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25HC Depleted PMs-Accessible Cholesterol to Restrict SFTSV Entry and Infectious-EVs Mediated Infection
Abstract:
Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease caused by a novel tick-borne phlebitis virus of Bunyaviridae, newly named as Banda virus, characterized by high fever, thrombocytopenia, and leukopenia with high case fatality. Currently, no specific antiviral drugs are available to treat patients. Here, we report a natural lipid metabolite 25-Hydroxycholesterol (25HC) that inhibited SFTSV entry by activating the activity of acetyl-CoA-cholesterol acyltransferase (ACAT), a lipid metabolism enzyme, affecting the accessible cholesterol translocation between the cytoplasm and plasma membranes (PMs). We also found that 25HC could inhibit the extracellular vesicles carrying virions into target cells, thus preventing the vesicles from mediating virus spread. In short, 25HC reduced the PMs-accessible cholesterol through modulating lipid metabolism, thereby inhibiting the double infection of cells by virions and infectious EVs, and potentially reducing the efficiency of SFTSV dissemination.
Insights
A natural lipid metabolite, 25-Hydroxycholesterol (25HC), shows promise in combating Severe Fever with Thrombocytopenia Syndrome (SFTS). This compound inhibits virus entry and spread by modulating cellular cholesterol, offering a potential new therapeutic avenue for this emerging infectious disease.
Area of Science:
- Virology
- Infectious Diseases
- Lipid Metabolism
Background:
- Severe Fever with Thrombocytopenia Syndrome (SFTS) is an emerging tick-borne viral illness.
- Caused by a novel Bunyaviridae virus (Banda virus), SFTS presents with high fever, thrombocytopenia, and leukopenia, leading to high mortality.
- No specific antiviral treatments are currently available for SFTS.
Purpose of the Study:
- To identify potential therapeutic agents against SFTSV.
- To investigate the role of lipid metabolism in SFTSV infection and dissemination.
- To explore the antiviral activity of natural lipid metabolites.
Main Methods:
- Investigated the effect of 25-Hydroxycholesterol (25HC) on SFTSV.
- Assessed the impact of 25HC on acetyl-CoA-cholesterol acyltransferase (ACAT) activity.
- Examined the role of 25HC in inhibiting extracellular vesicle-mediated virus spread.
Main Results:
- 25-Hydroxycholesterol (25HC) inhibited SFTSV entry into host cells.
- 25HC activated ACAT, altering cholesterol translocation between cytoplasm and plasma membranes.
- 25HC reduced extracellular vesicle-mediated SFTSV dissemination.
Conclusions:
- 25HC modulates lipid metabolism to reduce accessible cholesterol at the plasma membrane.
- This mechanism inhibits both direct virion infection and extracellular vesicle-mediated spread of SFTSV.
- 25HC represents a potential therapeutic strategy to reduce SFTSV dissemination.
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