Virus Details


VHFID4974

Pathogen Information

Virus Name Human papillomavirus type 16
Virus Short Name HPV16
Order Unassigned
Virus Family Papillomaviridae
Virus Subfamily N.A.
Genus Alphapapillomavirus
Species Human papillomavirus 16
Host Human, monkeys
Cell Tropism Epithelial cells of skin, mucous membranes
Associated Disease Malignant tumours
Mode of Transmission Sexual, indirect and direct contact, auto-inoculation
VIPR DB link N.A.
ICTV DB link https://talk.ictvonline.org/ictv-reports/ictv_9th_report/dsdna-viruses-2011/w/dsdna_viruses/121/papillomaviridae
Virus Host DB link http://www.genome.jp/virushostdb/view/?virus_lineage=Papillomaviridae

Publication Information

Paper Title The CXCL12/CXCR4 Signaling Pathway: A New Susceptibility Factor in Human Papillomavirus Pathogenesis
Author's Name Floriane Meuris, Laetitia Carthagena, Agnieszka Jaracz-Ros, Francoise Gaudin, Pasquale Cutolo, Claire Deback, Yuezhen Xue, Francoise Thierry, John Doorbar, Francoise Bachelerie
Journal Name PLOS Pathogens
Pubmed ID 27918748
Abstract The productive human papillomavirus (HPV) life cycle is tightly linked to the differentiation and cycling of keratinocytes. Deregulation of these processes and stimulation of cell proliferation by the action of viral oncoproteins and host cell factors underlies HPV-mediated carcinogenesis. Severe HPV infections characterize the wart, hypogammaglobulinemia, infection, and myelokathexis (WHIM) immunodeficiency syndrome, which is caused by gain-of-function mutations in the CXCR4 receptor for the CXCL12 chemokine, one of which is CXCR41013. We investigated whether CXCR41013 interferes in the HPV18 life cycle in epithelial organotypic cultures. Expression of CXCR41013 promoted stabilization of HPV oncoproteins, thus disturbing cell cycle progression and proliferation at the expense of the ordered expression of the viral genes required for virus production. Conversely, blocking CXCR41013 function restored virus production and limited HPV-induced carcinogenesis. Thus, CXCR4 and its potential activation by genetic alterations in the course of the carcinogenic process can be considered as an important host factor for HPV carcinogenesis.
Used Model NIKS cells
DOI 10.1371/journal.ppat.1006039