Abstract
Abstract Although a few mechanisms have explained how, for instance ectromelia virus (ECTV), is successful in causing fatal disease in certain strains of mice and how other strains are not susceptible, a global transcription overview of innate immunity genes is not entirely known. Poxviruses have evolved several mechanisms to avoid immune response of an infected host. Here we have studied the innate gene transcriptional response of BALB/c and C57BL/6 mice peritoneal macrophages to infection with ECTV Moscow strain (ECTV-Mos). Indeed, assessment of four categories of antiviral innate immune response receptors, downstream signalling and responsive components revealed generalized down regulation of many genes in both strains of mice. Of the 84 genes assessed in each mouse strain only 3 and 15 were significantly upregulated in BALB/c and C57BL/6 mice, respectively. The remaining genes were more or less down-regulated. Surprisingly, type I interferon genes were substantially upregulated. The observed upregulation strongly correlated with protein expression in the case of cathepsin genes as well as TLR genes. ECTV-Mos inhibits receptors and signalling components of the innate immune response in mice. Results provide an insight into initial factors that presumably lead to an ineffective antiviral immune response of BALB/c and C57BL/6 mice in the light of infection with ECTV.
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