PUBLICATION

pIgR-like4.2 enhances the antiviral immune response of zebrafish against spring viremia of carp virus

Authors
Chen, X., Cai, C., Li, S., Shi, Y., Zhang, Q., Cheng, G., Kong, W., Huang, Y., Xu, Z.
ID
ZDB-PUB-250419-5
Date
2025
Source
Fish & shellfish immunology : 110350110350 (Journal)
Registered Authors
Xu, Zhen
Keywords
CRISPR/Cas9, IFN, SVCV, Zebrafish, pIgRL4.2
MeSH Terms
  • Rhabdoviridae/physiology
  • Animals
  • Fish Proteins*/genetics
  • Fish Proteins*/immunology
  • Receptors, Polymeric Immunoglobulin*/genetics
  • Receptors, Polymeric Immunoglobulin*/immunology
  • Carps
  • Zebrafish*/genetics
  • Zebrafish*/immunology
  • Rhabdoviridae Infections*/immunology
  • Rhabdoviridae Infections*/veterinary
  • Rhabdoviridae Infections*/virology
  • Fish Diseases*/immunology
  • Fish Diseases*/virology
  • Immunity, Innate*/genetics
PubMed
40250506 Full text @ Fish Shellfish Immunol.
Abstract
The mucosal immune system plays a critical role in defending the body against external pathogens and preserving homeostasis. The polymeric immunoglobulin receptor (PIGR) is a critical component of this system, responsible for facilitating the transport and secretion of soluble polymeric immunoglobulins across epithelial cells, thereby contributing to immune defense. In zebrafish, a pIgR-like (pIgRL) family exists, among which pIgRL4.2 is highly expressed in multiple immune organs, suggesting its potential role in immunity. In this study, spring viremia of carp virus (SVCV) infection significantly downregulates pIgRL4.2 expression. Conversely, overexpression of pIgRL4.2 in EPC cells markedly delays SVCV-induced cytopathic effects and effectively suppresses SVCV replication. Additionally, overexpression of pIgRL4.2 enhances IFN activation induced by both poly(I:C) treatment and SVCV infection. Furthermore, CRISPR/Cas9 was used to generate pIgRL4.2-null zebrafish, and disruption of pIgRL4.2 in zebrafish has been demonstrated to result in a reduction in survival rates following SVCV challenge. This is accompanied by a consistent downregulation of antiviral responsive genes, concomitant with an increase in SVCV replication in pIgRL4.2-deficient zebrafish. Therefore, this study demonstrates that pIgRL4.2 inhibits viral replication by positively regulating the IFN signaling pathway.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping