
The Histopathological Characteristics Caused by <b><i>Trionyx sinensis</i></b> Hemorrhagic Syndrome Virus (TSHSV) and Comparative Proteomic Analysis of Liver Tissue in TSHSV-Infected Chinese Soft-Shelled Turtles (<b><i>Pelodiscus sinensis</i></b>)
Author(s) -
Li Liu,
Zheng Cao,
Feng Lin,
YE Xue-ping,
Shujuan Lü,
Sunjian Lyv
Publication year - 2017
Publication title -
intervirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.641
H-Index - 61
eISSN - 1423-0100
pISSN - 0300-5526
DOI - 10.1159/000479795
Subject(s) - kidney , pathology , biology , microbiology and biotechnology , medicine , endocrinology
Trionyx sinensis hemorrhagic syndrome virus (TSHSV) is a pathogen that causes severe hemorrhagic syndrome and irreversible damage to different infected tissues of Pelodis cus sinensis, ending in the death of affected organisms. In the present study, the histopathological characteristics of TSHSV-infected P. sinensis were analyzed and compared by HE staining. Relative and absolute quantification (iTRAQ)-based proteomic analysis was employed to explore the molecular pathology of liver injury. Anatomical features indicated that TSHSV caused obvious congestion in the liver, kidney, intestine, and other tissues of P. sinensis. The typical clinical symptoms included hepatomegaly, fragility, spotty and severe congestion in liver tissue, and also obvious intestinal bleeding. The histopathological studies corroborated such lesions in the liver and kidney, etc. iTRAQ-based proteomic analysis revealed that there were 252 differentially expressed proteins in the liver tissue between healthy and infected P. sinensis, of which 118 proteins were upregulated and 134 proteins were downregulated. GO enrichment analysis and KEGG pathway analysis initially revealed the molecular mechanism of pathological changes in P. sinensis by TSHSV infection. The expression of some differentially expressed proteins was further confirmed by qRT-PCR. These results provided important information for the pathological diagnosis of TSHSV-caused disease, as well as the mechanism underlying TSHSV-caused disease.