ArticleJournal of virology2009
Severe acute respiratory syndrome coronavirus triggers apoptosis via protein kinase R but is resistant to its antiviral activity.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
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Who cites it
89 citing papers in PubMed, 147 citations in OpenAlex.
- Human coronaviruses: activation and antagonism of innate immune responses.Microbiology and molecular biology reviews : MMBR · 2025Review
- Coronavirus endoribonuclease antagonizes ZBP1-mediated necroptosis and delays multiple cell death pathways.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Swine Acute Diarrhea Syndrome Coronavirus: An Overview of Virus Structure and Virus-Host Interactions.Animals : an open access journal from MDPI · 2025Review
- Indomethacin inhibits human seasonal coronaviruses at late stages of viral replication in lung cells: Impact on virus-induced COX-2 expression.Journal of virus eradication · 2024Article
- NS7a of SADS-CoV promotes viral infection via inducing apoptosis to suppress type III interferon production.Journal of virology · 2024Article
- Machine Learning to Identify Critical Biomarker Profiles in New SARS-CoV-2 Variants.Microorganisms · 2024Article
- Innate IRE1α-XBP1 activation by viral single-stranded RNA and its influence on lung cytokine production during SARS-CoV-2 pneumonia.Genes and immunity · 2024Article
- Human Betacoronavirus OC43 Interferes with the Integrated Stress Response Pathway in Infected Cells.Viruses · 2024Article
- SARS-CoV-2 variant-specific differences in inhibiting the effects of the PKR-activated integrated stress response.Virus research · 2024Article
- Coronavirus takeover of host cell translation and intracellular antiviral response: a molecular perspective.The EMBO journal · 2024Review
- Human Challenge Studies with Coronaviruses Old and New.Current topics in microbiology and immunology · 2024Review
- Molecular mechanisms of human coronavirus NL63 infection and replication.Virus research · 2023Review
- SARS-CoV-2 Harnesses Host Translational Shutoff and Autophagy To Optimize Virus Yields: the Role of the Envelope (E) Protein.Microbiology spectrum · 2023Article
- Self-amplifying RNA vaccine protects mice against lethal Ebola virus infection.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Role of different types of RNA molecules in the severity prediction of SARS-CoV-2 patients.Pathology, research and practice · 2023Article
- Immunometabolic interference between cancer and COVID-19.Frontiers in immunology · 2023Article
- Ebola Virus Activates IRE1α-DependentViruses · 2022Article
- RNASeq profiling of COVID19-infected patients identified an EIF2AK2 inhibitor as a potent SARS-CoV-2 antiviral.Clinical and translational medicine · 2022Article
- Review
- Type-I interferons in the immunopathogenesis and treatment of Coronavirus disease 2019.European journal of pharmacology · 2022Review
29 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, infection of 293/ACE2 cells with severe acute respiratory syndrome coronavirus (SARS-CoV) activated several apoptosis-associated events, namely, cleavage of caspase-3, caspase-8, and poly(ADP-ribose) polymerase 1 (PARP), and chromatin condensation and the phosphorylation and hence inactivation of the eukaryotic translation initiation factor 2alpha (eIF2alpha). In addition, two of the three cellular eIF2alpha kinases known to be virus induced, protein kinase R (PKR) and PKR-like endoplasmic reticulum kinase (PERK), were activated by SARS-CoV. The third kinase, general control nonderepressible-2 kinase (GCN2), was not activated, but late in infection the level of GCN2 protein was significantly reduced. Reverse transcription-PCR analyses revealed that the reduction of GCN2 protein was not due to decreased transcription or stability of GCN2 mRNA. The specific reduction of PKR protein expression by antisense peptide-conjugated phosphorodiamidate morpholino oligomers strongly reduced cleavage of PARP in infected cells. Surprisingly, the knockdown of PKR neither enhanced SARS-CoV replication nor abrogated SARS-CoV-induced eIF2alpha phosphorylation. Pretreatment of cells with beta interferon prior to SARS-CoV infection led to a significant decrease in PERK activation, eIF2alpha phosphorylation, and SARS-CoV replication. The various effects of beta interferon treatment were found to function independently on the expression of PKR. Our results show that SARS-CoV infection activates PKR and PERK, leading to sustained eIF2alpha phosphorylation. However, virus replication was not impaired by these events, suggesting that SARS-CoV possesses a mechanism to overcome the inhibitory effects of phosphorylated eIF2alpha on viral mRNA translation. Furthermore, our data suggest that viral activation of PKR can lead to apoptosis via a pathway that is independent of eIF2alpha phosphorylation.
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