Why patients with diabetes or heart disease are more likely to die: Covid-1 patients are more likely to die: A study shows that viruses on cholesterol molecules for cell retrieval
- Researchers studied the role of cholesterol in coronavirus infections
- The presence of high cholesterol is associated with an increase in cellular infection
- Coronavirus is thought to bind to cholesterol and hijack a lift to the cell surface.
- Once here it can then easily bind to ACE2, a receptor that allows viruses to enter human cells
Cholesterol, acting as a taxi service, could help infect coronaviruses into human cells, new laboratory studies show.
People with metabolic conditions such as diabetes and cardiovascular disease, who have frequently elevated cholesterol levels, may explain the findings as to why a disproportionate number of patients develop severe Covid-19 symptoms.
The researchers found that SARS-CoV-2, the virus that causes Covid-19, sticks to cholesterol molecules because they attach to their regular cell receptor, called SR-B1.
This helps locate the pathogen so that its spike protein can bind to the ACE2 receptor, which can infect it to the cell.
This graphic shows how cholesterol can be hijacked by SARS-Cavi-2 to aid in the infection of human cells. The virus attaches to cholesterol and when cholesterol then attaches to its SR-B1 receptor on the surface of its cells, it brings the virus with it, allowing it to infect ACE2 so that it can infect cells.
A study published in Nature Metabolism by researchers from the Chinese Academy of Military Medical Sciences looked at the role of ‘good’ cholesterol in coronavirus infections, known as ‘high density lipoprotein (HDL)’.
The study looked specifically at the SR-B1 receptor, which binds to cholesterol molecules and is found on all cells of the human body, including the lungs, where the coronavirus is the target.
SARS-CoV-2 may not directly absorb this receptor, the study found, but it may benefit from the process of cholesterol binding to SR-B1 to infiltrate cells.
The viral spike on the coronavirus – the same one that runs on ACE2 – has two sections, dub subbanit one and subnet 2.
In their experiments, Chinese scientists thought that anyone could attach cholesterol. This means that when cholesterol naturally migrates to its receptor, it also carries the coronavirus to the cell surface.
The researchers report that this ‘increases viral consumption’ and the cholesterol receptor ‘facilitates the entry of SARS-CoV-2 into ACE2-expressing cells by increasing the attachment of the virus’.
The coronavirus uses the ACE2 receptor to infect cells but can also leach cholesterol and, like a taxi, use it to bind to ACE2 (stock).
The researchers later found that by blocking and neutralizing SR-B1, the infection was prevented.
Targeting the SR-B1 receptor could be a potential route for future treatment, they say.
‘The results of our study show that SR-B1 facilitates SARS-CV-2 cellular attachment, penetration and infection,’ the researchers said in their paper.
‘Thus … SRS-B1 represents a therapeutic goal to limit SARS-Covi-2 infection.’
This is likely to benefit people with more specific commodities than others. People with heart disease and diabetes, who are likely to have elevated HDL levels, are among the people who will benefit the most.
“Cardiovascular disease and diabetes are associated with an increased risk of severe COVID-19,” the researchers wrote.
About half of the patients with Covid-19 have acute underlying diseases, mainly cardiovascular and cerebrovascular diseases and diabetes.
‘In addition, patients with obesity or diabetes have been shown to have increased mortality from COVID-19.’
April’s NHS Statistics show that a third (29 percent) of coronavirus patients had heart disease and about a fifth (19 percent) were diabetic.
An earlier study by NHS and Imperial College Ledge found that patients with type 2 diabetes died twice as much as Covid-19, and patients with type 1 diabetes were three and a half times more likely to die.
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