Distinct usage of three C-type lectins by Japanese encephalitis virus: DC-SIGN, DC-SIGNR, and LSECtin

Abstract

Infection with West Nile virus and dengue virus, two mosquito-borne flaviviruses, is enhanced by two calcium-dependent lectins: dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN), and its related molecule (DC-SIGNR). The present study examined the relationship between Japanese encephalitis virus (JEV) infection and three lectins: DC-SIGN, DC-SIGNR, and liver sinusoidal endothelial cell lectin (LSECtin). Expression of DC-SIGNR resulted in robust JEV proliferation in a lymphoid cell line, Daudi cells, which was otherwise non-permissive to infection. DC-SIGN expression caused moderate JEV proliferation, with effects that varied according to the cells in which JEV was prepared. LSECtin expression had comparatively minor, but consistent, effects, in all cell types used in JEV preparation. While DC-SIGN/DC-SIGNR-mediated JEV infection was inhibited by yeast mannan, LSECtin-mediated infection was inhibited by N-acetylglucosamine β1-2 mannose. Although involvement of DC-SIGN/DC-SIGNR in infection seems to be a common characteristic, this is the first report on usage of LSECtin in mosquito-borne flavivirus infection.

Sensitivity of Kupffer cells and liver sinusoidal endothelial cells to ricin toxin and ricin toxin–Ab complexes

“…One candidate is LSECtin, a single domain CTL with homology to DC‐SIGN and DC‐SIGNR expressed exclusively in the liver . LSECtin serves as a receptor for Ebola virus, SARS coronavirus, and Japanese encephalitis virus . We found that recombinant LSECtin recognized ricin toxin in a solid phase binding assay and that the interaction was inhibited by mannan.…”

Valosin-containing protein (VCP/p97) plays a role in the replication of West Nile virus

“…WNV attaches to host cells through the interaction of the viral E protein and cellular receptors on the surface of host cells (Fields et al, 2013). Several attachment receptors of WNV have been reported and include the laminin receptor (Bogachek et al, 2010;Perera-Lecoin et al, 2014;Zaitsev et al, 2014;Zidane et al, 2013), TIM (T cell/transmembrane, immunoglobulin and mucin) and TAM (Tyro3, Axl and Mer) families (Carnec et al, 2016;Morizono and Chen, 2014;Perera-Lecoin et al, 2014), DC-SIGN/L-SIGN (dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin) (Davis et al, 2006;Denizot et al, 2012;Martina et al, 2008;Shimojima et al, 2014) and integrin ␣v␤3 (Bogachek et al, 2010;Fields et al, 2013;Perera-Lecoin et al, 2014;Smit et al, 2011;Zaitsev et al, 2014). Following attachment, the virus is then internalized into the cytoplasm via clathrin-mediated endocytosis (Brinton, 2014;Chu and Ng, 2004;Fields et al, 2013).…”

Severe Fever with Thrombocytopenia Syndrome Virus Antigen Detection Using Monoclonal Antibodies to the Nucleocapsid Protein

“…Forecariah virus (FORV) and Palma virus (PALV), which were kindly gifted from Robert Tesh, University of Texas Medical Branch, USA, were handled in BSL-2. The infectious dose of the SFTSV and RVFV stock solutions was determined by calculating the 50% tissue culture infectious dose (TCID 50 ) as described previously [ 11 , 13 , 34 ]. Preliminary experiments indicated that treatment of sera containing SFTSV (10 7 TCID 50 /ml) with 1% triton X-100 in combination with UV-irradiation (312 nm, 2.5 mW/cm 2 ) on a trans-illuminator for 10 min caused complete loss of viral infectivity in cells.…”