Author(s): McKeever DJ, Jenkinson DM, Hutchison G, Reid HW
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Abstract Damage to the skin is essential for the establishment of orf virus infection and the development of typical lesions. However, analysis of the pathogenesis of experimental lesions induced by viral challenge of mildly abraded skin, indicated that the virus does not establish in the damaged epidermis, but replicates in the cells of an underlying replacement epidermal layer derived from the walls of the wool follicles. The skin reaction consists of a cellular response with necrosis and sloughing of the affected epidermis and underlying stratum papillare of the dermis. Healing is then completed by the formation of a third epidermis derived from the deeper portions of the wool follicles. Previous cutaneous infection did not prevent reintroduction of the disease, even on the same area of skin although the lesions were less severe and persisted for a shorter period.
This article was published in J Comp Pathol
and referenced in Journal of Antivirals & Antiretrovirals