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Ultraviolet Light Induces Reactivation in a Murine Model of Cutaneous Herpes Simplex Virus‐1 Infection ¶
Author(s) -
Goade Diane E.,
Nofchissey Robert A.,
Kusewitt Donna F.,
Hjelle Brian,
Kreisel John,
Moore Julene,
Lyons C. Richard
Publication year - 2001
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1562/0031-8655(2001)0740108uliria2.0.co2
Subject(s) - hairless , herpes simplex virus , virus , pathology , alphaherpesvirinae , immunosuppression , viral shedding , virology , necrosis , immunohistochemistry , syncytium , biology , herpesviridae , medicine , immunology , viral disease , genetics
ABSTRACT We have developed a model of cutaneous herpes simplex virus‐1 (HSV‐1) reactivation in SKH‐1 hairless mice which closely mimics the condition in humans. Sixty plaque‐forming units of HSV‐1 strain 17 syn + were applied to a superficially abraded area on the lateral body wall. More than 85% of mice developed primary HSV‐1 infection characterized by a zosteriform pattern of cutaneous vesiculation and ulceration. Approximately one‐third of mice with primary skin lesions succumbed to neurologic disease and in the remaining mice cutaneous lesions healed completely. Subsequent exposure of healed areas to two minimal inflammatory doses of UV resulted in recrudescence of skin lesions in the irradiated areas in almost 60% of mice. Lesions appeared approximately 4 days after irradiation, persisted for 3–5 days and then resolved completely. Reactivation rarely resulted in death due to neurologic disease. Primary lesions had a histologic appearance typical of cutaneous HSV‐1 infection with vesicles and focal epithelial necrosis accompanied by the formation of epithelial syncytial cells and the presence of herpetic intranuclear inclusion bodies. In primary lesions HSV‐1 was demonstrated by immunohistochemistry, polymerase chain reaction and culture. In reactivated lesions epithelial syncytia and inclusion bodies were not seen; however, virus was demonstrable by polymerase chain reaction and culture. Exposure of the uninfected side to UV did not stimulate disease recurrence suggesting that local effects of UV rather than systemic immunosuppression were responsible for reactivation. Reactivation could also be obtained with two minimal inflammatory doses of UV from a UV‐340 light source which emits light approximating the solar spectrum.