Illustration of a SARS-CoV-2 viral particle entering a cell. The particle pierces through a cell’s membrane, made of two layers of lipids. A PNNL-OHSU team has shown how lipids are key to the ability of the virus to replicate.
Illustration: Michael Perkins | Pacific Northwest National Laboratory)
Creationist mode: 
No doubt the more they learn about the SARS-CoV-2 which is causing the current COVID-19 pandemic, the more creationists will come to admire the sheer brilliance of the divine malevolence they believe created it for the sole purpose of killing millions of people and making hundreds of millions sicker, to generally increase the suffering in the world. At least that's what it achieved and is still achieving so, since it is supposedly omniscient, we have to believe it knew precisely what it would do and designed it for that purpose.
Now a group of scientists has discovered yet another example of just what a brilliantly sophisticated machine for making us sick this nasty little virus is. They have found that it
but before creationists get too excited, the scientists from Oregon Health & Science University and the Department of Energy’s Pacific Northwest National Laboratory caution that these results were obtained from cell cultures, not living humans, so must be treated with caution pending more research. Nevertheless, what they found should be enough to impress devotees of the malevolence that they believe designed this virus.undertakes a massive takeover of the body’s fat-processing system, creating cellular storehouses of fat that empower the virus to hijack the body’s molecular machinery and cause disease.
The news release from the Pacific Northwest National Laboratory explains:
After scientists discovered the important role of fat for SARS-CoV-2, they used weight-loss drugs and other fat-targeting compounds to try to stop the virus in cell culture. Cut off from its fatty fuel, the virus stopped replicating within 48 hours.
The authors of the recent paper in Nature Communications caution that the results are in cell culture, not in people; much more research remains to see if such compounds hold promise for people diagnosed with COVID. But the scientists, from Oregon Health & Science University and the Department of Energy’s Pacific Northwest National Laboratory, call the work a significant step toward understanding the virus.This is exciting work, but it’s the start of a very long journey. We have an interesting observation, but we have a lot more to learn about the mechanisms of this disease.
As the virus replicates, it needs a continuous supply of energy. More triglycerides could provide that energy in the form of fatty acids. But we don’t know exactly how the virus uses these lipids to its advantage.
Fikadu Tafesse, corresponding author
Assistant professor of molecular microbiology and immunology
Oregon Health & Science University, Portland, OR, USA
Fat as fuelLipids are an important part of every cell. They literally hold us together by keeping our cells intact, and they’re a major source of energy storage for our bodies. They are an attractive target for a virus.
Jennifer Kyle, co-author
Biological Sciences Division
Earth and Biological Sciences Directorate
Pacific Northwest National Laboratory (PNNL), Richland, WA, USA.
The team embarked on the study based on observations that people with a high body-mass index and conditions like cardiovascular disease and diabetes are more sensitive to the disease.
The team studied the effect of SARS-CoV-2 on more than 400 lipids in two different human cell lines. Scientists found a massive shift in lipid levels, with some fats increasing as much as 64-fold. In one cell line, nearly 80 percent of fats were altered by the virus; in the other, levels of slightly more than half were changed.
The lipids affected most were triglycerides, those little packets of fat that most patients try to keep to a minimum. Triglycerides are crucial for our health, allowing us to store energy and to maintain healthy membranes in our cells.
It turns out that those oily blobs of fat are also critical for the COVID virus.
When we need energy, cells break up the triglycerides into useful raw material—three fatty acids that each triglyceride molecule contains. The team found that SARS-CoV2 doesn’t simply boost the number of triglycerides in our cells. The virus also changes much of our fat-processing system, changing the body’s ability to use fat as fuel. The scientists went further, looking at the effects of 24 of the virus’s 29 proteins on lipid levels. The painstaking laboratory work was done at OHSU, and then cells were sent to PNNL for measurement and analysis.
Cutting the fuel supply
The team identified a handful of viral proteins whose effect on triglyceride levels was particularly strong. Based on the findings, the team searched databases and identified several compounds that might have potential to disrupt the body’s fat-processing system. Several proved effective at stopping the virus from replicating in the laboratory. An approved weight-loss medication, Orlistat, a lipase inhibitor, stopped viral replication. An experimental compound known as GSK2194069 also stopped the virus. These and other compounds worked against all the SARS-CoV2 variants tested: alpha, beta, gamma and delta.
Creationist mode: 
The authors give more details of just how sophisticated this nasty little virus is in the abstract to their paper published open access recently in Nature Communications, although, being scientists, they make no mention at all of the malevolence of any entity that could come up with this design, or indeed a designer of any description.
AbstractWhat I'm still waiting for and what I've been waiting for since the COVID-19 pandemic began, is an explanation for why creationists seem to prefer people to have a view of their supposedly omni-benevolent god who supposedly loves its creation and who would seek to maximise the happiness in the world, is also the creative genius behind these parasites that increase the suffering in the world, rather than have them accept that there is an easily understood natural process more than capable of providing a complete explanation for their existence.
A comprehensive understanding of host dependency factors for SARS-CoV-2 remains elusive. Here, we map alterations in host lipids following SARS-CoV-2 infection using nontargeted lipidomics. We find that SARS-CoV-2 rewires host lipid metabolism, significantly altering hundreds of lipid species to effectively establish infection. We correlate these changes with viral protein activity by transfecting human cells with each viral protein and performing lipidomics. We find that lipid droplet plasticity is a key feature of infection and that viral propagation can be blocked by small-molecule glycerolipid biosynthesis inhibitors. We find that this inhibition was effective against the main variants of concern (alpha, beta, gamma, and delta), indicating that glycerolipid biosynthesis is a conserved host dependency factor that supports this evolving virus.
Farley, Scotland E.; Kyle, Jennifer E.; Leier, Hans C.; Bramer, Lisa M.; Weinstein, Jules B.; Bates, Timothy A.; Lee, Joon-Yong; Metz, Thomas O.; Schultz, Carsten; Tafesse, Fikadu G. (2022)
A global lipid map reveals host dependency factors conserved across SARS-CoV-2 variants
Nature Communications 13(1); DOI: 10.1038/s41467-022-31097-7
Copyright: © 2022 The authors.
Published by Springer Nature. Open access
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
And still the wait goes on...
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