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Transcriptomic sequencing analysis of PPRV-infected goat endometrial epithelial cells and the critical role of the STING signaling pathway in PPRV infection

ABSTRACT: 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. 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. A total of 1946 DEGs (1,078 up-regulated and 868 down-regulated) were identifie in PPRV-infected EECs. GO and KEGG enrichment analysis showed that the DEGs were κB and tumor necrosis factor signaling pathways. Western blot analysis showed that PPRV promotes STING and p-TBK1 expression. Specifically, overexpression of STING significantl enhanced PPRV replication, while the knockdown of STING by specific siRNA markedly reduced STING protein expression and significantly decreased the PPRV-N protein levels and viral titer (TCID50) in Vero CCL-81 and glomerular microvascular endothelial cells.

ORGANISM(S): Capra hircus

PROVIDER: GSE343985 | GEO | 2026/08/20

REPOSITORIES: GEO

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Project description:Peste des petits ruminants virus (PPRV) infection causes highly contagious and severe disease in domestic and wild ruminants. It is widely reported that PRRV infection causes considerable innate immunosuppression in its host and promotes viral replication. However, how does the host rescue the innate immune response to counteract this immunosuppression during viral replication is poorly understood. The goat fetal fibroblasts (GFFs) have been commonly used as host-original cells to investigate the pathogenesis of PPRV. To explore the mechanisms of how host counteracts PPRV-mediated innate immunosuppression, a high-throughput quantitation proteomic approach (iTRAQ in conjunction with LC-MS/MS) was used to investigate the proteome landscape of GFFs in response to PPRV infection. Eventually, the proteomic analysis gained 497 up-regulated proteins and 358 down-regulated proteins (PPRV-infected cells versus mock-infected cells). The complement and coagulation cascades, protein digestion and absorption, and cytokine-cytokine receptor interaction pathways were significantly regulated in response to PPRV infection. ErmineJ analysis of the differentially expressed proteins (DEPs) identified the significantly enriched GO categories for response to interferon-gamma and positive regulation of ERK1 and ERK2 cascade. In addition, many immune related proteins, such as interferon gamma, 2'-5'-oligoadenylate synthase-like protein, toll-like receptor 9, toll-like receptor 6, NOD1, plasminogen activator inhibitor 1, and Wnt-5a were significantly upregulated. This suggested that the innate immune response was triggered during PPRV infection in GFFs. We subsequently identified that the E3 ubiquitin ligase FANCL was critically involved in regulation of the innate immune response during PPRV infection. FANCL inhibited PPRV infection by enhancing type I interferon (IFN) and interferon-stimulated genes (ISGs) expression. Further study indicated that FANCL induced type I IFN production by promoting TBK1 phosphorylation, and therefore impairing PPRV-mediated immunosuppression and revealing an antiviral function against PPRV.

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Transcriptomic sequencing analysis of PPRV-infected goat endometrial epithelial cells and the critical role of the STING signaling pathway in PPRV infection

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