Cholesterol, a component of cell membranes and a precursor for steroid hormones and bile acids, is synthesized by body cells and additionally absorbed with food. The hydrophobic cholesterol is transported in plasma via lipoproteins, complexes between lipids and apolipoproteins. The ratio of the four classes of lipoproteins (High-density lipoproteins (HDL), low-density lipoproteins (LDL), very low density lipoproteins (VLDL) and chylomicrons) can be used as risk factors for cardiovascular disease and to access lipid metabolism. While LDL is mostly associated with apolipoprotein-B, apolipoprotein-A is primarily present in HDL, directing the lipoproteins to different receptors. In addition to antioxidant effects, HDL also serves as a powerful mediator of the cellular inflammatory and antithrombotic responses. (1, 2)
Several viruses showed to utilize host cell metabolism for their own purposes. Dengue, hepatitis, and human cytomegalovirus appear to increase lipid synthesis, while hepatitis virus B increased the cholesterol metabolism. (3) Various roles of cholesterol in the stages of viral infection were reviewed for flavivirus by Osuna-Ramos et al. in 2018. (4)
Over 28 million cases and 900.000 deaths due to COVID-19 have been reported to the WHO by September 14, 2020.
A retrospective analysis of 228 COVID-19 patients showed lower levels of total cholesterol, triglycerides, LDL-cholesterol (LDL-c), and HDL-cholesterol (HDL-c) in comparison to the control group. HDL-c was at the lower reference ranges in both groups but was lower in severe cases compared to non-severe COVID-19 patients. (5)
Sterol regulated element binding protein-2 (SREBP-2) is a transcription factor, regulating gene expression for cholesterol biosynthesis. Cholesterol synthesis appears to be reduced by downregulation in some viral infections. (6)
The activation of SREBP-2 is reported in COVID-19 together with decreased cholesterol levels. Activated SREBP-2 appears to induce inflammatory responses, while the SREBP-2 mediated cholesterol pathway remains inhibited due to additional effects of the disease. (7)
While low levels of HDL-c can be related to severe cases in COVID-19, the role of HDL-c and lipid metabolism should be further investigated to understand the impacts on different pathways in this complex disease.
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1. Dati F, Metzmann E. Proteins: laboratory testing and clinical use. Holzheim: DiaSys, Diagnostic Systems; 2005.
2. Thomas L, editor. Labor und Diagnose: Indikation und Bewertung von Laborbefunden für die medizinische Diagnostik. 6. Aufl. Frankfurt/Main: TH-Books-Verl.-Ges; 2005.
3. Thaker SK, Ch’ng J, Christofk HR. Viral hijacking of cellular metabolism. BMC Biol. 2019;17:59.
4. Osuna-Ramos JF, Reyes-Ruiz JM, del Ángel RM. The Role of Host Cholesterol During Flavivirus Infection. Front Cell Infect Microbiol. 2018;8:388.
5. Wang G, Zhang Q, Zhao X, Dong H, Wu C, Wu F, et al. Low high-density lipoprotein level is correlated with the severity of COVID-19 patients: an observational study. Lipids Health Dis. 2020;19:204.
6. Blanc M, Hsieh WY, Robertson KA, Watterson S, Shui G, Lacaze P, et al. Host Defense against Viral Infection Involves Interferon Mediated Down-Regulation of Sterol Biosynthesis. Virgin SW, editor. PLoS Biol. 2011;9:e1000598.
7. Lee W, Ahn JH, Park HH, Kim HN, Kim H, Yoo Y, et al. COVID-19-activated SREBP2 disturbs cholesterol biosynthesis and leads to cytokine storm. Sig Transduct Target Ther. 2020;5:186.