ArticleViruses2016
Porcine Circovirus 2 Deploys PERK Pathway and GRP78 for Its Enhanced Replication in PK-15 Cells.
Article in Viruses, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 91 citations in OpenAlex.
- A multi species autophagy-inducing nano-vaccine platform: uncovering immunoenhancement properties of PCV2 cap nanoparticles.Journal of nanobiotechnology · 2026Article
- Pseudorabies virus infection induces lymphocyte depletion associated with cellular apoptosis and endoplasmic reticulum stress in the mouse spleen.BMC veterinary research · 2025Article
- PCV2 Infection Upregulates SOCS3 Expression to Facilitate Viral Replication in PK-15 Cells.Viruses · 2025Article
- Seneca Valley virus induces mitochondrial apoptosis by activating ER stress or the PERK pathway based on CaJournal of virology · 2025Article
- The roles and mechanisms of endoplasmic reticulum stress-mediated autophagy in animal viral infections.Veterinary research · 2024Review
- ATF4 Signaling in HIV-1 Infection: Viral Subversion of a Stress Response Transcription Factor.Biology · 2024Review
- Mechanisms of circovirus immunosuppression and pathogenesis with a focus on porcine circovirus 2: a review.The veterinary quarterly · 2023Review
- Porcine epidemic diarrhea virus activates PERK-ROS axis to benefit its replication in Vero E6 cells.Veterinary research · 2023Article
- Matrine combined with Osthole inhibited the PERK apoptosis of splenic lymphocytes in PCV2-infected mice model.BMC veterinary research · 2023Article
- Endoplasmic Reticulum Stress in Elderly Patients with COVID-19: Potential of Melatonin Treatment.Viruses · 2023Review
- Porcine Circovirus Type 2 Hijacks Host IPO5 to Sustain the Intracytoplasmic Stability of Its Capsid Protein.Journal of virology · 2022Article
- Review
- Porcine Circovirus 2 Activates the PERK-Reactive Oxygen Species Axis To Induce p53 Phosphorylation with Subsequent Cell Cycle Arrest at S Phase in Favor of Its Replication.Journal of virology · 2022Article
- Induction and modulation of the unfolded protein response during porcine deltacoronavirus infection.Veterinary microbiology · 2022Article
- Review
- PCV2 and PRV Coinfection Induces Endoplasmic Reticulum Stress via PERK-eIF2α-ATF4-CHOP and IRE1-XBP1-EDEM Pathways.International journal of molecular sciences · 2022Article
- Article
- Classical swine fever virus employs the PERK- and IRE1-dependent autophagy for viral replication in cultured cells.Virulence · 2021Article
- Porcine Circovirus 2 Manipulates the PERK-ERO1α Axis of the Endoplasmic Reticulum To Favor Its Replication by Derepressing Viral DNA from HMGB1 Sequestration within Nuclei.Journal of virology · 2021Article
- The Regulation of Integrated Stress Response Signaling Pathway on Viral Infection and Viral Antagonism.Frontiers in microbiology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porcine circovirus type 2 (PCV2) infection induces autophagy and apoptosis. These cellular responses could be connected with endoplasmic reticulum (ER) stress. It remains unknown if PCV2 induces ER stress and if autophagy or apoptosis is primary to PCV2 infection or secondary responses following ER stress. Here, we demonstrate that PCV2 triggered unfolded protein response (UPR) in PK-15 cells by activating the PERK/eIF2α pathway without concomitant activation of IRE1 or ATF6. Since ATF4 and CHOP were induced later than PERK/eIF2α, it is clear that persistent PCV2 infection could lead to selective activation of PERK via the PERK-eIF2α-ATF4-CHOP axis. Therefore, PERK activation could be part of the pro-apoptotic signaling via induced expression of CHOP by PCV2. Since PERK inhibition by GSK2606414 or RNA silencing or suppression of eIF2α dephosphorylation by salubrinal limited viral replication, we suppose that PCV2 deploys UPR to enhance its replication. Over-expression of GRP78 or treatment with tauroursodeoxycholic acid could enhance viral capsid expression and/or viral titers, indicating that these chaperones, endogenous or exogenous, could help correct folding of viral proteins. Our findings provide the first evidence that ER stress plays a role in the pathogenesis of PCV2 infection probably as part of autophagic and apoptotic responses.
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