MHC class II molecules that are constitutively expressed on professional antigen presenting cells, present peptides derived from exogenous antigens to CD4 T helper cells playing an important role in the induction and maintenance of CTL immunity. Epithelial cells can also constitutively express MHC II molecules fairly but at a lower level than professional APCs. In our exper iment, we detected a small subpopulation of uninfected PK15 cells constitutively expressing MHC class II mole cules. However, we did not detect modifications of the MHC class II expression at the cell surface. Since a down regulation of constitutive and IFN induced HLA class II expression has been observed in cells infected by other herpesviruses, our preliminary data suggest that it would be highly relevant to explore how PrV may interfere with the MHC class II presentation pathway in profes sional APCs.
In addition to genes belonging to MHC antigen presenta tion pathways, several other genes, playing Inhibitors,Modulators,Libraries a role in anti viral response are regulated during PrV infection such as genes belonging to the IFN signaling pathway. Inhibitors,Modulators,Libraries Indeed, it has been reported that in primary rat fibroblasts, PrV infection could suppress the establishment of the IFN induced viral state. IRF3, which is a transcriptional factor involved in IFN production by epithelial cells, is down regulated together with a set of other IRF. Constitu tively expressed in the cytosol, IRF3 is phosphorylated during herpesvirus infection and translocated into the nucleus to target the IFN promoter. Many viruses inter fere with IRF activities.
A decrease of IRF1 mRNA and protein levels has Inhibitors,Modulators,Libraries also been detected in cells infected with hepatitis C virus, resulting in the transcriptional repres sion of several IFN stimulated genes. In addition, TNF alpha, which is a multifunctional cytokine with potent antiviral activities and which mediates protection against HSV 1 in the mouse was analyzed Inhibitors,Modulators,Libraries by qRT PCR. A strong up regulation of TNF was detected from the beginning of PrV infection and until 12 h pi. These results suggest that Inhibitors,Modulators,Libraries the TNF transcription increase that is usually expected during an infection is not suppressed by PrV infection and that the cellular shutoff does not target TNF. Other cellular pathways modulated during PrV infection Our transcriptome analysis confirms that many other bio logical processes and functions are modulated during PrV inhibitor Pfizer infection in porcine PK15 cells as previously observed in rat embryonic fibroblast and human embryonic kidney cells. We have focused our study on a limited number of pathways and genes. Interestingly, we observe both by transcriptome analysis and qRT PCR that PPIA gene expression is clearly down regulated during PrV infection.
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