The Human papillomavirus type 16 E7 oncoprotein induces a transcriptional repressor complex on the Toll-like receptor 9 promoter

摘要: Human papillomavirus type 16 (HPV16) and other oncogenic viruses have been reported to deregulate immunity by suppressing the function of double-stranded DNA innate sensor TLR9. However, mechanisms leading these events remain be elucidated. We show that infection human epithelial cells with HPV16 promotes formation an inhibitory transcriptional complex containing NF-κBp50–p65 ERα induced E7 oncoprotein. The E7-mediated also recruited histone demethylase JARID1B deacetylase HDAC1. entire bound a specific region on TLR9 promoter, which resulted in decreased methylation acetylation histones upstream start site. involvement NF-κB down-regulation was fully confirmed cervical tissues from patients. Importantly, we present evidence HPV16-induced affects interferon response negatively regulates viral infection. Our studies highlight novel HPV16-mediated mechanism combines epigenetic suppress key immune sensor.