The zebrafish galectins Drgal1-L2 and Drgal3-L1 bind in vitro to the infectious hematopoietic necrosis virus (IHNV) glycoprotein and reduce viral adhesion to fish epithelial cells

Abstract

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.

Functional Aspects of Fish Mucosal Lectins—Interaction with Non-Self

“…The virus enters the host at the base of the fins. In vitro the galectins prevented the virus from adhering to fish epithelial cells [ 54 ] where it usually binds to a fibronectin at the cells surface [ 55 ]. Virus uptake can also be stimulated by lectins, for example SsLec1, a C-type lectin from black rockfish ( Sebastes schlegelii ) increases infectious spleen and kidney necrosis virus (ISKNV) copy numbers in black rockfish [ 31 ].…”

Infectious hematopoietic necrosis virus: advances in diagnosis and vaccine development

“…IHNV G proteins form trimeric peplomers, which are responsible for the viral interaction with its host’s receptor (Coll, 1995). The virus is believed to penetrate the host membrane through receptor-mediated fibronectin endocytosis (Bearzotti et al, 1999; Liu & Collodi, 2002; Nita-Lazar et al, 2016). The G protein alone is capable of inducing protective immunity against IHNV infection (Corbeil et al, 1999).…”

Peer Review #2 of "Infectious hematopoietic necrosis virus: advances in diagnosis and vaccine development (v0.1)"

“…IHNV G proteins form trimeric peplomers, which are responsible for the viral interaction with its host's receptor (Coll 1995). The virus is believed to penetrate the host membrane through receptormediated fibronectin endocytosis (Bearzotti et al 1999;Liu & Collodi 2002;Nita-Lazar et al 2016). The G protein alone is capable of inducing protective immunity against IHNV infection PeerJ reviewing PDF | (2019:01:34359:1:1:NEW 22 Apr 2019)…”