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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Mink cell focus-forming murine leukemia virus killing of mink cells involves apoptosis and superinfection
F K Yoshimura1, T Wang, S Nanua
1Department of Immunology and Microbiology, Wayne State University, 540 E. Canfield Ave., Detroit, MI 48201, USA. fyoshi@med.wayne.edu
Abstract:
Induction of apoptosis by different types of pathogenic retroviruses is an important step in disease development. We have observed that infection of thymic lymphocytes by the mink cell focus-forming murine leukemia virus (MCF MLV) during the preleukemic period resulted in an enhancement of apoptosis of these cells. To further study the ability of MCF MLVs to induce apoptosis and the role of this process in viral pathogenesis, we have developed an in vitro system of virus-induced apoptosis. MCF13 MLV infection of mink epithelial cells resulted in the production of cytopathic foci. In contrast, infection of mink cells with the 4070A amphotropic MLV did not produce any cytopathic effects. Staining of MCF13 MLV-infected cells with propidium iodide and annexin V-fluorescein isothiocyanate indicated that virus-induced cell death was due to apoptosis. At 6 days postinfection, the percentage of apoptotic MCF13 MLV-infected cells was 27% compared with 2 to 3% for mock- or amphotropic MLV-infected cells, representing a 9- to 14-fold difference. Assays for caspase-3 activation confirmed the detection by flow cytometry of apoptosis of MCF13 MLV-infected cells. Large amounts of unintegrated linear viral DNA were detectable by Southern blot analysis during the acute phase of infection, which indicated that MCF13 MLV is able to superinfect mink cells. Unintegrated viral DNA of only the linear form was detectable in thymic lymphocytes isolated from MCF13 MLV-inoculated mice during the preleukemic period. These results indicated that the ability of MCF13 MLV to induce apoptosis is correlated with its ability to superinfect cells and that this occurs as an early step in thymic lymphoma development.
Insights
Mink cell focus-forming murine leukemia virus (MCF MLV) infection enhances apoptosis in thymic lymphocytes, a key step in lymphoma development. This apoptosis induction correlates with the virus's ability to superinfect cells.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Apoptosis, or programmed cell death, is crucial in disease pathogenesis.
- Pathogenic retroviruses, including murine leukemia viruses (MLVs), can induce apoptosis.
Purpose of the Study:
- To investigate the role of apoptosis in viral pathogenesis.
- To characterize the ability of mink cell focus-forming MLV (MCF MLV) to induce apoptosis.
Main Methods:
- Developed an in vitro system using mink epithelial cells and MCF13 MLV.
- Assessed apoptosis using propidium iodide and annexin V staining, flow cytometry, and caspase-3 activation assays.
- Analyzed viral DNA integration using Southern blot analysis.
Main Results:
- MCF13 MLV infection induced significant apoptosis (27%) in mink cells, unlike amphotropic MLV.
- Apoptosis was confirmed by flow cytometry and caspase-3 activation.
- MCF13 MLV demonstrated superinfection capability, evidenced by detectable unintegrated linear viral DNA.
Conclusions:
- MCF MLV's ability to induce apoptosis is linked to its superinfection capacity.
- Apoptosis induction by MCF MLV is an early event in thymic lymphoma development.
