Department of Pathogenetic Veterinary Science, The United Graduate School of Veterinary Science, Gifu University, 1-1 Yanagido, Gifu, Japan.
Avian Pathol. 2009 Dec;38(6):469-83. doi: 10.1080/03079450903349162.
Chicken anaemia virus (CAV) is the most important confounding pathogen in Marek's disease virus (MDV) infection. The effect of CAV co-infection at 4 weeks of age after inoculation of virulent MDV (vMDV, KS strain) or very virulent MDV (vvMDV, Md/5 strain) in 1-day-old chicks was investigated by pathological and immunohistochemical studies. CAV increased the mortality rates induced by vMDV or vvMDV. The packed cell volume was reduced significantly in vMDV-CAV infection; however, no reduction or non-significant reduction was observed in vMDV infection. Bone marrow hypoplasia was related to CAV co-infection and none of the birds inoculated with vMDV or vvMDV had hypoplasia. Severe atrophy of the thymus and bursa of Fabricius was observed in the vvMDV-CAV and vvMDV groups. Complete regeneration of the thymus cortex and bursa of Fabricius in the vMDV group was noted and was in contrast to sequential lymphoid depletion after CAV inoculation in the vMDV-CAV group. The spleen was either regenerated, lymphoid depleted or had lymphoproliferative lesions. Lymphoid depletion in the spleen was not detected in the vMDV group; however, it was prominent in the vMDV-CAV and vvMDV-CAV groups during the first 2 weeks after CAV inoculation. CAV inclusions and antigens were detected in the thymus cortex and spleen of vMDV-CAV and vvMDV-CAV groups during the experiment. Severe depletion of CD8(+) T cells was observed in depleted spleen and thymus. The neoplastic foci appeared around splenic arterioles and venules, and stained mainly by CD4 antibody; however, CD8(+) T cells were singly dispersed or were present in clusters. It could be concluded that CAV was responsible for bone marrow hypoplasia, severe anaemia and hindrance of lymphoid organ regeneration in MDV-CAV co-infection.
鸡贫血病毒(CAV)是马立克氏病病毒(MDV)感染中最重要的干扰病原体。通过病理学和免疫组织化学研究,在 1 日龄雏鸡中接种强毒 MDV(KS 株)或超强毒 MDV(Md/5 株)4 周后,研究了 CAV 合并感染的影响。CAV 增加了强毒 MDV 或超强毒 MDV 引起的死亡率。CAV 合并感染导致红细胞压积显著降低;而强毒 MDV 感染则没有降低或没有显著降低。骨髓发育不良与 CAV 合并感染有关,接种强毒 MDV 或超强毒 MDV 的鸡无一例发生骨髓发育不良。在 vvMDV-CAV 和 vvMDV 组中观察到严重的胸腺和法氏囊萎缩。vMDV 组的胸腺皮质和法氏囊完全再生,而在 vMDV-CAV 组中,在接种 CAV 后,连续发生淋巴细胞耗竭。脾再生、淋巴细胞耗竭或发生淋巴增生性病变。vMDV 组未检测到脾淋巴细胞耗竭;然而,在 vMDV-CAV 和 vvMDV-CAV 组中,在接种 CAV 后的前 2 周内,脾淋巴细胞耗竭明显。在 vMDV-CAV 和 vvMDV-CAV 组的胸腺皮质和脾中检测到 CAV 包涵体和抗原。在耗竭的脾和胸腺中观察到 CD8+T 细胞严重耗竭。肿瘤灶出现在脾小动脉和小静脉周围,主要用 CD4 抗体染色;然而,CD8+T 细胞呈单个分散或成簇存在。可以得出结论,CAV 是 MDV-CAV 合并感染中导致骨髓发育不良、严重贫血和淋巴器官再生受阻的原因。