Pantin-Jackwood M J, Spackman E, Day J M
Southeast Poultry Research Laboratory, US Department of Agriculture, Agricultural Research Service, 934 College Station Road, Athens, GA 30605, USA.
Vet Pathol. 2007 Mar;44(2):185-95. doi: 10.1354/vp.44-2-185.
The pathogenesis of 4 isolates of turkey-origin reovirus (NC/SEP-R44/03, NC/98, TX/98, and NC/85) and 1 chicken-origin reovirus (1733) was examined by infecting specific pathogen free (SPF) poults. These turkey-origin reovirus (TRV) isolates were collected from turkey flocks experiencing poult enteritis and are genetically distinct from previously reported avian reoviruses. Microscopic examination of the tissues collected from the TRV-infected poults revealed different degrees of bursal atrophy characterized by lymphoid depletion and increased fibroplasia between the bursal follicles. To understand the relationship between virus spread and replication, and the induction of lesions, immunohistochemical staining (IHC) for viral antigen, in situ hybridization (ISH) for the detection of viral RNA, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay for the detection of apoptosis in affected tissues was performed. Both IHC and ISH revealed viral antigen and RNA in the surface epithelial cells of the bursa, in macrophages in the interstitium of the bursa and, to lesser degree, in splenic red pulp macrophages and intestinal epithelial cells. Increased apoptosis of bursal lymphocytes and macrophages was observed at 2 and 5 days postinoculation. No lesions were found in tissues from poults inoculated with the virulent chicken-origin strain, however viral antigen was detected in the bursa and the intestine. Although all TRVs studied displayed similar tissue tropism, there were substantial differences in the severity of the lesions produced. Poults inoculated with NC/SEP-R44/03 or NC/98 had moderate to severe bursal atrophy, whereas poults inoculated with TX/98 or NC/85 presented a mild to moderate bursal lymphoid depletion. The lymphoid depletion observed in the bursa appears to be the effect of an indirectly induced apoptosis and would most likely result in immune dysfunction in poults infected with TRV.
通过感染无特定病原体(SPF)的雏火鸡,研究了4株火鸡源呼肠孤病毒(NC/SEP-R44/03、NC/98、TX/98和NC/85)和1株鸡源呼肠孤病毒(1733)的发病机制。这些火鸡源呼肠孤病毒(TRV)分离株从患有雏火鸡肠炎的火鸡群中收集,在基因上与先前报道的禽呼肠孤病毒不同。对感染TRV的雏火鸡采集的组织进行显微镜检查,发现不同程度的法氏囊萎缩,其特征为淋巴细胞耗竭以及法氏囊滤泡之间的纤维增生增加。为了解病毒传播与复制以及病变诱导之间的关系,进行了病毒抗原的免疫组织化学染色(IHC)、病毒RNA检测的原位杂交(ISH)以及受影响组织中凋亡检测的末端脱氧核苷酸转移酶介导的dUTP缺口末端标记(TUNEL)分析。IHC和ISH均显示法氏囊表面上皮细胞、法氏囊间质中的巨噬细胞以及程度较轻的脾红髓巨噬细胞和肠上皮细胞中有病毒抗原和RNA。接种后2天和5天观察到法氏囊淋巴细胞和巨噬细胞凋亡增加。接种强毒鸡源毒株的雏火鸡组织中未发现病变,但在法氏囊和肠道中检测到病毒抗原。虽然所研究的所有TRV均表现出相似的组织嗜性,但所产生病变严重程度存在显著差异。接种NC/SEP-R44/03或NC/98的雏火鸡有中度至重度法氏囊萎缩,而接种TX/98或NC/85的雏火鸡表现为轻度至中度法氏囊淋巴细胞耗竭。在法氏囊中观察到的淋巴细胞耗竭似乎是间接诱导凋亡的结果,很可能导致感染TRV的雏火鸡免疫功能障碍。