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Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
Good Cholesterol Gone Bad? HDL and COVID-19
George E G Kluck1, Jeong-Ah Yoo1, Emmanuel H Sakarya1
1Thrombosis and Atherosclerosis Research Institute and Department of Biochemistry and Biomedical Sciences, McMaster University and Hamilton Health Sciences, Hamilton, ON L8L 2X2, Canada.
Insights
High-density lipoprotein (HDL) and its receptor SR-B1 play a complex role in COVID-19 severity. Their interaction with SARS-CoV-2 influences viral infection and disease outcomes, impacting cholesterol metabolism.
Area of Science:
- Cardiovascular biology
- Virology
- Immunology
Background:
- COVID-19, caused by SARS-CoV-2, shows inverse correlation between HDL levels and disease severity.
- Low HDL levels are linked to increased risk of severe COVID-19 outcomes.
- HDL's interaction with SARS-CoV-2 spike protein and ACE2 receptor is complex, with studies showing both facilitation and suppression of infection.
Purpose of the Study:
- To review the multifaceted role of HDL and SR-B1 in SARS-CoV-2 infection and COVID-19.
- To explore recent advancements in understanding HDL's structure, properties, and function during SARS-CoV-2 infection.
Main Methods:
- Literature review of existing studies on HDL, SR-B1, and SARS-CoV-2.
- Analysis of the interplay between HDL, SR-B1, and viral entry mechanisms.
- Synthesis of current knowledge on HDL's impact on COVID-19 pathogenesis.
Main Results:
- HDL's effect on SARS-CoV-2 infection is context-dependent, influenced by HDL concentration and SR-B1 expression.
- HDL can facilitate viral entry by binding to the spike protein and promoting interaction with ACE2 under specific conditions.
- Conversely, HDL has also been shown to suppress SARS-CoV-2 infection, with SR-B1 mediating this effect.
Conclusions:
- HDL and SR-B1 are critical mediators in cholesterol metabolism and play a significant, complex role in COVID-19.
- Understanding HDL's dual role in viral infection is crucial for developing therapeutic strategies against SARS-CoV-2.
- Further research into HDL structure and function during infection is warranted to elucidate its precise impact on COVID-19.
Abstract:
The transmissible respiratory disease COVID-19, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has affected millions of people worldwide since its first reported outbreak in December of 2019 in Wuhan, China. Since then, multiple studies have shown an inverse correlation between the levels of high-density lipoprotein (HDL) particles and the severity of COVID-19, with low HDL levels being associated with an increased risk of severe outcomes. Some studies revealed that HDL binds to SARS-CoV-2 particles via the virus's spike protein and, under certain conditions, such as low HDL particle concentrations, it facilitates SARS-CoV-2 binding to angiotensin-converting enzyme 2 (ACE2) and infection of host cells. Other studies, however, reported that HDL suppressed SARS-CoV-2 infection. In both cases, the ability of HDL to enhance or suppress virus infection appears to be dependent on the expression of the HDL receptor, namely, the Scavenger Receptor Class B type 1 (SR-B1), in the target cells. SR-B1 and HDL represent crucial mediators of cholesterol metabolism. Herein, we review the complex role of HDL and SR-B1 in SARS-CoV-2-induced disease. We also review recent advances in our understanding of HDL structure, properties, and function during SARS-CoV-2 infection and the resulting COVID-19 disease.
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