DIFFERENTIAL-EFFECTS OF HSV-1 AND HCMV INFECTION ON ADHESION MOLECULEEXPRESSION ON HUMAN CORNEAL KERATOCYTES

Citation
Pm. Stuart et al., DIFFERENTIAL-EFFECTS OF HSV-1 AND HCMV INFECTION ON ADHESION MOLECULEEXPRESSION ON HUMAN CORNEAL KERATOCYTES, Current eye research, 16(5), 1997, pp. 496-502
Citations number
41
Categorie Soggetti
Ophthalmology
Journal title
ISSN journal
02713683
Volume
16
Issue
5
Year of publication
1997
Pages
496 - 502
Database
ISI
SICI code
0271-3683(1997)16:5<496:DOHAHI>2.0.ZU;2-S
Abstract
Purpose. Previous studies have shown that keratoplasty buttons obtaine d at surgery from patients with herpes simplex virus-1 (HSV-1) keratit is have elevated localized expression of the adhesion molecule ICAM-1, which plays a critical role in the initiation and amplification of an immune response. We performed studies to determine whether changes in expression of ICAM-1 and HLA class I are direct effects of productive infection of human corneal fibroblasts with HSV-1. Methods. Immunocyt ologic and flow cytometric analyses were performed to analyze the abil ity of HSV-1 to induce ICAM-1 and HLA class I expression in a primary cornea-derived keratocyte cell line, E-2. Positive controls for these experiments were E-2 cells infected with human cytomegalovirus (HCMV), which has been shown to increase ICAM-1 expression in selected cells, and E-2 cells treated with IFN-gamma, which upregulates both ICAM-1 a nd KLA class I expression in most cell types. Results. Kinetic cytomet ric analysis indicated decreased ICAM-1 expression 3 hours following H SV-1 infection of E-2 cells. In contrast, HCMV led to delectable incre ases in ICAM-1 expression starting 6 hours after infection. Infections with either HSV-1 or HCMV resulted in reduced HLA class I expression on E-2 and SF cells. Conclusions. These studies suggest that increased ICAM-1 expression seen on corneal stromal cells during clinical HSV-1 infection is not a direct result of productive viral infection, but o f other mechanisms such as cytokine release by infiltrating mononuclea r cells.