In vitro activity of VEGF-E produced by orf virus strains isolated from classical and severe persistent contagious ecthyma

• Published in: Veterinary microbiology 2006-04, Vol.114 (1), p.142-147
• Main Authors: Scagliarini, Alessandra, Dal Pozzo, Fabiana, Gallina, Laura, Guercio, Annalisa, Vaccari, Francesca, Battilani, Mara, Ciulli, Sara, Prosperi, Santino
• Format: Article
• Language: English
• Subjects: Analysis of Variance; Angiogenesis; Animals; Biological and medical sciences; Cell Line; Culture Media, Conditioned; Cytokines - physiology; Ecthyma, Contagious - pathology; Ecthyma, Contagious - virology; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation, Viral; Humans; Microbiology; Miscellaneous; Neovascularization, Pathologic - virology; Orf virus; Orf virus - genetics; Orf virus - pathogenicity; Pathogenesis; Polymerase Chain Reaction - methods; Proliferative infection; RNA, Messenger - biosynthesis; Sheep; Time Factors; VEGF-E; Viral Proteins - biosynthesis; Viral Proteins - genetics; Viral Proteins - physiology; Virology
• ISSN: 0378-1135; 1873-2542
• DOI: 10.1016/j.vetmic.2005.11.052

Proliferative orf virus infections in adult sheep have increased in Italy in the past few years: these extreme cases are frequently fatal and difficult to differentiate from other infectious diseases of sheep such as blue tongue. A probable explanation for the proliferative and highly vascularized nature of the lesions was found in the expression of the VEGF-E gene encoded by the orf virus. To investigate a possible role of the viral VEGF in the pathogenesis of severe persistent orf virus lesions, the activity of four VEGF-E variants was compared by an angiogenesis in vitro model. Similar angiogenic activity was found between strains isolated from the classical and the proliferative forms of the disease, even if the latter was able to develop a higher number of vessels during the first 24 h of infection. Our in vitro findings seems to exclude that the VEGF variants encoded by the strain isolated from the atypical form of the disease could be the responsible for the histopathological aspect of the proliferative lesions.