Subcellular Trafficking of the Papillomavirus Genome during Initial Infection: The Remarkable Abilities of Minor Capsid Protein L2.
Since 2012, our understanding of human papillomavirus (HPV) subcellular trafficking has undergone a drastic paradigm shift. Work from multiple laboratories has revealed that HPV has evolved a unique means to deliver its viral genome (vDNA) to the cell nucleus, relying on myriad host cell proteins and processes. The major breakthrough finding from these recent endeavors has been the realization of L2-dependent utilization of cellular sorting factors for the retrograde transport of vDNA away from degradative endo/lysosomal compartments to the Golgi, prior to mitosis-dependent nuclear accumulation of L2/vDNA. An overview of current models of HPV entry, subcellular trafficking, and the role of L2 during initial infection is provided below, highlighting unresolved questions and gaps in knowledge.
['Campos|Samuel K|SK|']
D001692:Biological Transport D036022:Capsid Proteins D004279:DNA, Viral D054884:Host-Pathogen Interactions D006801:Humans D027383:Papillomaviridae D060066:Protein Interaction Maps D053586:Virus Internalization
subcellular trafficking L2 human papillomavirus HPV16 fusion peptide gamma secretase membrane penetration mitosis retromer toxin translocation transmembrane domain