HPV-16 virions can remain infectious for 2 weeks on senescent cells but require cell cycle re-activation to allow virus entry

[1]  K. Akashi,et al.  Cyclophosphamide-Induced Tolerance in Allogeneic Transplantation: From Basic Studies to Clinical Application , 2020, Frontiers in Immunology.

[2]  M. Sapp,et al.  Human Papillomavirus Major Capsid Protein L1 Remains Associated with the Incoming Viral Genome throughout the Entry Process , 2017, Journal of Virology.

[3]  P. Meneses,et al.  HPV entry into cells. , 2017, Mutation research. Reviews in mutation research.

[4]  D. Pim,et al.  The VPS4 component of the ESCRT machinery plays an essential role in HPV infectious entry and capsid disassembly , 2017, Scientific Reports.

[5]  S. Tenzer,et al.  The CD63-Syntenin-1 Complex Controls Post-Endocytic Trafficking of Oncogenic Human Papillomaviruses , 2016, Scientific Reports.

[6]  M. Sapp,et al.  Topography of the Human Papillomavirus Minor Capsid Protein L2 during Vesicular Trafficking of Infectious Entry , 2015, Journal of Virology.

[7]  D. Pim,et al.  A Novel PDZ Domain Interaction Mediates the Binding between Human Papillomavirus 16 L2 and Sorting Nexin 27 and Modulates Virion Trafficking , 2015, Journal of Virology.

[8]  Miranda Thomas,et al.  The Human Papillomavirus E6 PDZ Binding Motif: From Life Cycle to Malignancy , 2015, Viruses.

[9]  L. Banks,et al.  Human Papillomavirus Infectious Entry and Trafficking Is a Rapid Process , 2015, Journal of Virology.

[10]  C. Burd,et al.  Direct Binding of Retromer to Human Papillomavirus Type 16 Minor Capsid Protein L2 Mediates Endosome Exit during Viral Infection , 2015, PLoS pathogens.

[11]  L. Banks,et al.  Human papillomavirus infection requires the TSG101 component of the ESCRT machinery. , 2014, Virology.

[12]  Lucas Pelkmans,et al.  Large Scale RNAi Reveals the Requirement of Nuclear Envelope Breakdown for Nuclear Import of Human Papillomaviruses , 2014, PLoS pathogens.

[13]  A. Lipovsky,et al.  Genome-wide siRNA screen identifies the retromer as a cellular entry factor for human papillomavirus , 2013, Proceedings of the National Academy of Sciences.

[14]  D. Lowy,et al.  Identification of a Role for the trans-Golgi Network in Human Papillomavirus 16 Pseudovirus Infection , 2013, Journal of Virology.

[15]  Wim Quint,et al.  The biology and life-cycle of human papillomaviruses. , 2012, Vaccine.

[16]  Chad K. Park,et al.  A Transmembrane Domain and GxxxG Motifs within L2 Are Essential for Papillomavirus Infection , 2012, Journal of Virology.

[17]  R. Garcea,et al.  Cyclophilins Facilitate Dissociation of the Human Papillomavirus Type 16 Capsid Protein L1 from the L2/DNA Complex following Virus Entry , 2012, Journal of Virology.

[18]  Mario Schelhaas,et al.  Entry of Human Papillomavirus Type 16 by Actin-Dependent, Clathrin- and Lipid Raft-Independent Endocytosis , 2012, PLoS pathogens.

[19]  L. Banks,et al.  Human Papillomavirus L2 Facilitates Viral Escape from Late Endosomes via Sorting Nexin 17 , 2012, Traffic.

[20]  Z. Surviladze,et al.  Essential Roles for Soluble Virion-Associated Heparan Sulfonated Proteoglycans and Growth Factors in Human Papillomavirus Infections , 2012, PLoS pathogens.

[21]  R. Roden,et al.  Papillomavirus Infection Requires γ Secretase , 2010, Journal of Virology.

[22]  S. Lank,et al.  Establishment of Human Papillomavirus Infection Requires Cell Cycle Progression , 2009, PLoS pathogens.

[23]  D. Lowy,et al.  Heparan Sulfate-Independent Cell Binding and Infection with Furin-Precleaved Papillomavirus Capsids , 2008, Journal of Virology.

[24]  B. Trus,et al.  Arrangement of L2 within the Papillomavirus Capsid , 2008, Journal of Virology.

[25]  D. Lowy,et al.  Generation of HPV pseudovirions using transfection and their use in neutralization assays. , 2005, Methods in molecular medicine.

[26]  D. Lowy,et al.  Establishment of papillomavirus infection is enhanced by promyelocytic leukemia protein (PML) expression. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[27]  Masashi Narita,et al.  Reversal of human cellular senescence: roles of the p53 and p16 pathways , 2003, The EMBO journal.

[28]  R. Roden,et al.  Cell Surface-Binding Motifs of L2 That Facilitate Papillomavirus Infection , 2003, Journal of Virology.

[29]  Y. Modis,et al.  Atomic model of the papillomavirus capsid , 2002, The EMBO journal.

[30]  H. Hausen.  Papillomaviruses and cancer: from basic studies to clinical application , 2002, Nature Reviews Cancer.

[31]  Luise Florin,et al.  Human Papillomavirus Infection Requires Cell Surface Heparan Sulfate , 2001, Journal of Virology.

[32]  K. Jansen,et al.  The L1 Major Capsid Protein of Human Papillomavirus Type 11 Recombinant Virus-like Particles Interacts with Heparin and Cell-surface Glycosaminoglycans on Human Keratinocytes* , 1999, The Journal of Biological Chemistry.

[33]  D. Lowy,et al.  The Papillomavirus Minor Capsid Protein, L2, Induces Localization of the Major Capsid Protein, L1, and the Viral Transcription/Replication Protein, E2, to PML Oncogenic Domains , 1998, Journal of Virology.

[34]  J. Dillner,et al.  Surface conformational and linear epitopes on HPV-16 and HPV-18 L1 virus-like particles as defined by monoclonal antibodies. , 1996, Virology.

[35]  H. zur Hausen,et al.  Papillomavirus infections--a major cause of human cancers. , 1996, Biochimica et biophysica acta.

[36]  D. Lowy,et al.  Interaction of papillomaviruses with the cell surface , 1994, Journal of virology.

[37]  T. Crook,et al.  HPV-16 E7 functions at the G1 to S phase transition in the cell cycle. , 1990, Oncogene.

[38]  L. Hayflick.  THE LIMITED IN VITRO LIFETIME OF HUMAN DIPLOID CELL STRAINS. , 1965, Experimental cell research.