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Comparison of Host Gene Expression Profiles in Spleen Tissues of Genetically Susceptible and Resistant Mice during

Wen-Yu Cheng1, Huai-Jie Jia1, Xiao-Bing He1

  • 1State Key Laboratory of Veterinary Etiological Biology, Key Laboratory of Veterinary Public Health of Agriculture Ministry, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, Gansu 730046, China.

Biomed Research International
|February 13, 2018
PubMed

Insights

Ectromelia virus (ECTV) infection reveals distinct gene expression differences between susceptible and resistant mouse strains. Understanding these host genetic factors is key to deciphering Orthopoxvirus-host interactions and developing effective countermeasures.

Area of Science:

  • Virology
  • Immunology
  • Genomics

Background:

  • Ectromelia virus (ECTV) causes mousepox and serves as a model for Orthopoxvirus pathogenesis.
  • Mouse strains exhibit varying susceptibility to ECTV, with BALB/c being susceptible and C57BL/6 resistant.
  • Host genetic factors influence disease outcome during viral infections.

Purpose of the Study:

  • To investigate host genetic differences influencing ECTV infection outcomes.
  • To compare gene expression profiles in susceptible versus resistant mouse strains post-ECTV infection.

Main Methods:

  • Microarray analysis of spleen tissues from BALB/c and C57BL/6 mice at 3 and 10 days post-ECTV infection.
  • Differential Gene Expression (DEG) analysis.
  • Gene Ontology (GO) and KEGG pathway enrichment analysis.

Main Results:

  • Susceptible BALB/c mice displayed significantly more DEGs than resistant C57BL/6 mice.
  • DEGs in BALB/c mice were associated with innate immunity, apoptosis, metabolism, and cancer pathways.
  • DEGs in C57BL/6 mice were linked to MAPK signaling and leukocyte transendothelial migration.
  • Interferon-induced gene expression was stronger in susceptible BALB/c mice compared to resistant C57BL/6 mice.

Conclusions:

  • Differential host gene expression profiles correlate with ECTV susceptibility.
  • These findings provide insights into molecular mechanisms underlying Orthopoxvirus-host interactions.
  • Transcriptome data can guide future research on host-specific antiviral responses.

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