Format

Send to

Choose Destination
See comment in PubMed Commons below
Virology. 2013 Nov;446(1-2):378-88. doi: 10.1016/j.virol.2013.08.018. Epub 2013 Sep 17.

HIV-associated disruption of mucosal epithelium facilitates paracellular penetration by human papillomavirus.

Author information

1
Department of Medicine, University of California San Francisco, 513 Parnassus Ave, San Francisco, CA 94143-0512, USA; Department of Orofacial Sciences, University of California San Francisco, 513 Parnassus Ave, San Francisco, CA 94143-0512, USA. Electronic address: sharof.tugizov@ucsf.edu.

Abstract

The incidence of human papillomavirus (HPV)-associated epithelial lesions is substantially higher in human immunodeficiency virus (HIV)-infected individuals than in HIV-uninfected individuals. The molecular mechanisms underlying the increased risk of HPV infection in HIV-infected individuals are poorly understood. We found that HIV proteins tat and gp120 were expressed within the oral and anal mucosal epithelial microenvironment of HIV-infected individuals. Expression of HIV proteins in the mucosal epithelium was correlated with the disruption of epithelial tight junctions (TJ). Treatment of polarized oral, cervical and anal epithelial cells, and oral tissue explants with tat and gp120 led to disruption of epithelial TJ and increased HPV pseudovirion (PsV) paracellular penetration in to the epithelium. PsV entry was observed in the basal/parabasal cells, the cells in which the HPV life cycle is initiated. Our data suggest that HIV-associated TJ disruption of mucosal epithelia may potentiate HPV infection and subsequent development of HPV-associated neoplasia.

KEYWORDS:

Disruption of tight junctions; HIV; HPV; HPV paracellular penetration; Mucosal epithelium

PMID:
24074602
PMCID:
PMC3809142
DOI:
10.1016/j.virol.2013.08.018
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center