Infectious salmon anaemia virus infection of Atlantic salmon gill epithelial cells

Abstract

Infectious salmon anaemia virus (ISAV), a member of the Orthomyxoviridae family, infects and causes disease in farmed Atlantic salmon (Salmo salar L.). Previous studies have shown Atlantic salmon endothelial cells to be the primary targets of ISAV infection. However, it is not known if cells other than endothelial cells play a role in ISAV tropism. To further assess cell tropism, we examined ISAV infection of Atlantic salmon gill epithelial cells in vivo and in vitro. We demonstrated the susceptibility of epithelial cells to ISAV infection. On comparison of primary gill epithelial cell cultures with ISAV permissive fish cell cultures, we found the virus yield in primary gill epithelial cells to be comparable with that of salmon head kidney (SHK)-1 cells, but lower than TO or Atlantic salmon kidney (ASK)-II cells. Light and transmission electron microscopy (TEM) revealed that the primary gill cells possessed characteristics consistent with epithelial cells. Virus histochemistry showed that gill epithelial cells expressed 4-O-acetylated sialic acid which is recognized as the ISAV receptor. To the best of our knowledge, this is the first demonstration of ISAV infection in Atlantic salmon primary gill epithelial cells. This study thus broadens our understanding of cell tropism and transmission of ISAV in Atlantic salmon.

Dual Mutation Events in the Haemagglutinin-Esterase and Fusion Protein from an Infectious Salmon Anaemia Virus HPR0 Genotype Promote Viral Fusion and Activation by an Ubiquitous Host Protease

“…Therefore, like in influenza viruses and NDV, ISAV fusion is an important determinant of virulence and together with other factors, such as receptor availability on the cell surface [99], interferon antagonistic properties [100][101][102] and certain polymerase features [103], partly contributes to the varying degree of virulence reported for different HPR genotypes. Variation in fusion ability linked to HE HPR deletions and F protein mutations may also explain the different tissue [4] and cell tropism reported in ISAV [15,99,104]. We propose that the fusion protein of viruses carrying full length HPR HE may be mainly activated by trypsinlike proteases, most likely at the cell surface.…”

Infectious salmon anaemia – pathogenesis and tropism

“…Weli et al . () showed replication on gill epithelial cells using immersion challenged Atlantic salmon and primary isolated gill epithelial cells. This demonstrates the potential of ISAV virus replication in gill epithelium and points to the gill as a possible port of entry and primary replication site as previously suggested.…”

“…; Weli et al . ) essential to the spread systemically (viraemia). The causative agent is taken up in the host and spread systemically (viraemia).…”

Fish mucosal immunity: gill

“…A transient replication in few epithelial cells followed by increasing replication in endothelial cells of the gills has been observed by immunohistochemistry (Aamelfot et al, 2012;Weli et al, 2013). A transient replication in few epithelial cells followed by increasing replication in endothelial cells of the gills has been observed by immunohistochemistry (Aamelfot et al, 2012;Weli et al, 2013).…”

“…To a lesser extent, ISAV also replicates in leukocytes (Aamelfot et al, 2012;Moneke et al, 2005) and gill epithelial cells (Aamelfot et al, 2012;Weli et al, 2013). ISAV attaches to its target cells using glycoprotein-bound 4-O-acetylated sialic acids (Hellebø et al, 2004).…”