Modulation of lipid metabolism by thapsigarin inhibits hepatitis C virus infection by multiple mechanisms

Thapsigargin inhibits hepatitis C virus infection by blocking both RNA replication and extracellular egress, linked to enlarged lipid droplets and reduced apolipoprotein B/E secretion.

• Why it matters: Broad antiviral effects of thapsigargin are known, but the specific mechanisms—especially whether they involve UPR versus lipid remodeling—were unclear for HCV.
• What they did: Using HCV as a model, cells were pre-treated with thapsigargin; lipid synthesis genes (including FASN and DGAT1/2) and CIDE-C were measured, CIDEC was silenced, and secretion was assessed via apolipoprotein B/E and Gaussia luciferase.
• The result: Thapsigargin partially reduced HCV RNA replication and more strongly lowered extracellular viral RNA/titer; CIDEC knockdown rescued replication but not extracellular titer, while intracellular titers stayed intact and apolipoprotein B/E secretion dropped, implying a secretion defect.

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