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KLF16 inhibits PEDV replication by activating the type I IFN signaling pathway

Sujie Dong1, Ning Kong2, Haiyan Shen3

  • 1Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Shanghai, China; College of Animal Science, Tarim University, Xinjiang, China.

Veterinary Microbiology
|October 10, 2022
PubMed

Insights

Krüppel-like factor 16 (KLF16) inhibits porcine epidemic diarrhea virus (PEDV) replication by activating the type I interferon signaling pathway. This discovery offers new strategies for controlling PEDV.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Krüppel-like factors (KLFs) are implicated in various cancers.
  • The specific role of KLF16 in viral replication and type I interferon (IFN) signaling remains unclear.

Purpose of the Study:

  • To investigate the role of KLF16 in porcine epidemic diarrhea virus (PEDV) replication.
  • To elucidate the underlying signaling mechanisms involving type I IFN.

Main Methods:

  • Cell culture experiments using LLC-PK1 and Vero cells.
  • Analysis of KLF16 expression levels post-PEDV infection.
  • Overexpression and knockdown studies of KLF16.
  • Investigation of the TRAF6-pTBK1-pIRF3 signaling pathway.

Main Results:

  • KLF16 expression was downregulated upon PEDV infection.
  • Overexpression of KLF16 inhibited PEDV replication, while KLF16 knockdown promoted it.
  • KLF16 upregulates interferon (IFN) expression via the TRAF6-pTBK1-pIRF3 pathway.
  • KLF16 enhances the host's antiviral innate immune response.

Conclusions:

  • KLF16 plays a significant role in antiviral defense against PEDV.
  • KLF16 acts through the type I IFN signaling pathway to inhibit viral replication.
  • KLF16 presents a novel target for developing strategies to prevent and control PEDV infections.
Keywords:
IFNKLF16PEDVReplicationTRAF6

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