Section 10
Chapter 9,106

Nonneutralizing antibody against the glycoprotein K of herpes simplex virus type-1 exacerbates herpes simplex virus type-1-induced corneal scarring in various virus-mouse strain combinations

Ghiasi, H.; Cai, S.; Slanina, S.; Nesburn, A.B.; Wechsler, S.L.

IOVS Investigative Ophthalmology and Visual Science 38(6): 1213-1221


ISSN/ISBN: 0146-0404
PMID: 9152241
Accession: 009105351

Purpose. To determine whether the exacerbation of herpes simplex virus type-1 (HSV-1) induced corneal scarring that the authors reported previously in HSV-1 glycoprotein K (gK) vaccinated BALB/c mice challenged with HSV-1 strain McKrae was a general phenomenon independent of virus and mouse strains. To determine the gK-induced immune response leading to exacerbation of HSV-1-induced corneal scarring. Methods. BALB/c or C57BL/6 mice were vaccinated with gK, ocularly challenged with HSV1 strain KOS or McKrae, and the relative amount of corneal scarring determined 28 days after challenge. The T cells, total serum, or purified immunoglobulin G (IgG) isolated from gK-vaccinated mice was transferred individually to naive mice, and the affects on corneal scarring after HSV-1 challenge were determined. Results. The KOS challenge of gK-vaccinated BALB/c mice resulted in significant corneal scarring (P = 0.0003), despite the fact that KOS normally produces no corneal scarring. McKrae challenge of gK-vaccinated C57BL/6 mice resulted in significant corneal scarring (P lt 0.0001), despite the fact that C57BL/6 mice are normally refractory to HSV-1-induced corneal scarring. Passive transfer of total anti-gK mouse sera or purified anti-gK mouse IgG but not adoptive transfer of total anti-gK T-cells to naive mice, resulted in exacerbation of corneal scarring after HSV-1 challenge (P lt 0.0001). Mice defective for T-cell-dependent antibody production were not susceptible to exacerbation of HSV-1-induced corneal scarring by gK vaccination (P lt 0.0001). Conclusions. The ability of gK vaccination to exacerbate HSV-1-induced corneal scarring was not mouse strain or HSV-1 strain specific. The gK-induced exacerbation of corneal scarring was related to anti-gK IgG. How anti-gK IgG exacerbated HSV-1 induced corneal scarring remains to be determined.

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