Human papillomavirus type 16 minor capsid protein L2 (RG1 epitope) - host cell receptor interface (HPV16 L2 RG1 interface)

The Human papillomavirus type 16 (HPV16) minor capsid protein L2 (RG1 epitope) - host cell receptor interface is a critical molecular junction required for the successful infection of host epithelial cells by HPV16 (Gambhira et al., 2007, Journal of Virology). The L2 protein, specifically the highly conserved RG1 epitope located within residues 17–36, becomes accessible on the viral surface only after the virus binds to primary heparan sulfate proteoglycan (HSPG) receptors and undergoes conformational changes mediated by cyclophilin B and furin cleavage (Day et al., 2008, Journal of Virology). This interface facilitates the interaction with secondary host cell receptors or entry factors, such as the retromer complex and annexin A2, which are essential for endosomal escape and the subsequent trafficking of the viral episome to the nucleus (Schellenbacher et al., 2009, Journal of Virology). Because the RG1 epitope is highly conserved across diverse high-risk and low-risk HPV types, it is a primary target for the development of next-generation, broad-spectrum "pan-HPV" vaccines (Tumban et al., 2011, PLoS ONE). Therapeutic interventions, including monoclonal antibodies like RG1 and chimeric virus-like particle (VLP) vaccines, aim to block this interface to neutralize viral entry and prevent the establishment of chronic infections that lead to cervical and oropharyngeal cancers (Wang & Roden, 2013, Expert Review of Vaccines). Despite its potential, the L2 protein is significantly less immunogenic than the L1 protein, necessitating innovative delivery systems or potent adjuvants to elicit a robust and sustained immune response (Jagu et al., 2013, PLoS ONE).

Other names

HPV16 L2 (17-36) epitopeRG1 epitopeHPV16 minor capsid protein L2L2-host receptor interfaceHPV16 L2 N-terminal interface

Neutralization of viral infection by blocking the interaction between the L2 minor capsid protein and host cell entry factors, thereby preventing endosomal escape and nuclear import of the viral genome.