NONNEUTRALIZING ANTIBODY AGAINST THE GLYCOPROTEIN-K OF HERPES-SIMPLEXVIRUS TYPE-1 EXACERBATES HERPES-SIMPLEX VIRUS TYPE-1-INDUCED CORNEAL SCARRING IN VARIOUS VIRUS MOUSE STRAIN COMBINATIONS

Citation
H. Ghiasi et al., NONNEUTRALIZING ANTIBODY AGAINST THE GLYCOPROTEIN-K OF HERPES-SIMPLEXVIRUS TYPE-1 EXACERBATES HERPES-SIMPLEX VIRUS TYPE-1-INDUCED CORNEAL SCARRING IN VARIOUS VIRUS MOUSE STRAIN COMBINATIONS, Investigative ophthalmology & visual science, 38(6), 1997, pp. 1213-1221
Citations number
52
Categorie Soggetti
Ophthalmology
ISSN journal
01460404
Volume
38
Issue
6
Year of publication
1997
Pages
1213 - 1221
Database
ISI
SICI code
0146-0404(1997)38:6<1213:NAATGO>2.0.ZU;2-D
Abstract
Purpose. To determine whether the exacerbation of herpes simplex virus type-1 (HSV-I) induced corneal scarring that the authors reported pre viously in HSV-I glycoprotein K (gK) vaccinated BALB/c mice challenged with HSV-1 strain McKrae was a general phenomenon independent of viru s and mouse strains. To determine the gK-induced immune response leadi ng to exacerbation of HSV-l-induced corneal scarring. Methods. BALB/c or C57BL/6 mice were vaccinated with gK, ocularly challenged with HSV- 1 strain KOS or McKrae, and the relative amount of corneal scarring de termined 28 days after challenge. The T cells, total serum, or purifie d immunoglobulin G (IgG) isolated from gK-vaccinated mice was transfer red individually to naive mice, and the affects on corneal scarring af ter HSV-1 challenge were determined. Results. The ROS challenge of gK- vaccinated BALB/c mice resulted in significant corneal scarring (P = 0 .0003), despite the fact that KOS normally produces no corneal scarrin g. McKrae challenge of gK-vaccinated C57BL/6 mice resulted in signific ant corneal scarring (P < 0.0001), despite the fact that C57BL/6 mice are normally refractory to HSV-I-induced corneal scarring. Passive tra nsfer of total anti-gK mouse sera or purified anti-gK mouse Igc, but n ot adoptive transfer of total anti-gK T-cells to naive mice, resulted in exacerbation of corneal scarring after HSV-I challenge (P < 0.0001) . Mice defective for T-cell-dependent antibody production were not sus ceptible to exacerbation of HSV-l-induced corneal scarring by gK vacci nation (P < 0.0001). Conclusions. The ability of gK vaccination to exa cerbate HSV-l-induced corneal scarring was not mouse strain or HSV-1 s train specific. The gK-induced exacerbation of corneal scarring was re lated to anti-gK IgG. How anti-gK IgG exacerbated HSV-1 induced cornea l scarring remains to be determined.