Explainer: Why COVID-19 is more lethal for patients with heart disease or diabetes

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RESTRICTIONS: Broadcast: NO USE JAPAN, NO USE TAIWAN Digital: NO USE JAPAN, NO USE TAIWAN
Molecular biologists at the Chinese Academy of Military Medical Sciences have found a reason why COVID-19 patients with heart disease and diabetes are more likely to suffer serious complications.

The researchers, who published their findings in the journal Nature Metabolism, found that the spike protein of the SARS-CoV-2 coronavirus binds to cholesterol and possibly to HDL, or high-density lipoprotein. This allows the coronavirus to essentially hitch a ride on cholesterol molecules as they seek to bind to their regular cell receptor, SR-B1.

SARS-CoV-2 cannot exploit the SR-B1 receptor directly, but this brings it into close proximity to the ACE2 receptors it uses to gain entry to cells.

RUNDOWN SHOWS:
1. SARS-CoV-2 viruses and HDL cholesterol
2. SARS-CoV-2 spike protein
3. Subunits 1 and 2 of SARS-CoV-2 spike protein
4. SARS-CoV-2 transported to cell by HDL cholesterol
5. HDL cholesterol binds with cell's SR-B1 receptor, SARS-CoV-2 exploits ACE2 receptor
6. Blocking SR-B1 receptors inhibits coronavirus infection

VOICEOVER (in English):
"Molecular biologists at the Chinese Academy of Military Medical Sciences have found a reason why COVID-19 patients with heart disease and diabetes are more likely to suffer serious complications."

"The SARS-CoV-2 coronavirus is coated in spike proteins. The spike protein possesses receptor binding domains that the coronavirus uses to pry open a cell's ACE2 receptors before penetrating the cellular membrane."

"The spike protein has two sections, subunit one and subunit 2. The S1 subunit of SARS-CoV-2 binds to cholesterol and possibly to high-density lipoprotein, or HDL, a particle that transports cholesterol."

"This allows the coronavirus to essentially hitch a ride on cholesterol molecules as they seek to bind to their regular cell receptor, SR-B1."

"SARS-CoV-2 cannot exploit the SR-B1 receptor directly, but this brings it into close proximity to the ACE2 receptors that it uses to gain entry to cells."

"The researchers, who published their findings in the journal Nature Metabolism, discovered that blocking SR-B1 inhibits infection. They propose using drugs that target SR-B1 as antivirals to limit SARS-CoV-2 infection."

SOURCE: Nature Metabolism
https://www.nature.com/articles/s42255-020-00324-0