress, multiorgan dysfunction and, in some cases, death. The virus is also responsible for post-COVID-19 condition (commonly referred to as 'long COVID'). SARS-CoV-2 is a single-stranded, positive-sense RNA virus with a genome of approximately 30 kb, which encodes 26 proteins. It has been reported to affect multiple pathways in infected cells, resulting, in many cases, in the induction of a 'cytokine storm' and cellular senescence. Perhaps because it is an RNA virus, replicating largely in the cytoplasm, the effect of SARS-Cov-2 on genome stability and DNA damage responses (DDRs) has received relatively little attention. However, it is now becoming clear that the virus causes damage to cellular DNA, as shown by the presence of micronuclei, DNA repair foci and increased comet tails in infected cells. This review considers recent evidence indicating how SARS-CoV-2 causes genome instability, deregulates the cell cycle and targets specific components of DDR pathways. The significance of the virus's ability to cause cellular senescence is also considered, as are the implications of genome instability for patients suffering from long COVID.
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.