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Transcriptome analysis of PK-15 cells expressing CSFV NS4A.
Huifang Lv1, Zhifeng Peng1, Bingxin Jia1
1Key Laboratory of Veterinary Biological Products, College of Veterinary Medicine, Henan University of Animal Husbandry and Economy, 450046, Zhengzhou, China.
BMC Veterinary Research
|December 12, 2022
Summary
Classical swine fever virus (CSFV) nonstructural protein 4A (NS4A) impacts host cells. This study reveals CSFV NS4A suppresses immune responses and regulates cell adhesion, apoptosis, and autophagy.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- Classical swine fever (CSF) is an economically significant swine disease caused by the classical swine fever virus (CSFV).
- CSFV nonstructural protein 4A (NS4A) is vital for infectious CSFV particle formation, but its precise function during infection remains unclear.
Purpose of the Study:
- To elucidate the functional role of CSFV NS4A in host cells.
- To investigate the impact of NS4A on gene expression during CSFV infection.
Main Methods:
- RNA sequencing (RNA-seq) was employed to analyze gene expression in PK-15 cells expressing CSFV NS4A.
- Differentially expressed genes (DEGs) were identified and further validated using RT-qPCR.
- Gene Ontology (GO) and KEGG pathway enrichment analyses were performed on the identified DEGs.
Main Results:
- A total of 3893 DEGs were identified in PK-15 cells expressing NS4A compared to control cells.
- Enrichment analyses indicated that DEGs are involved in cell adhesion, apoptosis, host defense, inflammatory response, immune response, and autophagy.
- Notably, genes related to host immune and inflammatory responses were downregulated, while those linked to apoptosis and autophagy were upregulated.
Conclusions:
- CSFV NS4A plays a significant role in modulating host cell processes.
- CSFV NS4A inhibits the innate immune response and suppresses antiviral and inflammatory gene expression.
- CSFV NS4A regulates host cell adhesion, apoptosis, and autophagy during infection.
