Project description:Ectromelia virus (ECTV) has emerged as a valuable model for investigating the host-orthopoxvirus relationship as it relates to pathogenesis and the immune response. ECTV causes mousepox in most strains of mice, including BALB/c and DBA/2, and these are therefore classified as susceptible mice. Conversely, C57BL/6 and certain 129 strains display limited pathology and a very low mortality, and are thus classified as resistant. To understand the host genetic factors of different mouse strains in response to ECTV infection, we carried out a microarray analysis using Affymetrix Gene-Chip Mouse Genome Arrays of spleen tissues from BALB/c and C57BL/6 mice at 3 and 10 days post-ECTV infection. Differential Expression of Genes (DEGs) analyses revealed distinct differences in the gene profiles of resistant and susceptible mice infected with ECTV. Gene ontology and KEGG pathway analysis showed that the DEGs of susceptible mice were involved mainly in immunity, apoptosis, spliceosomes and cancer-related pathways, while the DEGs of resistant mice were largely involved in MAPK signaling and leukocyte transendothelial migration. This suggests that the susceptible BALB/c mice have a stronger response than the resistant C57BL/6 mice to ECTV infection. The BALB/c mice showed a strong induction of interferon-induced genes (ISGs), including guanylate binding proteins (GBPs), myxovirus resistance protein (Mx) GTPases, oligoadenylate synthetase (OAS) and IFN-induced protein with tetratricopeptide repeats (IFIT) family proteins, while the C57BL/6 mice upregulated more genes related to metabolic pathways. This suggests that the susceptible BALB/c mice have a stronger response than the resistant C57BL/6 mice to ECTV infection.
Project description:Ectromelia virus (ECTV) has emerged as a valuable model for investigating the host-orthopoxvirus relationship as it relates to pathogenesis and the immune response. We analyzed the transcriptional signatures of BALB/3T3 cells at different times after infection with Ectromelia virus. Mouse Genome 430 2.0 arrays were used to analyze global changes in gene transcripts to generate a pool of genes that was a fold change cut-off of ≥ 1.5 or ≤ 0.5 in infected samples versus non-infected samples. Gene ontology and KEGG pathway analysis showed that the DEGs were involved mainly in immunity, apoptosis, spliceosomes, MAPK signaling and cancer-related pathways.
