Autophagy as a control mechanism in human papilloma virus infection
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Date
29/11/2016Item status
Restricted AccessEmbargo end date
31/12/2100Author
Charsou, Chara
Metadata
Abstract
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.