Reactivation of latent herpes simplex virus type 1 (HSV-1) has been shown to occur in response to localized
inflammation.
Prostaglandins and
lipoxygenase products [eg.
hydroxyeicosatetraenoic acids, (HETEs)] are associated with
inflammation and, therefore, may play a role in HSV-1
infection and reactivation. In the rabbit cornea,
alkali injury, cryogenic injury, and acute HSV-1
infection promote the synthesis of HETEs. Recently, a
platelet activating factor antagonist,
ginkgolide B (
BN 52021) has been found to specifically inhibit the corneal synthesis of HETEs after
alkali injury. If the induction of HETEs after injury is related to HSV reactivation and severity of
infection,
BN 52021 may alter HSV reactivation and the severity of
infection by reducing the production of HETEs. To study the effect of
BN 52021 on HSV-1 reactivation, cryogenic corneal lesions were produced in ten HSV-1 latently infected rabbits. Five rabbits were treated with topical and intravenous
BN 52021 while the remaining five rabbits received topical
artificial tears and intravenous saline. In the
BN 52021 treated group, 90% (9/10) of the eyes and 53% (35/66) of the total ocular cultures were positive for HSV-1. In the control group, 60% (6/10) of the eyes, and 27% (18/66) of the ocular swabs were positive for HSV-1. The total number of positive cultures was significantly greater (p less than .05) in the
BN 52021 treated rabbits. By increasing the number of positive HSV ocular cultures,
BN 52021 appeared to act similarly to other inhibitors of
arachidonic acid metabolism such as steroidal and
nonsteroidal anti-inflammatory agents.