Researchers uncover how SARS-CoV-2 rewires cholesterol metabolism, highlighting a novel target to combat COVID-19's metabolic and cardiovascular effects. Study: Manipulation of Host Cholesterol by SARS-CoV-2 . Image Credit: Kateryna Kon / Shutterstock *Important notice: bioRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.
In a recent research paper posted to the bioRxiv preprint* server, researchers in the United States investigated the potential effect of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on cholesterol metabolism, focusing on the role of the viral protein open reading frame 3a (ORF3a). They found that SARS-CoV-2 causes cholesterol sequestration in lysosomes via the ORF3a protein, which disrupts protein trafficking and reduces the levels of bis(monoacylglycero)phosphate (BMP) in the cell, enhancing viral survival. Background Coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, disrupts lipid metabolism, particularly cholesterol homeostasis, which can persist during and after infection.
This is linked to disease severity and long-term complications like dyslipidemia and cardiovascular diseases. Cholesterol is crucial for cellular function and is primarily transported through lysosomes, where proteins like Niemann-Pick C1 and C2 (NPC1 and NPC2) facilitate its release. SARS.