Human papillomavirus early entry process

The Human papillomavirus (HPV) early entry process is a complex, multi-step mechanism by which the virus attaches to and enters host basal keratinocytes (PMID: 23723222). It begins with the initial attachment of the major capsid protein L1 to heparan sulfate proteoglycans (HSPGs) on the basement membrane or cell surface (PMID: 20089160). This binding triggers conformational changes in both L1 and the minor capsid protein L2, often facilitated by host factors like cyclophilin B and furin (PMID: 23723222). Subsequently, the virus interacts with a secondary uptake receptor complex, which may include alpha-6 integrin, annexin A2, and tetraspanins like CD151 (PMID: 20089160, PMID: 23723222). The virion is then internalized through a slow, asynchronous endocytic pathway that is typically clathrin-independent and actin-dependent (PMID: 20089160). This process is a critical target for prophylactic vaccines (which induce antibodies against L1) and experimental entry inhibitors (such as carrageenan or L2-targeting peptides) aimed at preventing the establishment of infection and subsequent diseases like cervical cancer (PMID: 35412144).

Other names

HPV entry pathwayHPV infectious entryHPV cell entryHPV attachment and internalization

Inhibition of viral attachment to heparan sulfate proteoglycans, inhibition of furin-mediated capsid cleavage, inhibition of cyclophilin-mediated conformational changes, and blockade of secondary receptor interactions.