Coronavirus Disease 2019—also known as COVID-19—is a respiratory infection caused by syndrome coronavirus (SARS-CoV-2) which originated in Wuhan China in late 2019 and has since resulted in a global pandemic affecting nearly 13 million people and spiking a total, global death toll to almost 500,000 as of late July 2020.
COVID-19 is known to affect the elderly notably and severely as well as those people with pre-existing, underlying chronic conditions. While this isn’t fully understood—especially the factors that make children largely resistant and the elderly vulnerable—it’s vital to try to understand these differences. Why? Because this understanding is critical for safeguarding the vulnerable populations and guiding the right type of policy and treatments.
A recent study published in 2020 shows how loading cells with cholesterol from blood serum enhances the endocytic entry of pseudotyped SARS-CoV-2. In other words, through super-resolution imaging, the study shows that SARS-Co-2 entry points with high cholesterol have a substantially increased diameter and almost twice the number of viral entry points.
How? According to the study, cholesterol traffics angiotensinogen converting enzyme (also known as ACE2) to the entry sites where SARS-CoV-2 docks to gain entry to the cell and exploit it.
In order to test the theory of cholesterol dependency of SARS-CoV-2 on viral entry, scientists, researchers, and other stud participants loaded cholesterol into HEK293T cells with apolipoprotein E (apoE) and blood serum. Then, participants treated the cells with retrovirus pseudotyped with the SARS-CoV-2 protein binds.
The study shows that cholesterol enhances the binding of SARS-CoV-2 to a cell’s surface, allowing it to increase its own association with the endocytic pathway. By this logic, what happens when a cell’s cholesterol levels decrease? It has the opposite effect.
The findings of this study show that as cholesterol increases with age and inflammation (through things like diabetes, smoking, etc.), the cell surface is more and more coated with viral entry points, which, of course, allow for an optimally assembled viral entry for virus proteins.
It’s suggested in this study that high levels of cholesterol are actually the most alarming in the tissue—not actually blood. The study’s model even suggests that dropping cholesterol in blood could indicate severe loading of cholesterol in peripheral tissue—causing a potentially dangerous situation and escalated SARS-CoV-2 infectivity.
Whereas PUFAs (polyunsaturated fatty acids) that oppose the effects of cholesterol could provide a molecular basis for eating healthy diets which could help avoid severe cases of COVID-19.