期刊
DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY
卷 55, 期 -, 页码 241-252出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.dci.2015.09.007
关键词
Infectious hematopoietic necrosis virus (IHNV); Zebrafish; Epithelial cells; Galectin; Viral adhesion; IHNV envelope glycoprotein
资金
- National Institutes of Health [R01 GM070589-01, 5T32AI095190-03, 5T32A195190-02]
- Department of Biotechnology, New Delhi, India
- Biotechnology and Biological Sciences Research Council [BB/K016164/1, BB/F008309/1]
- Wellcome Trust Senior Investigator Award
- BBSRC [BB/F008309/1, BB/K016164/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/K016164/1, BB/F008309/1] Funding Source: researchfish
The infectious hematopoietic necrosis virus (IHNV; Rhabdoviridae, Novirhabdovirus) infects teleost fish, such as salmon and trout, and is responsible for significant losses in the aquaculture industry and in wild fish populations. Although IHNV enters the host through the skin at the base of the fins, the viral adhesion and entry mechanisms are not fully understood. In recent years, evidence has accumulated in support of the key roles played by protein-carbohydrate interactions between host lectins secreted to the extracellular space and virion envelope glycoproteins in modulating viral adhesion and infectivity. In this study, we assessed in vitro the potential role(s) of zebrafish (Danio rerio) proto type galectin-1 (Drgal1-L2) and a chimera galectin-3 (Drgal3-L1) in IHNV adhesion to epithelial cells. Our results suggest that the extracellular Drgal1-L2 and Drgal3-L1 interact directly and in a carbohydrate-dependent manner with the IHNV glycosylated envelope and glycans on the epithelial cell surface, significantly reducing viral adhesion. (C) 2015 Elsevier Ltd. All rights reserved.
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