Bioproject ID: PRJNA597622


bioproject id PRJNA597622      to NCBI
key word Challenge; GCRV; autophagy; grass carp; grass carp reovirus; inflammatory responses; HEPATITIS-B-VIRUS; LC3; SUBVERSION; MECHANISMS; EXPRESSION; MACHINERY; ZEBRAFISH; PROTEINS; PATHWAY; SITE
experiment type challenge
publication Chu, P. , et al. "Autophagy Inhibits Grass Carp Reovirus (GCRV) Replication and Protects Ctenopharyngodon idella Kidney (CIK) Cells from Excessive Inflammatory Responses after GCRV Infection." Biomolecules 10.9(2025).
description To explore the related markers of disease resistance and growth in genome data, and then apply them to production and breeding
abstract Autophagy is an essential and highly conserved process in mammals, which is critical to maintaining physiological homeostasis, including cell growth, development, repair, and survival. However, the understanding of autophagy in fish virus replication is limited. In this study, we found that grass carp reovirus (GCRV) infection stimulated autophagy in the spleen of grass carp (Ctenopharyngodon idella). Moreover, both Western blot (WB) analysis and fluorescent tracer tests showed that GCRV infection induced the enhancement of autophagy activation in Ctenopharyngodon idella kidney (CIK) cells. Autophagy inducer rapamycin and autophagy inhibitor 3-MA pretreatment can inhibit and promote the proliferation of GCRV, respectively. In addition, grass carp autophagy-related gene 5 (CiATG5)-induced autophagy, as well as rapamycin, showed effects on GCRV replication in CIK cells. Transcriptome analysis revealed that the total number of differentially expressed genes (DEGs) in CiATG5 overexpression groups was less than that of the control during GCRV infection. Enrichment analysis showed that CiATG5 overexpression induced the enhancement of autophagy, lysosome, phagosome, and apoptosis in the early stage of GCRV infection, which led to the clearance of viruses. In the late stage, steroid biosynthesis, DNA replication, terpenoid backbone biosynthesis, and carbon metabolism were upregulated, which contributed to cell survival. Moreover, signaling pathways involved in the immune response and cell death were downregulated in CiATG5 overexpression groups. Further study showed that CiATG5 repressed the expression of inflammatory response genes, including cytokines and type I interferons. Taken together, the results demonstrate that autophagy represses virus replication and attenuates acute inflammatory responses to protect cells.


Sample Information


sample id sample name tissue strain treatment description
1. SRR10767221 GCRV_33 kidney cells Grass carp reovirus (GCRV) 6 hours after GCRV infecton of empty vector tansfected CIK cells nan
2. SRR10767224 GCRV_27 kidney cells Grass carp reovirus (GCRV) 0 hours after GCRV infecton of empty vector tansfected CIK cells nan
3. SRR10767225 GCRV_35 kidney cells Grass carp reovirus (GCRV) 6 hours after GCRV infecton of empty vector tansfected CIK cells nan
4. SRR10767226 GCRV_25 kidney cells Grass carp reovirus (GCRV) 0 hours after GCRV infecton of empty vector tansfected CIK cells nan
5. SRR10767222 GCRV_31 kidney cells Grass carp reovirus (GCRV) 6 hours after GCRV infecton of empty vector tansfected CIK cells nan
6. SRR10767223 GCRV_29 kidney cells Grass carp reovirus (GCRV) 0 hours after GCRV infecton of empty vector tansfected CIK cells nan