Figure 1. Mechanism whereby HPV-16 promotes TLR9 downregulation. Infection of human epithelial cells with human papillomavirus type 16 (HPV-16) promotes the formation of an inhibitory transcriptional complex which relies the on the E7-dependent, IκB kinase (IKK)-mediated activation of NF-κB p50/p65 dimers as well as of estrogen receptor 1 (α) (ERα). Such an E7-elicited transcriptional complex also recruits histone deacetylase 1 (HDAC1) and lysine-specific demethylase 5B (JARID1B) to a specific region of the Toll-like receptor 9 (TLR9) promoter, resulting in a decreased methylation and acetylation of histones upstream of the TLR9 transcriptional start site.