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Published on: July 1, 2022
Feline immunodeficiency virus infection is enhanced by feline bone marrow-derived dendritic cells
F J U M van der Meer1, N M P Schuurman1, H F Egberink1
1Department of Immunology and Infectious Diseases, Division of Virology, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 1, 3584 CL Utrecht, The Netherlands.
Insights
Feline dendritic cells (feDCs) enhance feline immunodeficiency virus (FIV) replication in lymphocytes. Direct cell contact is required, suggesting feDCs play a key role in FIV pathogenesis.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Feline dendritic cells (feDCs) are implicated in feline immunodeficiency virus (FIV) pathogenesis.
- feDCs are hypothesized to transport and transfer FIV to lymphocytes.
Purpose of the Study:
- To investigate the role of feDCs in FIV infection of feline peripheral blood mononuclear cells (PBMCs) and thymocytes.
- To determine if feDCs influence FIV replication and T cell proliferation.
Main Methods:
- feDCs were generated from bone marrow mononuclear cells using feline interleukin-4 and granulocyte-macrophage colony-stimulating factor.
- Co-culture experiments were performed with feDCs and resting PBMCs or thymocytes.
- Transwell assays were used to differentiate between direct cell contact and soluble factor involvement.
Main Results:
- feDCs upregulated FIV replication in co-cultured PBMCs.
- feDCs enhanced FIV infection in co-cultured thymocytes.
- Direct cell contact between feDCs and lymphocytes was necessary for enhanced FIV infection.
- feDCs induced proliferation of resting thymocytes.
Conclusions:
- feDCs promote FIV replication in feline leukocytes, similar to human and simian DCs.
- Direct cell-to-cell contact is crucial for feDC-mediated enhancement of FIV infection.
- feDCs may influence FIV pathogenesis through T cell activation and direct viral transfer.
Abstract:
In the pathogenesis of feline immunodeficiency virus (FIV) infection, feline dendritic cells (feDCs) are thought to play an important role. As with DCs in other species, feDCs are believed to transport virus particles to lymph nodes and transfer them to lymphocytes. Our investigation has focused on the ability of feDCs to influence the infection of syngeneic peripheral blood mononuclear cells (PBMCs) and allogeneic thymocytes. feDCs were derived from bone marrow mononuclear cells that were cultured under the influence of feline interleukin-4 and feline granulocyte-macrophage colony-stimulating factor. By using these feDCs in co-culture with resting PBMCs, an upregulation of FIV replication was shown. An enhancement of FIV infection was also detected when co-cultures of feDCs/feline thymocytes were infected. To obtain this enhancement, direct contact of the cells in the co-culture was necessary; transwell cultures showed that the involvement of only soluble factors produced by feDCs in this process is not likely. These feDCs were also able to induce the proliferation of resting thymocytes, which might explain the enhanced FIV replication observed. Together, these data suggest that feDCs have abilities similar to those shown for simian and human DCs in the interaction with leukocytes. This system is suitable for further investigations of the interplay of DC and T cells during FIV infection in vitro.
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