Senecavirus A
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ABSTRACT:
PROVIDER: PRJNA1245008 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the mRNA m6A modification profiling in Mesocricetus auratus cells that infected with Senecavirus, we used passage-5 Senecavirus A to infect BSR-T7/5 cells. We then performed m6A MeRIP-seq(GenSeq®️ m6A MeRIP Kit) at at two time points (12hrs or 72 hrs after infection), each time point with three replicates.
2022-06-30 | GSE206974 | GEO
Project description:Senecavirus A isolate:SVA-715 Genome sequencing
| PRJNA353236 | ENA
Project description:Senecavirus A (SVA) belongs to the family of small RNA viruses, the genus Senecavirus, and has become a research hotspot because of the oncolytic viral characteristics. PIWI-interacting RNAs (piRNAs) are a class of small RNAs found in mammalian cells in recent years; however, the host piRNA expression profile during SVA infection and their role in viral infection is not well understood. In this study, we obtained small RNA transcriptome expression profiles from SVA-infected pig kidney cell lines (PK-15) by high-throughput sequencing. Differential expression (DE) analysis, GO annotation, and KEGG analysis of piRNAs in SVA-infected and non-infected PK-15 cells were performed. qRT-PCR was used to validate the DE of piRNAs. The results showed that 981 and 1,370 novel piRNAs were identified in SVA-infected and non-infected PK-15 cells; expression of 129 piRNAs was upregulated while that of 44 piRNAs was downregulated after SVA infection. The DE of 10 piRNAs was further verified by qRT-PCR. GO annotation analysis results showed the metabolism, proliferation, and differentiation were significantly activated after SVA infection. KEGG results showed that after SVA infection, piRNA was mainly enriched in AMPK signaling pathway, Rap1 signaling pathway, circadian rhythm, and VEGF signaling pathway, which suggested that piRNAs may play a role in regulating antiviral immunity, intracellular homeostasis, and tumor processes during SVA infection. This is the first report of the piRNA transcriptome in pig kidney cells and will contribute to the research of piRNA regulatory mechanism during SVA infections and provide an important reference for the prevention and treatment of SVA.
2023-01-05 | GSE222010 | GEO
Project description:Senecavirus A strain:SVA/MN/US/2015 Genome sequencing and assembly
| PRJNA553255 | ENA
Project description:Study of Conserved Motifs in Senecavirus A Genome
| PRJNA1328620 | ENA
Project description:Ribosome sequencing (Ribo-seq) technology was employed to analyze key sequences regulating translation elongation in the Senecavirus A (SVA) genome and to evaluate their impact on viral replication, thereby providing a theoretical foundation for elucidating the molecular mechanisms of SVA.First, the translation rate of the whole genome of SVA was analyzed using rSVA-GFP as a model via Ribo-seq technology. Based on the significant ribosome enrichment peaks detected by Ribo-seq, synonymous mutations were introduced into the corresponding sequences. After chemical synthesis, these sequences were substituted into the full-length cDNA backbone to obtain recombinant plasmids. Subsequently, reverse genetics was employed to transfect the plasmid into BHK-21 cells to rescue the replication-competent recombinant virus. A series of experiments, including blind passage, RT-PCR, Sanger sequencing, and growth curve analysis, were conducted on the recombinant virus to characterize its biological properties. Representative recombinant viruses were selected for secondary Ribo-seq analysis to elucidate the effects of the modification site on viral replication and protein translation.Ribo-seq data revealed significant ribosomal translation -stall peaks in VP1, 2C, and 3D genes, suggesting that key motifs impeding ribosomal translocation may be present in these regions. It was hypothesized that these regions may contain key motifs that impede ribosomal translocation. To test this hypothesis, these regions were further synonymously mutated to construct recombinant viruses. The results indicated that only the mutant in the 3D region successfully rescued replication-competent viruse that remained genetically stable through 20 passages and had no significant impact on viral growth kinetics. It suggested that the motifs in the 3D region were nonessential for viral replication. In contrast, the motifs, corresponding to the Ribo-seq-specific peaks in the VP1 and 2C regions, were essential for viral replication. The further Ribo-seq analysis of the rescued virus revealed the absence of ribosomal stalling peaks in both the 2C and 3D regions. This suggested that the key motifs in the 2C region, if any, were not the sole determinant of the translation rate of viral proteins. In contrast, disrupting any such structures in the 3D region did not impact viral replication but could affect the rates of viral protein translation.
2025-09-20 | GSE308036 | GEO