Autophagy as a control mechanism in human papilloma virus infection
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Human Papilloma Virus (HPV) is a conserved DNA virus, which infects mucosal and cutaneous epithelia. Although over 200 types of HPV have been identified which can infect humans, only around 15 high-risk (HR) types have been shown to be responsible for the development of cancer. HPV-16 is the most abundant HR-HPV type being responsible for almost 70% of cervical cancers. HPV-16 consists of 8 genes, the early genes (E1, E2, E4, E5 and the potential oncogenes E6 and E7) responsible for the infection, amplification and proliferation and the late genes (L1 and L2) responsible for the packaging and assembly of the virus. Autophagy, a physiological mechanism of intracellular digestion and recycling of unwanted cellular materials such as aggregated proteins and organelles has been shown to act as a first line defence against invading pathogens. An essential condition for this process is the formation of double membrane structures called the autophagosomes, which can engulf the pathogen or pathogenic proteins and digest them by fusing with endocytic vesicles (lysosomes). Beclin 1 and LC3 are vital proteins involved in the complicated process of the autophagosome formation while SQSTM1/p62 has a key role in the identification and transit of cargo into the forming autophagosomes. This novel work focuses on investigating the role of autophagy in HR-HPV related tumour development and progression in cervical epithelial cells both in vitro and ex vivo.