Research Papers: Pathology:
The neglected avian hepatotropic virus induces acute and chronic hepatitis in ducks: an alternative model for hepatology
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Xumin Ou1,2,*, Sai Mao1,2,*, Jingyu Cao1,2, Yunchao Ma1,2, Guangpeng Ma4, Anchun Cheng1,2,3,*, Mingshu Wang1,2,3,*, Dekang Zhu2,3, Shun Chen1,2,3, Renyong Jia1,2,3, Mafeng Liu1,2,3, Kunfeng Sun1,2,3, Qiao Yang1,2,3, Ying Wu1,2,3 and Xiaoyue Chen2,3
1 Institute of Preventive Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, Sichuan, People′s Republic of China
2 Key Laboratory of Animal Disease and Human Health of Sichuan Province, Sichuan Agricultural University, Wenjiang, Chengdu, Sichuan, People′s Republic of China
3 Avian Disease Research Center, College of Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu, Sichuan, People′s Republic of China
4 China Rural Technology Development Center, Beijing, People′s Republic of China
* These authors have contributed equally to this work
Anchun Cheng, email:
Mingshu Wang, email:
Keywords: duck hepatitis A virus, viral hepatitis, liver injury, pathogenesis, viral-host interaction, Pathology Section
Received: February 17, 2017 Accepted: June 20, 2017 Published: July 05, 2017
Duck Hepatitis A Virus (DHAV) belongs to the Avihepatovirus, which is also classified into Picornaviridae with Hepatovirus, Hepatitis A Virus (HAV). In humans, the pathogenesis of HAV is not well understood because of limited work with animal models. Here, we investigated the progress of duck viral hepatitis caused by DHAV and their potential for dissecting the pathogenesis of HAV. During the course of infection, the duck model had undergone hepatocellular lesions (vacuolation, acidophilic degeneration and steatosis), lymphocytes recruitment (neutrophil granulocytes, heterophilic granulocytes and T cells or plasm cells) and repair (activation of hepatic stellate cells, fibrosis and regeneration). Coincident with liver injury, the serum biomarkers, aspartate aminotransferase and alanine transaminase were significantly increased. Moreover, comparatively lower CD4+ and CD8+ T-cells were recruited to the liver, which might lead to a persistent infection (40 wk). Because DHAV and HAV have similar genomic structure, biological phenotypes and can easily replicate in liver. And half of fibrosis-related genes had high homology between humans and ducks. Considering these similarity in pathological and virological phenotypes, we proposed that the ducks might be an alternatively small animal model that would provide insight into the pathogenesis of viral hepatitis, fibrosis and liver regeneration.
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