Abstract
The 27.8kDa membrane protein from flounder (Paralichthys olivaceus) gill (FG) cells was previously identified as a putative cellular receptor involved in lymphocystis disease virus (LCDV) infection. In this paper, the expression of receptor-27.8kDa (27.8R) and LCDV loads in FG cells and hirame natural embryo (HINAE) cells were investigated upon LCDV infection and anti-27.8R monoclonal antibody (MAb) treatment. The results showed the 27.8R was expressed and co-localized with LCDV in both FG and HINAE cell surface. After LCDV infection, the expression of 27.8R exhibited a dose-dependent up-regulation with the increasing of LCDV titers, and demonstrated a tendency to increase firstly and then decrease during a time course up to 9 days; LCDV copies showed a similar variation trend to the 27.8R expression, however, it reached the highest level later than did the 27.8R expression. Additionally, the 27.8R expression and LCDV copies in FG cells were higher than those in HINAE cells. In the presence of increasing concentration of the anti-27.8R MAbs, the up-regulation of 27.8R expression and the copy numbers of LCDV significantly declined post LCDV infection, and the cytopathic effect induced by LCDV in the two cell lines was accordingly reduced, indicating anti-27.8R MAbs pre-incubation could inhibit the up-regulation of 27.8R expression and LCDV infection. These results suggested that LCDV infection could induce up-regulation of 27.8R expression, which in turn increased susceptibility and availability of FG and HINAE cells for LCDV entry, providing important new insights into the LCDV replication cycle and the interaction between this virus and the host cells.
Highlights
Lymphocystis disease virus (LCDV), which belongs to the genus lymphocystivirus within the Iridoviridae family [1, 2], is the causative agent of lymphocystis disease characterized by formation of hypertrophied cells on fish skin, fins and mouth, and has affected more than 140 marine and freshwater fish species worldwide, resulting in great economic losses [3, 4]
To confirm the expression of 27.8R protein in both flounder gill (FG) and hirame natural embryo (HINAE) cells, SDS-PAGE followed by western blotting was performed using the cell membrane proteins and cytoplasm proteins extracted from the two cell lines
The results showed that anti-27.8R monoclonal antibody (MAb) reacted with only one band at a molecular weight of 27.8kDa from both FG and HINAE cell membrane proteins (Fig 1, lane 6 and 7), suggesting 27.8R was expressed in the cell membrane
Summary
Lymphocystis disease virus (LCDV), which belongs to the genus lymphocystivirus within the Iridoviridae family [1, 2], is the causative agent of lymphocystis disease characterized by formation of hypertrophied cells on fish skin, fins and mouth, and has affected more than 140 marine and freshwater fish species worldwide, resulting in great economic losses [3, 4]. Receptor Expression and LCDV Infection the infected flounder (Paralichthys olivaceus) are investigated [5], and the antiviral molecules, vaccine and immunostimulants that enhance the innate immune response and disease resistance in LCDV infected fish have been reported [6,7,8]. It is well known that viral receptors mediate a physical interaction between virus and target cells and the initial entry. Several researches have been focused on the host cellular molecules and viral proteins involved in LCDV infection [9,10,11,12]. No information is known about the dynamic expression of the receptors in response to LCDV infection
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