McKeever D J, Jenkinson D M, Hutchison G, Reid H W
Moredun Research Institute, Edinburgh, UK.
J Comp Pathol. 1988 Oct;99(3):317-28. doi: 10.1016/0021-9975(88)90052-7.
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.
皮肤损伤对于羊痘病毒感染的建立和典型病变的发展至关重要。然而，对轻度擦伤皮肤经病毒攻击诱导的实验性病变发病机制的分析表明，病毒并非在受损的表皮中立足，而是在源自毛囊壁的下方替代表皮层的细胞中复制。皮肤反应包括细胞反应，伴有受影响表皮及真皮乳头层的坏死和脱落。然后通过形成源自毛囊较深部分的第三层表皮来完成愈合。先前的皮肤感染并不能预防疾病的再次引入，即使在同一皮肤区域也是如此，尽管病变较轻且持续时间较短。
