Productive human immunodeficiency virus-1 infection of epithelial cell lines of salivary gland origin

Citation
Y. Han et al., Productive human immunodeficiency virus-1 infection of epithelial cell lines of salivary gland origin, ORAL MICROB, 15(2), 2000, pp. 82-88
Citations number
35
Categorie Soggetti
Microbiology
Journal title
ORAL MICROBIOLOGY AND IMMUNOLOGY
ISSN journal
09020055 → ACNP
Volume
15
Issue
2
Year of publication
2000
Pages
82 - 88
Database
ISI
SICI code
0902-0055(200004)15:2<82:PHIVIO>2.0.ZU;2-U
Abstract
To ascertain whether epithelial cells of oral cavity origin may be infected with human immunodeficiency virus (HIV-1), a study to determine susceptibi lity to infection of salivary gland epithelial cell lines (HSY and HSG) was undertaken. Because of the potential for oral-genital transmission, an end ometrial cell line, HEC-1, was also studied. Epithelial cell monolayers wer e infected with cell-free HTLVIIIB or a primary HIV-1 isolate. Several line s of evidence indicated that inoculation of these cell lines with HIV-1 led to productive infection: 1) p24 antigen was present in supernatants, with levels peaking on days 3-4; 2) provirus was found in cells by polymerase ch ain reaction; 3) virions present in supernatants were infectious as confirm ed by coculture with the T-lymphoblastoid line CEM-NKr. Following a period of virus production, HIV-1 entered a latency phase over 10 weeks. All epith elial cell lines were positive for galactosylceramide (GalC) and CXCR4. HSY was weakly positive for surface CD4, and also expressed mRNA for CD4 and C CR5, as did HEC-1. Blocking studies indicated that anti-GalC, but not anti- CD4, significantly reduced productive infection, and that regulated on acti vation normal T cell expressed and secreted (RANTES) but not stromal cell-d erived factor (SDF-1) could partially block infection of the M-tropic prima ry isolate. These results suggest that epithelial cells in the oral cavity and the genital tract might be targets of HIV-1 and potentially serve as a mediator of systemic infection.