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Updated: Aug 22, 2026

Merkel Cell Polyomavirus Infection and Detection
Published on: February 7, 2019
Establishment of papillomavirus infection is enhanced by promyelocytic leukemia protein (PML) expression
Patricia M Day1, Carl C Baker, Douglas R Lowy
1Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. pmd@nih.gov
Abstract:
Previous studies have suggested that most papillomaviruses enter the host cell via clathrin-dependent receptor-mediated endocytosis but have not addressed later steps in viral entry. To examine these events, we followed the localization of L2 and packaged DNA after entry of infectious virions or L1/L2 pseudovirions. Confocal microscopic analyses of HeLa cells showed a time-dependent uncoating of capsids in cytoplasmic vesicles and the accumulation of both L2 and viral DNA at distinct nuclear domains identified as nuclear domain 10 (ND10). Both L2 and the pseudogenome had a punctate distribution and localized to ND10 in promyelocytic leukemia protein (PML)-expressing cells, whereas L2 had a diffuse nuclear distribution in PML-/- cells. The number of pseudovirus-infected cells was an order of magnitude higher in the PML+ cells compared with the PML-/- cells, and viral genome transcription after infection with authentic bovine papillomavirus virions was similarly elevated in PML+ cells. The results identify a role for PML in the enhancement of viral infectivity in the early part of the life cycle. We propose a model in which L2 chaperones the viral genome to ND10 to efficiently initiate viral transcription.
Insights
Papillomaviruses utilize promyelocytic leukemia protein (PML) to enhance viral infectivity. PML facilitates the transport of viral DNA to nuclear domain 10 (ND10) for efficient transcription and infection.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Papillomaviruses are known to enter host cells via endocytosis.
- Later steps in viral entry and nuclear targeting remain less understood.
Purpose of the Study:
- To investigate the intracellular trafficking and nuclear localization of papillomavirus components post-entry.
- To determine the role of promyelocytic leukemia protein (PML) in papillomavirus infection.
Main Methods:
- Confocal microscopy was used to track L2 and viral DNA in HeLa cells.
- Infectious virions and L1/L2 pseudovirions were utilized.
- Experiments were conducted in both PML-expressing and PML-deficient cells.
Main Results:
- Papillomavirus capsids uncoated in cytoplasmic vesicles.
- Both L2 and viral DNA localized to nuclear domain 10 (ND10).
- PML presence significantly increased viral infectivity and genome transcription, with L2 showing punctate localization at ND10.
Conclusions:
- PML plays a crucial role in enhancing papillomavirus infectivity early in the viral life cycle.
- A model is proposed where L2 chaperones the viral genome to ND10 for efficient transcription initiation.
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