ArticlePloS one2015
Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Infection Induced Apoptosis and Autophagy in Thymi of Infected Piglets.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 52 citations in OpenAlex.
- The mechanisms by which hypothalamic neuroinflammation induced by neonatal cerebral ischemia-hypoxia leads to decreased thymic function via the HPA axis.Cell & bioscience · 2026Article
- Quercetin Regulates Autophagy to Inhibit PRRSV Replication Through the PI3K/Akt/mTOR Signaling Pathway.Viruses · 2025Article
- Article
- Cytoplasmic translocation of tripartite motif-containing 28 is critical for PRRSV-induced autophagy through promoting Vps34-Beclin1 complex formation.Journal of virology · 2025Article
- Review
- Article
- METTL3 governs thymocyte development and thymic involution by regulating ferroptosis.Nature aging · 2024Article
- A Comprehensive Review on Porcine Reproductive and Respiratory Syndrome Virus with Emphasis on Immunity.Vaccines · 2024Review
- Molecular mechanism of autophagy in porcine reproductive and respiratory syndrome virus infection.Frontiers in cellular and infection microbiology · 2024Review
- Article
- Article
- Evasion strategies of porcine reproductive and respiratory syndrome virus.Frontiers in microbiology · 2023Review
- The Multi-Faceted Role of Autophagy During Animal Virus Infection.Frontiers in cellular and infection microbiology · 2022Review
- Virus, Exosome, and MicroRNA: New Insights into Autophagy.Advances in experimental medicine and biology · 2022Article
- Activation of regulated cell death in the lung of piglets infected with virulent PRRSV-1 Lena strain occurs earlier and mediated by cleaved Caspase-8.Veterinary research · 2021Article
- Infection-Associated Thymic Atrophy.Frontiers in immunology · 2021Review
- PRRSV Promotes MARC-145 Cells Entry Into S Phase of the Cell Cycle to Facilitate Viral ReplicationFrontiers in veterinary science · 2021Article
- Porcine Reproductive and Respiratory Syndrome Virus Promotes SLA-DR-Mediated Antigen Presentation of Nonstructural Proteins To Evoke a Nonneutralizing Antibody ResponseJournal of virology · 2020Article
- Molecular and Cellular Mechanisms for PRRSV Pathogenesis and Host Response to Infection.Virus research · 2020Review
- The tail domain of PRRSV NSP2 plays a key role in aggrephagy by interacting with 14-3-3ε.Veterinary research · 2020Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previously, we demonstrated that the highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) HuN4 strain causes obvious thymic atrophy and thymocytes apoptosis in infected piglets after birth, which is more severe than that induced by classical PRRSV. In this study, we investigated apoptosis and autophagy in the thymus of piglets infected with the HP-PRRSV HuN4 strain, and found that both apoptosis and autophagy occurred in the thymus of piglets infected with HP-PRRSV. In addition to a few virus-infected cells, CD14+ cells, the main autophagic cells in the thymus were thymic epithelial cells. These findings demonstrated that HP-PRRSV induces apoptosis in bystander cells, and induces autophagy in both infected and bystander cells in the thymus of infected piglets. Herein, we first present new data on the thymic lesions induced by HP-PRRSV, and show that apoptosis and autophagy are key mechanisms involved in cell survival and determinants of the severity of thymic atrophy in infected piglets. Finally, future studies of the mechanism underlying immune responses are proposed based on our current understanding of PRRSV-host interactions.
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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.