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Feb 20, 2025;17 (3):

Early Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Infection Induces Necroptosis in Immune Cells of Peripheral Lymphoid Organs.

Jiawei Xu, Caiyun Huo, Yaling Yang, Jun Han, Lei Zhou, Yanxin Hu, Hanchun Yang
Author Information
  1. Jiawei Xu: Key Laboratory of Animal Epidemiology of Ministry of Agriculture and Rural Affairs, National Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, No. 2 Yuanmingyuan West Road, Beijing 100193, China.
  2. Caiyun Huo: Key Laboratory of Animal Epidemiology of Ministry of Agriculture and Rural Affairs, National Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, No. 2 Yuanmingyuan West Road, Beijing 100193, China.
  3. Yaling Yang: Key Laboratory of Animal Epidemiology of Ministry of Agriculture and Rural Affairs, National Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, No. 2 Yuanmingyuan West Road, Beijing 100193, China.
  4. Jun Han: Key Laboratory of Animal Epidemiology of Ministry of Agriculture and Rural Affairs, National Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, No. 2 Yuanmingyuan West Road, Beijing 100193, China. ORCID
  5. Lei Zhou: Key Laboratory of Animal Epidemiology of Ministry of Agriculture and Rural Affairs, National Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, No. 2 Yuanmingyuan West Road, Beijing 100193, China. ORCID
  6. Yanxin Hu: Key Laboratory of Animal Epidemiology of Ministry of Agriculture and Rural Affairs, National Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, No. 2 Yuanmingyuan West Road, Beijing 100193, China. ORCID
  7. Hanchun Yang: Key Laboratory of Animal Epidemiology of Ministry of Agriculture and Rural Affairs, National Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, No. 2 Yuanmingyuan West Road, Beijing 100193, China. ORCID
PMID: 40143222 DOI: 10.3390/v17030290

Abstract

The highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) has caused huge economic losses to the pig industry in China. This study evaluated the damage to peripheral immune tissues in the early infection of HP-PRRSV, including the hilar lymph nodes, mandibulares lymph nodes, inguinales superficials lymph nodes, spleens, and tonsils. HP-PRRSV infection led to a reduction in CD4 and CD8 T cells, as well as CD19 B cells, in the tonsils. Additionally, CD163 macrophages and CD56 NK cells increased in all peripheral lymphoid organs, with NK cells migrating toward the lymphoid follicles. However, no significant changes were observed in CD11c dendritic cells. RNA-seq analysis showed the down-regulation of T and B cell functions, while macrophage and NK cell functions were enhanced. Gene Ontology (GO) and KEGG pathway analysis indicated the up-regulation of necroptosis processes. Western blotting and immunofluorescence confirmed that HP-PRRSV induced PKR-mediated necroptosis in immunocytes. This study provides new insights into the effects of early HP-PRRSV infection on peripheral immune organs, highlighting dynamic shifts in immune cell populations, virus-induced immunosuppression, and the role of PKR-mediated necroptosis. These findings improve our understanding of the immunomodulation induced by PRRSV infection.

Keywords

highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) immune cell necroptosis peripheral lymphoid organs

