Toyoda T, Ochiai K, Hatai H, Murakami M, Ono E, Kimura T, Umemura T
Laboratory of Comparative Pathology, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan.
Vet Pathol. 2006 May;43(3):294-301. doi: 10.1354/vp.43-3-294.
Fowl glioma-inducing virus (FGV), which belongs to subgroup A of avian leukosis virus (ALV), shows tumorigenicity and pathogenicity, mainly in the nervous system, and causes astrocytoma and perineurioma. Apart from these neoplasms, cerebellar anomaly was found in chickens infected with FGV in ovo. The study reported here describes the morphologic characteristics of the affected cerebellum. Specific-pathogen-free chickens (C/O) were inoculated with FGV through the yolk sac on the 7th day of incubation. The cerebellar anomaly included diffuse depletion of granular cells of the internal granular layer (IGL), remnants of the external granular layer (EGL), and disorganization of the Purkinje cell layer. These cerebellar changes were observed in all birds except one. In the infected embryos, the EGL was thicker and had an irregular arrangement with a thin molecular layer (ML) and IGL, compared with the control. The granular cells were immunohistochemically positive for ALV common antigen. Immunohistochemical analysis for vimentin revealed disarrangement and decreased number of Bergmann's fibers. Use of the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling method and electron microscopy indicated that apoptotic granular cells were frequently observed in the EGL and ML. These results suggested that the cerebellar anomaly was hypoplasia, principally resulting from the apoptosis of granular cells in the EGL and ML caused by FGV infection and that the cell loss induced obstruction of granular cell migration and disarrangement of Bergmann's fibers in the ML.
禽胶质瘤诱导病毒（FGV）属于禽白血病病毒（ALV）A亚群，具有致瘤性和致病性，主要作用于神经系统，可引发星形细胞瘤和神经束膜瘤。除了这些肿瘤外，还在经卵感染FGV的鸡中发现了小脑异常。本文报道的研究描述了受影响小脑的形态学特征。在孵化第7天，通过卵黄囊给无特定病原体鸡（C/O）接种FGV。小脑异常包括内颗粒层（IGL）颗粒细胞弥漫性减少、外颗粒层（EGL）残留以及浦肯野细胞层紊乱。除一只鸡外，所有鸡均观察到这些小脑变化。与对照组相比，感染胚胎的EGL更厚，排列不规则，分子层（ML）和IGL较薄。颗粒细胞对ALV共同抗原免疫组化呈阳性。波形蛋白免疫组化分析显示伯格曼纤维排列紊乱且数量减少。使用末端脱氧核苷酸转移酶介导的dUTP-生物素缺口末端标记法和电子显微镜观察表明，在EGL和ML中经常观察到凋亡的颗粒细胞。这些结果表明，小脑异常是发育不全，主要是由FGV感染导致EGL和ML中颗粒细胞凋亡引起的，并且细胞丢失导致颗粒细胞迁移受阻以及ML中伯格曼纤维排列紊乱。
