Transcriptome analysis of 3D4/21 cells expressing CSFV NS4B.
Wang Dong1, Huifang Lv1, Yuzhen Song1
1Key Laboratory of Veterinary Biological Products, College of Veterinary Medicine and Pharmacy, Henan University of Animal Husbandry and Economy, Zhengzhou, China.
Frontiers in Microbiology
|February 19, 2025
Summary
Classical swine fever virus (CSFV) non-structural protein 4B (NS4B) impacts host cell processes. This study reveals NS4B regulates endocytosis, autophagy, and immune responses, offering insights into CSFV pathogenesis.
Area of Science:
- * Virology
- * Molecular Biology
- * Cell Biology
Background:
- * Classical swine fever (CSF) causes significant global economic losses in the pig industry.
- * Classical swine fever virus (CSFV) non-structural protein 4B (NS4B) is vital for viral replication and pathogenicity.
- * The precise functions of CSFV NS4B during infection remain incompletely understood.
Purpose of the Study:
- * To investigate the molecular mechanisms and cellular functions of CSFV NS4B.
- * To identify host genes differentially expressed in response to CSFV NS4B expression using RNA-sequencing.
- * To elucidate the role of NS4B in host cell processes such as endocytosis, autophagy, and immune response.
Main Methods:
- * RNA-sequencing (RNA-seq) was employed to profile gene expression in 3D4/21 cells expressing CSFV NS4B.
- * Differentially expressed genes (DEGs) were identified by comparing NS4B-expressing cells to control cells (empty vector).
- * Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed. RT-qPCR was used for validation of selected DEGs.
Main Results:
- * A total of 4397 DEGs were identified in cells expressing CSFV NS4B.
- * Enrichment analyses indicated involvement of DEGs in endocytosis, autophagy, cell adhesion, transport, immune response, and apoptosis.
- * Key findings include regulation of endocytosis-related genes, downregulation of antiviral immune genes (e.g., RIG-I, MDA5), and upregulation of autophagy-related genes (e.g., WIPI2, ATG16L2).
Conclusions:
- * CSFV NS4B plays a significant role in modulating host cellular processes crucial for viral invasion and intracellular trafficking.
- * NS4B actively induces host autophagy and suppresses the host's antiviral immune response.
- * This research provides valuable insights into the multifaceted functions of CSFV NS4B during infection, aiding in understanding viral pathogenesis.
