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Updated: Dec 16, 2025

Confocal Imaging of Double-Stranded RNA and Pattern Recognition Receptors in Negative-Sense RNA Virus Infection
Published on: January 26, 2019
Long non-coding RNAs are associated with Seneca Valley virus infection
Mengyan Zhu1, Yuchen Cai1, Wen Zhao1
1MOE Joint International Research Laboratory of Animal Health and Food Safety, Engineering Laboratory of Animal Immunity of Jiangsu Province, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
Seneca Valley virus (SVV) outbreaks cause significant pig industry losses. Researchers identified a specific long non-coding RNA (lncRNA), lnc-MSTRG.18940.1, that regulates immune responses and inhibits SVV replication.
Area of Science:
- Veterinary Virology
- Molecular Biology
- Immunology
Background:
- Sporadic Seneca Valley virus (SVV) outbreaks cause substantial economic losses in the swine industry.
- SVV infection in pigs manifests as oral, nasal, and hoof lesions, accompanied by fever and inflammation.
- The role of long non-coding RNAs (lncRNAs) in regulating antiviral and inflammatory responses is established, but their specific involvement in SVV-induced inflammation is unknown.
Purpose of the Study:
- To investigate the role of lncRNAs in the host response to SVV infection.
- To identify specific lncRNAs involved in regulating inflammation during SVV pathogenesis.
- To explore potential therapeutic targets for SVV infection.
Main Methods:
- RNA sequencing (RNA-seq) was employed to analyze differential gene expression in SVV-infected ST cells.
- Functional annotation analysis was performed on differentially expressed lncRNAs and mRNAs.
- The function of a candidate lncRNA, lnc-MSTRG.18940.1, was investigated through gene silencing experiments.
Main Results:
- RNA-seq identified 1332 differentially expressed lncRNAs and 3299 differentially expressed mRNAs in SVV-infected cells.
- Functional analysis indicated that regulated transcripts are primarily involved in host immunity and inflammatory signaling pathways.
- Silencing of lnc-MSTRG.18940.1 significantly reduced SVV replication and the production of key inflammatory factors (TNF-α, IL-1, IL-6, IL-8).
Conclusions:
- lnc-MSTRG.18940.1 acts as a crucial immune regulator during SVV infection.
- This lncRNA plays a significant role in controlling SVV replication and modulating the inflammatory response.
- The findings provide insights into the molecular mechanisms of SVV pathogenesis and highlight lncRNAs as potential targets for therapeutic intervention.
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