ArticleThe Journal of infectious diseases2007
Open reading frame 8a of the human severe acute respiratory syndrome coronavirus not only promotes viral replication but also induces apoptosis.
Article in The Journal of infectious diseases, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
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86 citing papers in PubMed, 122 citations in OpenAlex.
- PANoptosis as a Therapeutic Target for COVID-19.Current microbiology · 2026Review
- SADS-CoV NS3 induces apoptosis by blocking the formation of Bcl-xL-BAK complex.Journal of virology · 2026Article
- Roles of Reactive Oxygen Species in Relationships Between Viral Infections and Alzheimer's Disease and Related Dementia.Antioxidants (Basel, Switzerland) · 2026Review
- The citrus tristeza virus p33 protein functions as a viroporin.PLoS pathogens · 2025Article
- Spatial Transcriptomics and Single Cell-RNASeq Reveals Cellular Heterogeneity of SARS-CoV-2 in Lung Tissues and Global Mutational Patterns in COVID-19 Patients.Journal of medical virology · 2025Article
- Aggregation potency and proinflammatory effects of SARS-CoV-2 proteins.Scientific reports · 2025Article
- Immuno-epigenetic paradigms in coronavirus infection.Frontiers in immunology · 2025Review
- A glimpse into viral warfare: decoding the intriguing role of highly pathogenic coronavirus proteins in apoptosis regulation.Journal of biomedical science · 2024Review
- SARS-CoV-2 Viroporin E Induces CaInternational journal of molecular sciences · 2024Article
- Review
- SARS-CoV-2 Accessory Protein Orf7b Induces Lung Injury via c-Myc Mediated Apoptosis and Ferroptosis.International journal of molecular sciences · 2024Article
- The 29-nucleotide deletion in SARS-CoV: truncated versions of ORF8 are under purifying selection.BMC genomics · 2023Article
- Talk to Me-Interplay between Mitochondria and Microbiota in Aging.International journal of molecular sciences · 2023Review
- Possible Pathogenesis and Prevention of Long COVID: SARS-CoV-2-Induced Mitochondrial Disorder.International journal of molecular sciences · 2023Review
- Canine Coronavirus Infection Modulates the Biogenesis and Composition of Cell-Derived Extracellular Vesicles.Biomedicines · 2023Article
- Severe acute respiratory syndrome coronaviruses contributing to mitochondrial dysfunction: Implications for post-COVID complications.Mitochondrion · 2023Review
- Contribution to pathogenesis of accessory proteins of deadly human coronaviruses.Frontiers in cellular and infection microbiology · 2023Review
- Ubiquitination of SARS-CoV-2 ORF7a Prevents Cell Death Induced by Recruiting BclXL To Activate ER Stress.Microbiology spectrum · 2022Article
- Common mitochondrial haplogroups as modifiers of the onset-age for critical COVID-19.Mitochondrion · 2022Article
- The First Geographic Identification by Country of Sustainable Mutations of SARS-COV2 Sequence Samples: Worldwide Natural Selection Trends.bioRxiv : the preprint server for biology · 2022Article
26 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA unique genomic difference between human and civet severe acute respiratory syndrome coronaviruses (SARS-CoVs) is that the former has a deletion of 29 nucleotides from open reading frame (orf) 8a' that results in the generation of orf8a and orf8b. The objectives of the present study were to analyze antibody reactivity to ORF8a in patients with SARS and to elucidate the function of ORF8a.
methodsWestern-blot and immunofluorescent antibody assays were used to detect anti-ORF8a antibody. SARS-CoV HKU39849 was used to infect stable clones expressing ORF8a and cells transfected with small interfering RNA (siRNA). The virus loads (VLs) and cytopathic effects (CPEs) were recorded. Confocal microscopy and several mitochondria-related tests were used to study the function of ORF8a.
resultsTwo (5.4%) of 37 patients with SARS had anti-ORF8a antibodies. The VLs in the stable clones expressing ORF8a were significantly higher than those in control subjects 5 days after infection. siRNA against orf8a significantly reduced VLs and interrupted the CPE. ORF8a was found to be localized in mitochondria, and overexpression resulted in increases in mitochondrial transmembrane potential, reactive oxygen species production, caspase 3 activity, and cellular apoptosis.
conclusionsORF8a not only enhances viral replication but also induces apoptosis through a mitochondria-dependent pathway.
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