Epidemiology Division, Animal Health Research Institute, New Taipei City, Taiwan.
Fishhead Labs, LLC, Stuart, FL, USA.
Avian Pathol. 2021 Feb;50(1):41-51. doi: 10.1080/03079457.2020.1832199. Epub 2020 Nov 20.
Goose haemorrhagic polyomavirus (GHPV) is the aetiological agent of haemorrhagic nephritis enteritis of geese (HNEG), a fatal disease that impacts geese and has been recorded only in Europe. The present study describes the first clinical cases of HNEG in Taiwan and the phylogenesis of Taiwanese GHPV, and it elucidates the pathogenesis of GHPV infection using hybridization (ISH). The genomes of Taiwanese GHPV were highly similar to the previously reported strains. The diseased geese showed various degrees of vascular damage, especially in the digestive tract. The affected geese in the early stage showed transmural haemorrhagic enteritis in the intestine. In the middle to late stages, the most obvious lesion was hypoxic necrosis of renal tubules around intralobular central veins. Mineralization deposited in the kidney and systemic gout were also found. ISH revealed GHPV DNA in the vascular endothelial cells throughout the body, but not in the parenchymal cells of organs. Accordingly, the pathogenesis of GHPV infection was consistent with viral tropism in the endothelial cells. Specific attack of vascular endothelium by GHPV resulted in endothelial cell necrosis and subsequent increases of blood vessel permeability, as well as secondary circulation disorders, such as oedema, haemorrhage, and ischaemic necrosis in the adjacent parenchyma. Cell tropism of GHPV is determined by hybridization. The tropism results in vascular dysfunction and subsequent pathobiology. Haemorrhagic nephritis and enteritis of geese described outside Europe for the first time.
鹅出血性多瘤病毒(GHPV)是鹅出血性肾炎肠炎(HNEG)的病原体,HNEG 是一种致命疾病,仅在欧洲有记录。本研究描述了台湾首例 HNEG 临床病例和台湾 GHPV 的系统发生,并通过杂交(ISH)阐明了 GHPV 感染的发病机制。台湾 GHPV 的基因组与先前报道的毒株高度相似。患病鹅表现出不同程度的血管损伤,特别是在消化道。早期受影响的鹅表现出肠壁全层出血性肠炎。在中后期,最明显的病变是小叶间中心静脉周围肾小管缺氧性坏死。还发现肾脏和全身痛风中矿物质沉积。ISH 显示 GHPV DNA 存在于全身血管内皮细胞中,但不存在于器官实质细胞中。因此,GHPV 感染的发病机制与内皮细胞中的病毒嗜性一致。GHPV 对血管内皮细胞的特异性攻击导致内皮细胞坏死,随后血管通透性增加,以及继发性循环障碍,如相邻实质中的水肿、出血和缺血性坏死。GHPV 的细胞嗜性由杂交决定。嗜性导致血管功能障碍和随后的病理生物学。在欧洲以外首次描述了鹅出血性肾炎和肠炎。