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Why patients with diabetes or Covid-19 heart disease are more likely to die REVEALED: Virus locks onto cholesterol molecules to access cells, study finds
- Researchers studied the role of cholesterol in coronavirus infection
- Found that the presence of high cholesterol is linked to increased infection of cells
- Coronavirus is thought to bind to cholesterol and hijack a cell surface lift
- Once here, it can then easily attach to ACE2, the receptor that allows the virus to enter human cells.
Cholesterol can help the coronavirus infect human cells by acting like a taxi service, new lab studies show.
The results may explain why people with metabolic disorders such as diabetes and cardiovascular disease, who often have high cholesterol levels, constitute a disproportionate number of patients who develop severe symptoms of Covid-19.
Researchers have found that SARS-CoV-2, the virus that causes Covid-19, can stick to cholesterol molecules as they bind to their normal cellular receptor, called SR-B1.
This helps position the pathogen so that its spike protein can bind to the ACE2 receptor, allowing it to infect the cell.
This graph shows how cholesterol can be diverted by SARS-CoV-2 to promote infection of human cells. The virus binds to cholesterol and when cholesterol then attaches to its SR-B1 receptor on the surface of human cells, it brings the virus with it, allowing it to cling to ACE2 allowing it to infect cells.
A study published in Nature Metabolism by researchers at the Chinese Academy of Military Medical Sciences examined the role of “ good ” cholesterol, also known as high density lipoprotein (HDL), in coronavirus infection .
The study looked specifically at the SR-B1 receptor, which connects to cholesterol molecules and is found on cells throughout the human body, including the lungs, where the coronavirus targets.
According to the study, SARS-CoV-2 cannot directly harness this receptor, but it can take advantage of the process of connecting cholesterol to SR-B1 to infiltrate cells.
The viral peak on the coronavirus – the same one that locks onto ACE2 – has two sections, called subunit one and subunit 2.
In their experiments, Chinese scientists found that a subunit could attach to cholesterol. This means that when cholesterol naturally migrates to its receptor, it also brings the coronavirus to the cell surface.
The researchers claim that this “improves viral uptake” and that the cholesterol receptor “facilitates entry of SARS-CoV-2 into cells expressing ACE2 by increasing virus attachment.”
The coronavirus uses the ACE2 receptor to infect cells, but it can also cling to cholesterol and use it as a cab to help it attach to ACE2 (stock)
The researchers then found that by blocking SR-B1 and neutralizing it, it inhibits the infection.
They say targeting the SR-B1 receptor could be a potential avenue for future treatments.
“The results of our study demonstrate that SR-B1 facilitates cellular attachment, entry and infection of SARS-CoV-2,” the researchers explain in their article.
“So … SR-B1 could represent a therapeutic target to limit infection with SARS-CoV-2.”
This would likely benefit people with specific comorbidities more than others. People with heart disease and diabetes, who are most likely to have high HDL levels, are among those who would benefit the most.
“Cardiovascular disease and diabetes are associated with an increased risk of severe COVID-19,” the researchers write.
“About half of patients with COVID-19 have underlying chronic illnesses, mainly cardiovascular and cerebrovascular disease and diabetes.
“In addition, an increase in mortality from COVID-19 has been observed in patients with obesity or diabetes.
NHS data from April reveals that almost a third (29%) of coronavirus patients had heart disease and almost a fifth (19%) had diabetes.
A previous study by the NHS and Imperial College found that patients with type 2 diabetes are twice as likely to die from Covid-19 and type 1 diabetics are three and a half times more likely to die.
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