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Published on: June 22, 2016
Relationship between Expression of Cellular Receptor-27.8 kDa and Lymphocystis Disease Virus (LCDV) Infection
Ronghua Wu1, Xiaoqian Tang1, Xiuzhen Sheng1
1Laboratory of Pathology and Immunology of Aquatic Animals, Ocean University of China, 5 Yushan Road, Qingdao 266003, P. R. China.
Abstract:
The 27.8 kDa 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-27.8 kDa (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.
Insights
Lymphocystis disease virus (LCDV) infection up-regulates a 27.8 kDa membrane receptor (27.8R) in fish cells. Blocking this receptor with antibodies inhibits viral replication and cell damage, revealing a key host-pathogen interaction.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- A 27.8 kDa membrane protein in flounder gill (FG) cells was identified as a potential receptor for lymphocystis disease virus (LCDV).
- Understanding the interaction between LCDV and its cellular receptor is crucial for comprehending viral pathogenesis.
Purpose of the Study:
- To investigate the expression of the 27.8 kDa receptor (27.8R) and LCDV loads in FG and hirame natural embryo (HINAE) cells.
- To determine the effect of anti-27.8R monoclonal antibodies (MAbs) on LCDV infection and receptor expression.
Main Methods:
- Quantification of 27.8R expression and LCDV copies in FG and HINAE cells via infection and MAb treatment.
- Confocal microscopy to assess co-localization of 27.8R and LCDV.
- Evaluation of cytopathic effects post-infection and MAb intervention.
Main Results:
- 27.8R is expressed on the cell surface and co-localizes with LCDV in both cell types.
- LCDV infection induces dose-dependent up-regulation of 27.8R, with expression peaking before viral load.
- Anti-27.8R MAbs significantly reduced 27.8R up-regulation, LCDV copies, and cytopathic effects.
Conclusions:
- LCDV infection triggers the up-regulation of the 27.8R, enhancing cellular susceptibility to viral entry.
- The 27.8R plays a critical role in facilitating LCDV infection and replication.
- Targeting the 27.8R with antibodies presents a potential strategy for controlling LCDV infections.
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