Classical swine fever virus infection suppresses claudin-1 expression to facilitate its replication in PK-15 cells

  • Microb Pathog. 2021 Aug;157:105012. doi: 10.1016/j.micpath.2021.105012.
Xiangmin Wang  1 ,  Yu'ai Yang  1 ,  Xiaoying Yang  1 ,  Xiao Liu  2 ,  Xiaochun Wang  1 ,  Libo Gao  1 ,  Chao Yang  1 ,  Rui Lan  1 ,  Junlong Bi  3 ,  Qian Zhao  4 ,  Guishu Yang  1 ,  Jing Wang  5 ,  Yingbo Lin  6 ,  Jianping Liu  7 ,  Gefen Yin  8
Affiliations
  • 1. College of Animal Veterinary Medicine, Yunnan Agricultural University, Kunming, 650201, Yunnan, China.
  • 2. College of Animal Veterinary Medicine, Yunnan Agricultural University, Kunming, 650201, Yunnan, China; Department of Oncology-Pathology, Karolinska Institutet, 17176, Stockholm, Sweden.
  • 3. Institute of Science and Technology, Chuxiong Normal University, 546 Lucheng South Rd, Chuxiong, 675000, Yunnna, China.
  • 4. Center for Animal Disease Control and Prevention, Chuxiong, 675000, Yunnan, China.
  • 5. School of Clinical Medicine, Dali University, Dali, 671003, Yunnan, China.
  • 6. Department of Oncology-Pathology, Karolinska Institutet, 17176, Stockholm, Sweden.
  • 7. School of Clinical Medicine, Dali University, Dali, 671003, Yunnan, China. Electronic address: [email protected].
  • 8. College of Animal Veterinary Medicine, Yunnan Agricultural University, Kunming, 650201, Yunnan, China. Electronic address: [email protected].
PMID: 34062228 DOI: 10.1016/j.micpath.2021.105012
Abstract

Classical swine fever (CSF) is one of the most epidemic viral diseases in swine industry. The causative pathogen is CSF virus (CSFV), a small enveloped RNA virus of Flaviviridae family. Claudin-1 was reported to be involved in the infections of a number of viruses, including many from Flaviviridae family, but no studies have investigated the role of porcine claudin-1 during CSFV Infection in PK-15 cells. In this study, on the one hand, we demonstrated that CSFV Infection reduced the claudin-1 expression at both mRNA and protein levels; on the Other hand, CSFV Infection was enhanced after claudin-1 knockdown, but inhibited by claudin-1 overexpression in a dose-dependent manner. Furthermore, negative correlation was demonstrated between the claudin-1 expression and CSFV titer. In conclusion, claudin-1 might be a barrier for CSFV Infection in PK-15 cells, while CSFV bypasses the barrier through lysosome mediated degradation of claudin-1, which could be repressed by bafilomycin A1. Although the elaborate mechanisms how claudin-1 plays its roles in CSFV Infection require further investigations, this study may advance our understanding of the molecular host-pathogen interaction mechanisms underlying CSFV Infection and suggests enhancement of porcine claudin-1 as a potential preventive or therapeutic strategy for CSF control.

Keywords
Classic swine fever virus; Claudin-1; Infection; Lysosome; NF-κB; PK-15 cells.
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