Transcriptome analysis of murine RAW264.7 macrophages infected with Nelson Bay virus
10.12007/j.issn.0258-4646.2025.04.010
- VernacularTitle:纳尔逊海湾病毒感染小鼠巨噬细胞RAW264.7的转录物组分析
- Author:
Zhuping MA
1
;
Miaojuan CHEN
;
Lüyin SUN
;
Wenrui FU
;
Jing TIAN
;
Yonggang LI
;
Xiaoli TAO
Author Information
1. 锦州医科大学基础医学院病原生物学教研室,辽宁锦州 121001
- Publication Type:Journal Article
- Keywords:
Nelson bay virus;
macrophage;
transcriptome
- From:
Journal of China Medical University
2025;54(4):340-345
- CountryChina
- Language:Chinese
-
Abstract:
Objective To analyze the transcriptome sequencing results of Nelson Bay virus(NBV)-infected murine RAW264.7 mac-rophages,and to screen for differentially expressed genes(DEGs)to provide a theoretical basis for exploring the mechanism of innate immune response in reovirus infection.Methods RAW264.7 cells were infected with the NBV-Miyazaki virus strain at a multiplicity of infection(MOI)of 30.We used transcriptome sequencing technologies,with q＜0.05 and|log2FC|≥ 1,for screening the DEGs in the infection and control groups.The Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)databases were used for enrichment analysis of DEGs.Results A total of 442 genes were differentially expressed in the infection group,of which 381 genes were significantly upregulated and 61 genes were significantly downregulated.In the GO analysis,the enrichment of DEGs was primarily related to the innate immune response,defense response to viruses,cytokine production,and cell response to cytokine stimulation.In the KEGG analysis,the enrichment of DEGs were primarily related to the Toll-like receptor,retinoid acid inducible gene Ⅰ-like receptor,PI3K/Akt,and other signaling pathways.Conclusion RAW264.7 macrophages infected with the NBV-Miyazaki virus can activate pattern recognition receptors;promote the release of cytokines,chemokines,and other immune-related factors;and enhance antibody-dependent cell-mediated cytotoxicity to exert an immune effect.This study provides a theoretical basis for exploring the mechanisms of innate immu-nity during NBV-Miyazaki virus infection.
