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Viruses. 2017 Dec 3;9(12). pii: E370. doi: 10.3390/v9120370.

Subcellular Trafficking of the Papillomavirus Genome during Initial Infection: The Remarkable Abilities of Minor Capsid Protein L2.

Campos SK1,2,3,4.

Author information

1
The Department of Immunobiology, The University of Arizona, Tucson, AZ 85721-0240, USA. skcampos@email.arizona.edu.
2
The Department of Molecular & Cellular Biology, The University of Arizona, Tucson, AZ 85721-0240, USA. skcampos@email.arizona.edu.
3
The Cancer Biology Graduate Interdisciplinary Program, The University of Arizona, Tucson, AZ 85721-0240, USA. skcampos@email.arizona.edu.
4
The BIO5 Institute, Tucson, AZ 85721-0240, USA. skcampos@email.arizona.edu.

Abstract

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.

KEYWORDS:

HPV16; L2; fusion peptide; gamma secretase; human papillomavirus; membrane penetration; mitosis; retromer; subcellular trafficking; toxin; translocation; transmembrane domain

PMID:
29207511
PMCID:
PMC5744145
DOI:
10.3390/v9120370
[Indexed for MEDLINE]
Free PMC Article

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