Journal of veterinary science · 2026
Transcriptomic sequencing reveals critical role of STING pathway in PPRV-infected goat endometrial epithelial cells.
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Liu Mengyuan, Chen Yaqi, Guo Yixian, Wang Xiaoge, Wu Minrui, Yang Xiaozhu, Wang Chenyang, Yin Hanwei, Wen Bo, Wang Hongnuan, Sun Zilong, Zhang Ding, Wang Jingyu, Gu Shaopeng, Yang Bo, Li Wei
Аннотация
IMPORTANCE: Peste des petits ruminants virus (PPRV) is the causative agent of peste des petits ruminants (PPR), a highly contagious disease in small ruminants that causes massive economic losses worldwide. Despite its impact, the mechanisms underlying PPRV infections remain elusive, hindering its control and prevention.
OBJECTIVE: This study examined the molecular mechanisms underlying PPRV infections by investigating the transcriptomic changes in PPRV-infected goat endometrial epithelial cells (EECs) and clarifying the regulatory role of the stimulator of interferon genes (STING) signaling pathway in PPRV replication.
METHODS: Transcriptome sequencing was performed on EECs at 72 h after a PPRV infection. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were conducted on the identified differentially expressed genes (DEGs). Western blot analysis was used to detect STING and p-TBK1 expression in various cell lines at different time points after the PPRV infection. The effects of STING on PPRV replication were evaluated by STING overexpression and knockdown using quantitative real-time polymerase chain reaction, immunofluorescence, and 50% tissue culture infectious dose (TCID₅₀) assay.
RESULTS: A total of 1946 DEGs (1,078 up-regulated and 868 down-regulated) were identified in PPRV-infected EECs. GO and KEGG enrichment analysis showed that the DEGs were significantly enriched in terms related to immune response. Western blot analysis showed that PPRV promotes STING and p-TBK1 expression. Specifically, overexpression of STING significantly enhanced PPRV-N protein levels (p < 0.05) and viral titers (p < 0.05) in Vero CCL-81 cells and glomerular microvascular endothelial cells, whereas knockdown of STING decreased viral protein expression (p < 0.05) and viral titers (p < 0.05) in these cells.
CONCLUSIONS AND RELEVANCE: A PPRV infection activates the STING pathway, which facilitates viral replication. This finding helps reveal the pathogenesis of PPRV and provides a theoretical basis for the prevention and control of PPR.
OBJECTIVE: This study examined the molecular mechanisms underlying PPRV infections by investigating the transcriptomic changes in PPRV-infected goat endometrial epithelial cells (EECs) and clarifying the regulatory role of the stimulator of interferon genes (STING) signaling pathway in PPRV replication.
METHODS: Transcriptome sequencing was performed on EECs at 72 h after a PPRV infection. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were conducted on the identified differentially expressed genes (DEGs). Western blot analysis was used to detect STING and p-TBK1 expression in various cell lines at different time points after the PPRV infection. The effects of STING on PPRV replication were evaluated by STING overexpression and knockdown using quantitative real-time polymerase chain reaction, immunofluorescence, and 50% tissue culture infectious dose (TCID₅₀) assay.
RESULTS: A total of 1946 DEGs (1,078 up-regulated and 868 down-regulated) were identified in PPRV-infected EECs. GO and KEGG enrichment analysis showed that the DEGs were significantly enriched in terms related to immune response. Western blot analysis showed that PPRV promotes STING and p-TBK1 expression. Specifically, overexpression of STING significantly enhanced PPRV-N protein levels (p < 0.05) and viral titers (p < 0.05) in Vero CCL-81 cells and glomerular microvascular endothelial cells, whereas knockdown of STING decreased viral protein expression (p < 0.05) and viral titers (p < 0.05) in these cells.
CONCLUSIONS AND RELEVANCE: A PPRV infection activates the STING pathway, which facilitates viral replication. This finding helps reveal the pathogenesis of PPRV and provides a theoretical basis for the prevention and control of PPR.