Project description:Human papillomaviruses (HPVs) target PML nuclear bodies during infectious entry and PML protein is important for efficient transcription of incoming viral genome.We used shRNA to knockdown PML protein in HaCaT keratinocytes to further investigate the role of PML protein in HPV entry. We used microarrays to compare the transcriptome of PML protein-deficient with vector control-transduced HaCaT cells.
Project description:Analysis of the effect of high-risk human papillomaviruses HPV16 and HPV18 in keratinocytes at gene expression level. The hypothesis tested in the present study was that HPVs inhibit the function of pathogen recognition receptors (PRRs), thereby evading the immune system. Results show that HPV-positive keratinocytes have a weaker response to poly(I:C), a synthetic double strand RNA agonist of viral PRRs, with IL1B as a central hub in a gene expression network of relative downregulation.
Project description:Analysis of the effect of high-risk human papillomaviruses HPV16 and HPV18 in keratinocytes at gene expression level. The hypothesis tested in the present study was that HPVs inhibit the function of pathogen recognition receptors (PRRs), thereby evading the immune system. Results show that HPV-positive keratinocytes have a weaker response to poly(I:C), a synthetic double strand RNA agonist of viral PRRs, with IL1B as a central hub in a gene expression network of relative downregulation. Total RNA from eight primary undifferentiated keratinocyte cultures, four uninfected and four HPV-positive, that were either left unstimulated, or stimulated for 4 or 24 hrs with 25 ug/ml poly(I:C).
