Human papillomavirus entry process

The **human papillomavirus (HPV) entry process** refers to the sequence of molecular and cellular events by which HPV virions gain access to and infect basal epithelial cells. HPV infection typically requires microabrasion or trauma to the epithelium, allowing virions to bind initially to heparan sulfate proteoglycans (HSPGs) present on the exposed basement membrane. This binding triggers conformational changes in the viral capsid proteins L1 and L2, which expose the N-terminus of L2 to cleavage by furin-like proprotein convertases. The processed virion is then able to engage a secondary, less well-defined, receptor on the surface of basal keratinocytes. Several molecules have been implicated as co-receptors or factors involved in HPV uptake, including integrins (especially α6 integrin), epidermal growth factor receptor (EGFR), syndecan-1, tetraspanins, annexin A2, laminin, and vimentin. Internalization occurs via endocytosis mechanisms similar to micropinocytosis, followed by vesicular trafficking to the trans-Golgi network, escape from endosomes, and ultimately delivery of the viral genome—accompanied by L2 protein—to the nucleus, often at promyelocytic leukemia nuclear bodies (PML-NBs), where early gene transcription and the viral life cycle commence. The entire process is notably slow compared to many other viruses, often requiring over 12-24 hours from attachment to initiation of transcription[1][3][4][6]. **Important note:** The "HPV viral entry process" is not a molecule, gene, protein, or canonical drug target, but rather a series of interacting molecular steps in the HPV infection cycle. While individual proteins and cell surface molecules involved in HPV entry (e.g., α6 integrin, HSPG, EGFR) can be considered therapeutic targets, the process itself is not a discrete molecule. Thus, it is not a canonical "target" for structured drug-target information systems[3][1][6].

Other names

HPV entryHPV viral entryHPV infection cycleHPV attachment and uptake