Human papillomavirus entry and fusion process

The "Human papillomavirus entry and fusion process" refers to the multi-step mechanism by which HPV virions attach to, enter, and release their genomes into host epithelial cells. Entry is initiated when **HPV L1 capsid protein binds to heparan sulfate proteoglycans (HSPGs)** on the exposed basement membrane, usually following microtrauma. This triggers **conformational changes that expose the L2 protein**, enabling cleaving by host furin protease and subsequent binding to an as-yet-unknown secondary cell surface receptor. The virus is then **internalized (mainly through clathrin-mediated endocytosis, possibly with actin involvement)**, trafficked through endosomal compartments, and delivered to the nucleus during mitosis for genome release. The HPV entry/fusion process is mechanistically essential for HPV infectivity but does not refer to a discrete molecule or receptor; it instead describes a **complex, multi-protein, multi-cellular pathway** involving both viral and cellular components[2][3][4][6]. Therefore, it is not considered a canonical therapeutic target in the way a receptor or enzyme would be. **Note:** This is a process, not a single molecule, receptor, or druggable target. Therefore, it is an "incorrect" entry by the standards of target-centric databases.

Other names

HPV entryHPV fusionHPV uptakeHPV internalization

Antibodies can neutralize HPV by blocking capsid binding or structural changes; some entry inhibitors block the interaction with cellular components[2][5]