References

  1. Vet Microbiol. 1997 May;56(1-2):9-19 [PMID: 9228678]
  2. Int Rev Immunol. 1990;6(2-3):151-61 [PMID: 1967103]
  3. Vet Res. 2017 Feb 27;48(1):15 [PMID: 28241868]
  4. Immunity. 2023 Aug 8;56(8):1778-1793.e10 [PMID: 37463581]
  5. Vet Microbiol. 2022 Sep;272:109498 [PMID: 35793585]
  6. PLoS One. 2015 Sep 23;10(9):e0138772 [PMID: 26397116]
  7. Eur J Immunol. 2023 Dec;53(12):e2250218 [PMID: 36792132]
  8. J Clin Invest. 2020 Apr 1;130(4):2111-2128 [PMID: 31961824]
  9. Trends Immunol. 2001 Nov;22(11):633-40 [PMID: 11698225]
  10. PLoS One. 2013 Jun 24;8(6):e66645 [PMID: 23826108]
  11. J Virol. 2022 Jul 27;96(14):e0212721 [PMID: 35758658]
  12. Viruses. 2022 Feb 22;14(3): [PMID: 35336858]
  13. Vet Sci. 2019 Mar 11;6(1): [PMID: 30862035]
  14. Theranostics. 2022 Jan 1;12(3):1267-1285 [PMID: 35154486]
  15. Vet Microbiol. 2017 Oct;210:124-133 [PMID: 29103681]
  16. Vet Microbiol. 2016 Jun 30;189:75-85 [PMID: 27259830]
  17. Front Immunol. 2022 Oct 20;13:960709 [PMID: 36341362]
  18. Cell Host Microbe. 2021 Jul 14;29(7):1186-1198.e8 [PMID: 34043960]
  19. Vaccines (Basel). 2020 Oct 09;8(4): [PMID: 33050150]
  20. Vet Microbiol. 2020 Apr;243:108639 [PMID: 32273018]
  21. Vet Res. 2021 Jan 22;52(1):12 [PMID: 33482914]
  22. J Virol. 2019 Sep 30;93(20): [PMID: 31341055]
  23. Viruses. 2020 Oct 31;12(11): [PMID: 33142752]
  24. Genome Biol. 2014;15(12):550 [PMID: 25516281]
  25. Int J Biol Sci. 2019 Jan 1;15(2):481-492 [PMID: 30745836]
  26. Virol J. 2015 Nov 14;12:185 [PMID: 26573719]
  27. Int J Biol Sci. 2019 Jul 25;15(9):1993-2005 [PMID: 31523199]
  28. J Virol. 2019 Aug 13;93(17): [PMID: 31189711]
  29. Cell Res. 2016 Sep;26(9):1007-20 [PMID: 27573174]
  30. Transbound Emerg Dis. 2013 Aug;60(4):351-9 [PMID: 22762447]
  31. Anal Bioanal Chem. 2021 Sep;413(23):5799-5810 [PMID: 34331087]
  32. Commun Biol. 2022 Jul 7;5(1):674 [PMID: 35798936]
  33. Virol J. 2014 Jan 06;11:2 [PMID: 24393149]
  34. Nat Commun. 2015 Feb 18;6:6282 [PMID: 25693118]
  35. Vet Microbiol. 2017 Mar;201:126-135 [PMID: 28284598]
  36. Immunity. 2017 Nov 21;47(5):820-833 [PMID: 29166586]
  37. Cell Rep. 2022 Nov 29;41(9):111764 [PMID: 36450255]
  38. Viruses. 2022 Jan 18;14(2): [PMID: 35215760]
  39. Cell. 2012 Jul 20;150(2):339-50 [PMID: 22817896]
  40. Nature. 2020 Apr;580(7803):391-395 [PMID: 32296175]
  41. Signal Transduct Target Ther. 2022 Jun 20;7(1):196 [PMID: 35725836]
  42. Vet Immunol Immunopathol. 2011 Aug 15;142(3-4):170-8 [PMID: 21612828]
  43. J Gen Virol. 2016 Jun;97(6):1356-1361 [PMID: 26963602]
  44. Front Microbiol. 2023 Apr 27;14:1159590 [PMID: 37180243]
  45. Vet Microbiol. 2018 Mar;216:85-92 [PMID: 29519531]
  46. Proc Natl Acad Sci U S A. 2013 Aug 13;110(33):E3109-18 [PMID: 23898178]

Grants

  1. 32372966/National Natural Science Foundation of China
  2. 32330106/National Natural Science Foundation of China
  3. CARS-35/China Agriculture Research System of MOF and MARA

MeSH Term

Animals
Porcine respiratory and reproductive syndrome virus
Swine
Porcine Reproductive and Respiratory Syndrome
Necroptosis
Lymphoid Tissue
Killer Cells, Natural
Macrophages
Lymph Nodes
B-Lymphocytes
Spleen
Palatine Tonsil
Journal Article

Word Cloud

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