Transcriptome profiling provided insights into the growth retardation and dwarfism caused by goose parvovirus in goslings

Keshan Zhang^1*Guangliang Gao¹Zhuping Chen¹Hongyuan zhang²Lecheng wang¹Xianzhi zhao¹Qin Li¹Hang Zhong¹Yi Luo¹Qigui Wang^1*

• ¹Chongqing Academy of Animal Science, Chongqing, China
• ²Southwest University, Chongqing, Chongqing Municipality, China

Goose parvovirus (GPV) poses a significant threat to the waterfowl industry, causing high mortality in goslings and stunted growth in survivors, leading to considerable economic losses.Despite its serious consequences, the molecular mechanisms underlying GPV-induced growth retardation and dwarfism remain poorly understood. Fourteen days post-infection with the GPV SYG61 strain, goslings exhibited a 63.33% mortality rate, along with dwarfism, significant weight loss, and severe histopathological lesions in the liver and jejunum. Serum analysis revealed a marked increase in the immunosuppressive factors TGF-β and IL-10 (p < 0.01 or p < 0.05), while pro-inflammatory cytokines such as IL-4, IFN-γ, TNF-α, and IgG remained unaffected.Additionally, GPV infection inhibited the proliferation of goose embryo fibroblasts (GEFs) and induced apoptosis, as evidenced by transcriptomic analysis, which identified 285 differentially expressed genes (DEGs). These DEGs were enriched in pathways involved in the negative regulation of cell proliferation (GO:0008285,19/276, LogP=-12.62) and skeletal system development (GO:0001501,25/227, LogP=-12.51) with key genes including IL6, CXCL8, PTGDS, PI15, MMP9, MMP13, MMP2, CCN3, and FAM180A. Further DEGs were linked to the IL-17 signaling pathway (hsa04657) and the regulation of programmed cell death (GO:0043068).Notably, GPV infection activated both apoptosis and ferroptosis through the upregulation of key regulatory genes such as PTGS2, TF, and ASCL1 (p < 0.01). These findings indicated that GPV infection triggers inflammatory responses and programmed cell death, leading to high mortality in goslings, disturbs the genes expression related to growth and skeletal development caused the growth retardation and dwarfism in infection survivors. This study provides valuable insights into the pathogenic mechanisms of GPV, offering potential strategies to mitigate its impact and improve the health and productivity of the waterfowl industry.