Orolabial human infections with herpes simplex virus type 1 (HSV-1) ar
e very common; following the primary epidermal infection, the virus is
retained in a latent form in the trigeminal ganglia from where it can
reactivate and cause a recrudescent lesion, Recrudescences are trigge
red by various stimuli including exposure to sunlight, In this review
three categories of mouse models are used to examine the effects of UV
irradiation on HSV infections: these are UV exposure prior to primary
infection, UV exposure as a triggering event for recrudescence and UV
exposure prior to challenge with virus in mice already immunized to H
SV, In each of these models immunosuppression occurs, which is manifes
t, in some instances, in increased morbidity or an increased rate of r
ecrudescence. Where known, the immunological mechanisms involved in th
e models are summarized and their relevance to human infections consid
ered.