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Macrophage Cholesterol Depletion and Its Effect on the Phagocytosis of Cryptococcus neoformans
Published on: December 19, 2014
Effect of cellular cholesterol depletion on rabies virus infection
Kozue Hotta1, Boldbarrtar Bazartseren, Yoshihiro Kaku
1Department of Veterinary Science, National Institute of Infectious Diseases, 162-8640 Toyama 1-23-1, Shinjuku-ku, Tokyo 162-8640, Japan. kozue@nagasaki-u.ac.jp
Abstract:
Although there are several reports on candidates for rabies virus (RABV) receptor, possible roles played by these receptor candidates in determination of highly neurotropic nature of RABV have not been well understood. Since these candidate receptors for RABV were reported to be frequently associated with cholesterol-rich microdomains characterized by lipid rafts and caveolae structures, we attempted to determine whether the disturbance of microdomains caused by the cholesterol depletion showed any effects on RABV infection. When the cellular cholesterol was depleted by methyl-beta-cyclodextrin (MBCD) treatment, increase in RABV adsorption and infection, but not multiplication rather than suppression was observed in both BHK-21 and HEp-2 cells. These effects exerted by MBCD treatment on RABV infection could be reversed by cholesterol reconstitution. These results suggest that RABV enters BHK-21 or HEp-2 cells through ports of entry other than those located on cholesterol-rich microdomains and raise the possibility that RABV uses different mechanisms to enter the non-neuronal cells.
Insights
Cholesterol depletion enhanced rabies virus (RABV) adsorption and infection in cells, suggesting RABV may use alternative entry pathways. This finding impacts understanding of RABV neurotropism and cell entry mechanisms.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Rabies virus (RABV) receptor candidates are linked to cholesterol-rich microdomains.
- The role of these microdomains in RABV's neurotropic nature remains unclear.
Purpose of the Study:
- To investigate the effect of cholesterol depletion on RABV infection.
- To determine if RABV entry depends on cholesterol-rich microdomains.
Main Methods:
- Depletion of cellular cholesterol using methyl-beta-cyclodextrin (MBCD).
- Assessing RABV adsorption, infection, and multiplication in treated and untreated cells.
- Cholesterol reconstitution to reverse MBCD effects.
Main Results:
- Cholesterol depletion by MBCD increased RABV adsorption and infection in BHK-21 and HEp-2 cells.
- RABV multiplication was not significantly affected by cholesterol depletion.
- MBCD-induced effects on RABV infection were reversible upon cholesterol replenishment.
Conclusions:
- RABV likely utilizes entry points independent of cholesterol-rich microdomains in non-neuronal cells.
- This suggests RABV may employ diverse entry mechanisms for different cell types.
- Findings contribute to understanding RABV cell entry and neurotropism.
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