Androutsopoulos Georgios, Thanatsis Nikolaos, Michail Georgios, Adonakis Georgios, Decavalas Georgios
Department of Obstetrics and Gynecology, University of Patras, Medical School, Rio, Greece
Correspondence: Androutsopoulos Georgios, Department of Obstetrics and Gynecology, University of Patras, Medical School, Rio, GR-26504, Greece, E – mail: email@example.com
Human papillomaviruses (HPV) are small, non-enveloped viruses. They have circular double-stranded DNA in an icosahedral capsid. Structural proteins of viral capsid, play important role in efficient virus infectivity. The viral L1 protein binds to the exposed basement membrane via heparan sulphate proteoglycans (primary receptor) and α6 integrin (secondary receptor). That binding
triggers receptor mediated endocytosis of HPV. Most HPV types use clathrin dependent endocytic pathway. Clathrin coated vesicles become uncoated after endocytosis and fuse with early endosomes. HPV can avoid lysosomal degradation and escape from the endosomes to the cytosol, with various mechanisms, including membrane disruption, transmembrane pore formation and pH decline. Finally, the complex of HPV genome and L2 protein enters the nucleus. Then, HPV transcription and replication occur in association with promyelocytic leukemia (PML) nuclear bodies. During latent infection, HPV genome maintain as autonomous replicating episome in the proliferating basal cells of the squamous epithelium.