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- Title
Comparison of Host Gene Expression Profiles in Spleen Tissues of Genetically Susceptible and Resistant Mice during ECTV Infection.
- Authors
Cheng, Wen-Yu; Jia, Huai-Jie; He, Xiao-Bing; Chen, Guo-Hua; Feng, Yuan; Wang, Chun-Yan; Wang, Xiao-Xia; Jing, Zhi-Zhong
- Abstract
Ectromelia virus (ECTV), the causative agent of mousepox, has emerged as a valuable model for investigating the host-Orthopoxvirus relationship as it relates to pathogenesis and the immune response. ECTV is a mouse-specific virus and causes high mortality in susceptible mice strains, including BALB/c and C3H, whereas C57BL/6 and 129 strains are resistant to the disease. To understand the host genetic factors in different mouse strains during the ECTV infection, we carried out a microarray analysis of spleen tissues derived from BALB/c and C57BL/6 mice, respectively, at 3 and 10 days after ECTV infection. Differential Expression of Genes (DEGs) analyses revealed distinct differences in the gene profiles of susceptible and resistant mice. The susceptible BALB/c mice generated more DEGs than the resistant C57BL/6 mice. Additionally, gene ontology and KEGG pathway analysis showed the DEGs of susceptible mice were involved in innate immunity, apoptosis, metabolism, and cancer-related pathways, while the DEGs of resistant mice were largely involved in MAPK signaling and leukocyte transendothelial migration. Furthermore, the BALB/c mice showed a strong induction of interferon-induced genes, which, however, were weaker in the C57BL/6 mice. Collectively, the differential transcriptome profiles of susceptible and resistant mouse strains with ECTV infection will be crucial for further uncovering the molecular mechanisms of the host-Orthopoxvirus interaction.
- Subjects
ANIMAL experimentation; APOPTOSIS; CELL motility; CELLULAR signal transduction; GENE expression; IMMUNITY; INTERFERONS; LEUCOCYTES; MICE; SPLEEN; TRANSGENIC animals; MICROARRAY technology; GENE expression profiling; SIGNAL peptides; DNA virus diseases
- Publication
BioMed Research International, 2017, Vol 2017, p1
- ISSN
2314-6133
- Publication type
Article
- DOI
10.1155/2017/6456180