Study of E6 and E7 proteins from HPV16 and HPV6 and its effects on Toll like receptors signaling pathways

Abstract

High risk or oncogenic Human Papillomavirus (HPV) are responsible for the development of cervical cancer. In 2008 there were 529.800 new cases and 275.100 registered deaths of cervical cancer worldwide.Integration of the viral genome is an essential step to the development of cancer, resulting in loss or disruption of E2 gene, causing the continuous expression of E6 and E7.Besides several other interactions, both E6 and E7 are involved in deregulating the innate immune system interfering with the expression of Toll like receptors (TLR), which is an important step in cancer progression.Numerous studies indicate that TLR signaling contributes to tumor growth in different organs and their activation in cancer cells with subsequent production of cytokines and chemokines promote angiogenesis, cell survival, chemo resistance and thus tumor progression. However little is known about how HPV affects TLR signaling pathways during infection and cervical cancer progression.This project aims to study the effects of HPV infection on Toll like receptors (TLR) signaling pathways in human primary keratinocytes and cervical lesions.