ArticlePLoS pathogens2011
Severe acute respiratory syndrome coronavirus envelope protein regulates cell stress response and apoptosis.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 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
142 citing papers in PubMed, 219 citations in OpenAlex.
- Large-scale genomic surveillance reveals immunosuppression drives mutation dynamics in persistent SARS-CoV-2 infections.Nature communications · 2026Article
- Interaction of coronavirus E protein with BRD2 plays important regulatory roles in viral replication and induction of pro-inflammatory response.Journal of virology · 2026Article
- Cell-cell fusion limits activation of the unfolded protein response induced by the Nipah virus glycoproteins.Journal of virology · 2026Article
- Article
- Article
- Coronaviruses in wild rodent and eulipotyphlan small mammals: a review of diversity, ecological implications and surveillance considerations.The Journal of general virology · 2025Review
- Human coronaviruses: activation and antagonism of innate immune responses.Microbiology and molecular biology reviews : MMBR · 2025Review
- Omics-based analysis of mitochondrial dysfunction and BBB integrity in post-COVID-19 sequelae.Scientific reports · 2024Article
- A glimpse into viral warfare: decoding the intriguing role of highly pathogenic coronavirus proteins in apoptosis regulation.Journal of biomedical science · 2024Review
- Developing inhibitory peptides against SARS-CoV-2 envelope protein.PLoS biology · 2024Article
- Research Advances on Swine Acute Diarrhea Syndrome Coronavirus.Animals : an open access journal from MDPI · 2024Review
- Antiviral responses in a Jamaican fruit bat intestinal organoid model of SARS-CoV-2 infection.Nature communications · 2023Article
- Deletion of a 7-amino-acid region in the porcine epidemic diarrhea virus envelope protein induces higher type I and III interferon responses and results in attenuationJournal of virology · 2023Article
- The unfolded protein response components IRE1α and XBP1 promote human coronavirus infection.mBio · 2023Article
- Article
- SARS-CoV-2 N protein enhances the anti-apoptotic activity of MCL-1 to promote viral replication.Signal transduction and targeted therapy · 2023Article
- Molecular mechanisms of human coronavirus NL63 infection and replication.Virus research · 2023Review
- Severe acute respiratory syndrome coronaviruses contributing to mitochondrial dysfunction: Implications for post-COVID complications.Mitochondrion · 2023Review
- Recent trends in next generation immunoinformatics harnessed for universal coronavirus vaccine design.Pathogens and global health · 2023Review
- Cellular Sensors and Viral Countermeasures: A Molecular Arms Race between Host and SARS-CoV-2.Viruses · 2023Review
82 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
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Severe acute respiratory syndrome virus (SARS-CoV) that lacks the envelope (E) gene (rSARS-CoV-ΔE) is attenuated in vivo. To identify factors that contribute to rSARS-CoV-ΔE attenuation, gene expression in cells infected by SARS-CoV with or without E gene was compared. Twenty-five stress response genes were preferentially upregulated during infection in the absence of the E gene. In addition, genes involved in signal transduction, transcription, cell metabolism, immunoregulation, inflammation, apoptosis and cell cycle and differentiation were differentially regulated in cells infected with rSARS-CoV with or without the E gene. Administration of E protein in trans reduced the stress response in cells infected with rSARS-CoV-ΔE or with respiratory syncytial virus, or treated with drugs, such as tunicamycin and thapsigargin that elicit cell stress by different mechanisms. In addition, SARS-CoV E protein down-regulated the signaling pathway inositol-requiring enzyme 1 (IRE-1) of the unfolded protein response, but not the PKR-like ER kinase (PERK) or activating transcription factor 6 (ATF-6) pathways, and reduced cell apoptosis. Overall, the activation of the IRE-1 pathway was not able to restore cell homeostasis, and apoptosis was induced probably as a measure to protect the host by limiting virus production and dissemination. The expression of proinflammatory cytokines was reduced in rSARS-CoV-ΔE-infected cells compared to rSARS-CoV-infected cells, suggesting that the increase in stress responses and the reduction of inflammation in the absence of the E gene contributed to the attenuation of rSARS-CoV-ΔE.
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.