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Cholesterol enhances mouse hepatitis virus-mediated cell fusion
1Department of Microbiology and Infectious Diseases, University of Calgary, Alberta, Canada.
Virology
|April 1, 1988
Summary
Cholesterol enhances mouse hepatitis virus (MHV) cell fusion but does not eliminate virus persistence. Membrane fusion resistance and MHV persistence are modulated, not abolished, by cell membrane cholesterol.
Area of Science:
- Virology
- Cell Biology
- Biochemistry
Background:
- Mouse hepatitis virus (MHV) infection causes distinct outcomes in different mouse fibroblast cell lines: acute infection with cell fusion in L-2 cells versus persistent infection with reduced fusion in LM-K cells.
- The role of host cell membrane lipid composition and cytoskeleton in modulating MHV-induced cell fusion and virus persistence is not fully understood.
Purpose of the Study:
- To investigate how host cell membrane lipid composition, specifically cholesterol and fatty acids, and the cytoskeleton influence MHV-induced cell fusion.
- To determine the impact of these modifications on MHV replication and persistence.
Main Methods:
- Treatment of mouse fibroblast cell lines (L-2 and LM-K) with cytoskeleton-disrupting drugs (cytochalasin B, colchicine).
- Supplementation of cell membranes with specific fatty acids (arachidonic acid, palmitic acid) and cholesterol.
- Assessment of MHV-induced cell fusion extent, virus replication, and virus persistence.
- Utilized a contact fusion assay to confirm cholesterol's role in later fusion events.
Main Results:
- Cytoskeleton disruption did not affect MHV-induced cell fusion.
- Fatty acid supplementation had minimal impact on fusion and replication.
- Increased membrane cholesterol significantly enhanced MHV-mediated cell fusion in both cell types.
- Cholesterol enhancement of fusion was independent of MHV internalization, acting at a later stage.
- Cholesterol-supplemented L-2 cells showed reduced virus replication, correlating with increased fusion.
- Cholesterol supplementation increased fusion susceptibility in LM-K cells but did not abolish their capacity for MHV persistence.
Conclusions:
- Host cell membrane cholesterol content plays a significant role in modulating MHV-induced cell fusion.
- While cholesterol enhances fusion, it does not eliminate the ability of cells to support MHV persistence.
- Both membrane fusion resistance and MHV persistence are influenced by, but not completely overcome by, alterations in cell membrane cholesterol.