High-density lipoprotein (HDL) is a type of cholesterol that has the reputation of being good for you. As the US Centres for Disease Control and Prevention (CDC) explains, while low-density lipoprotein (LDL or bad cholesterol) makes up for most of the cholesterol in your body, it's HDL that absorbs it from all over your system and carries it back to the liver. The liver then flushes out the LDL cholesterol and HDL gets back to work.
Most studies indicate that high levels of HDL in your body can lower your risks of heart disease and stroke. However, a new study published in the journal Nature Metabolism suggests that the SARS-CoV-2 virus, which causes COVID-19 infection, uses the body's cholesterol synthesis system to enter the host cells. The study, conducted by researchers at the Academy of Military Medical Sciences in China, shows that SARS-CoV-2 actually hijacks the essentially healthy process through which HDL works to gain entry into the body.
How SARS-CoV-2 piggybacks on HDL synthesis
The connection between cholesterol and COVID-19 is one which has been established for a while now; this is reflected in the fact that studies, and even the CDC, list high-cholesterol levels as a risk factor for severe COVID-19 disease. A study published in Trends in Anaesthesia and Critical Care in September 2020 explains that SARS-CoV-2 has ribonucleic acid (RNA) in its genetic material with a lipid envelope. So, cholesterol synthesis pathways play an important role in the assembly, replication and infectivity of SARS-CoV-2's viral RNA in any case.
This may also be the reason why this study and others have suggested that cholesterol-decreasing medications like statins that reduce the synthesis and absorption of cholesterol have antiviral effects too and can be prescribed to COVID-19 patients to reduce severe outcomes. The new study in Nature Metabolism expands on this role of lipids in COVID-19 infection by explaining the role played by HDL scavenger receptor B type 1 (SR-B1).
HDL, scavenger receptors and COVID-19
The study explains that the angiotensin-converting enzyme 2 (ACE2) receptor binds with the SARS-CoV-2 virus through a receptor-binding domain. This binding is a complex mechanism and research indicates that SARS-CoV-2 might also use other receptors in the host body to accomplish cell entry. SR-B1, the researchers suggest, is one such crucial co-receptor for SARS-CoV-2.
SR-B1 is a cell-surface HDL receptor that helps select bad cholesterol and other such components in the cells, which is a crucial cell mechanism in the body. SR-B1 expression has been recognised in all types of cells in the body, including adrenal, ovarian and testicular ones. SR-B1 is also responsible for the synthesis of vitamin E in the body, which is an essential micronutrient.
The researchers searched for cholesterol-regulated patterns in the SARS-CoV-2 virus and then evaluated the ability of the virus to associate with the host's cholesterol. They found that certain components of the virus' spike proteins quickly bound to cholesterol and successfully interacted with HDL and its components via SR-B1. This evaluation proved to the scientists that SARS-CoV-2 has specific affinities for host cholesterol and possibly even HDL components.
Further investigation proved that HDL actually enhanced the activity of SARS-CoV-2 proteins in a dose-dependent manner and significantly increased viral entry and replication. So, HDL actually mediates the entry of SARS-CoV-2 into the human body. On the other hand, the researchers found that depletion of HDL cholesterol in the cellular membranes inhibits the SARS-CoV-2 infection, ultimately suggesting that further research into blocking SR-B1 and other susceptible HDL components could potentially provide avenues to treat and prevent COVID-19 infection.
For more information, read our article on High cholesterol.
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