title: CXCR4-dependent HIV-1 infection of differentiated epithelial cells.
abstract: Epithelial cells constitute a physical barrier to sexual transmission of HIV, but are also a source of cytokines that could alter infection efficiency. We studied HIV infection of the human colonic epithelial cell line HCT116, which is a model for differentiation of intestinal mucosal epithelium. Differentiated HCT116 cells had increased expression of cell surface C-X-C chemokine receptor type-4 (CXCR4) that mediated HIV entry, despite the apparent absence of cell surface CD4. HIV infection in differentiated HCT116 cells increased the levels of IL-1alpha, and IFN-alpha mRNA even though only 1% of cells had integrated provirus. The inefficient, CXCR4-mediated infection of differentiated HCT116 cells supports the view that epithelial cells are a barrier and not a portal for HIV transmission. However, low level infection of epithelial cells could trigger the release of cytokines that indirectly increase the transmission rate.
authors.affiliation: Institute of Human Virology, University of Maryland Biotechnology Institute, 725 W Lombard Street, Baltimore, MD 21201, USA.
authors.forename: Douglas
authors.initials: D
authors.lastname: Horejsh
authors.forename: Tracy J
authors.initials: TJ
authors.lastname: Ruckwardt
authors.forename: C
authors.initials: C
authors.lastname: David Pauza
mesh_terms: D002454:Cell Differentiation; D003106:Colon / Q000166:cytology; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004847:Epithelial Cells / Q000166:cytology* / Q000821:virology*; D015658:HIV Infections / Q000821:virology*; D015497:HIV-1 / Q000472:pathogenicity* / Q000502:physiology; D006801:Humans; D019718:Receptors, CXCR4 / Q000378:metabolism*; D014162:Transfection; D015854:Up-Regulation
chemical_list: D016207:Cytokines; D019718:Receptors, CXCR4