Chloroquine inhibits Spring viremia of carp virus replication by modulating autophagy and metabolic pathways
5 affiliations
- 1College of Animal Science and Technology, Yangzhou University
- 2State Key Laboratory of Breeding Biotechnology and Sustainable Aquaculture, Institute of Hydrobiology, Chinese Academy of Sciences
- 3University of Chinese Academy of Sciences
- 4Innovative Academy of Seed Design, Chinese Academy of Sciences
- 5Yizheng Water World Agricultural Ecological Park Co., Ltd
Abstract
Spring viremia of carp virus (SVCV) severely threatens cyprinid aquaculture, yet the role of autophagy in SVCV infection remains unclear. Here, SVCV infection was associated with enhanced autophagic activity and autophagic flux in common carp and EPC cells. Pharmacological perturbation of autophagy revealed that rapamycin treatment increased SVCV gene expression and aggravated SVCV-induced cytopathic effects, whereas chloroquine blocked autophagic flux, suppressed viral gene expression, and mitigated virus-induced cellular damage. Transcriptomic analysis identified 1,868 differentially expressed genes after chloroquine treatment, with major changes in lysosome/autophagy-related pathways, glycan degradation, ion transport, cell cycle, DNA replication, and DNA repair. Metabolomic and integrated multi-omics analyses revealed changes in amino sugar and nucleotide sugar metabolism, steroid biosynthesis, riboflavin metabolism, and amino acid metabolism. Functional validation showed that diflorasone and all-trans-retinal reduced SVCV-G expression, alleviated cytopathic effects, and improved survival after SVCV infection. These findings suggest that SVCV infection is associated with enhanced autophagic flux, whereas chloroquine treatment blocks autophagic flux and is accompanied by reduced SVCV gene expression.
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BibTeX
@article{zhu2026chloroquine,
title = {{Chloroquine inhibits Spring viremia of carp virus replication by modulating autophagy and metabolic pathways}},
author = {Yuchao Zhu and Shuyang Chen and Yue Wang and Jian Shen and Libo He and Yaping Wang and Dong Wang and Shuyan Miao and Guobin Chang and Pengfei Chu},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1920055},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1920055/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Chloroquine inhibits Spring viremia of carp virus replication by modulating autophagy and metabolic pathways
AU - Yuchao Zhu
AU - Shuyang Chen
AU - Yue Wang
AU - Jian Shen
AU - Libo He
AU - Yaping Wang
AU - Dong Wang
AU - Shuyan Miao
AU - Guobin Chang
AU - Pengfei Chu
PY - 2026
DA - 2026/10/07
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1920055
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1920055/full
AB - Spring viremia of carp virus (SVCV) severely threatens cyprinid aquaculture, yet the role of autophagy in SVCV infection remains unclear. Here, SVCV infection was associated with enhanced autophagic activity and autophagic flux in common carp and EPC cells. Pharmacological perturbation of autophagy revealed that rapamycin treatment increased SVCV gene expression and aggravated SVCV-induced cytopathic effects, whereas chloroquine blocked autophagic flux, suppressed viral gene expression, and mitigated virus-induced cellular damage. Transcriptomic analysis identified 1,868 differentially expressed genes after chloroquine treatment, with major changes in lysosome/autophagy-related pathways, glycan degradation, ion transport, cell cycle, DNA replication, and DNA repair. Metabolomic and integrated multi-omics analyses revealed changes in amino sugar and nucleotide sugar metabolism, steroid biosynthesis, riboflavin metabolism, and amino acid metabolism. Functional validation showed that diflorasone and all-trans-retinal reduced SVCV-G expression, alleviated cytopathic effects, and improved survival after SVCV infection. These findings suggest that SVCV infection is associated with enhanced autophagic flux, whereas chloroquine treatment blocks autophagic flux and is accompanied by reduced SVCV gene expression.
SN - 1664-3224
ER -