On a brighter note, here's a snippet from the end of a fascinating paper looking at the detailed structure of SARS-CoV-2 and its fatty acid binding sites:
Free fatty acid binding pocket in the locked structure of SARS-CoV-2 spike protein
"We hypothesize that LA [linoleic acid] sequestration by SARS-CoV-2 could confer a tissue-independent mechanism by which pathogenic coronavirus infection may drive immune dysregulation and inflammation (35–37). Our findings provide a direct structural link between LA, COVID-19 pathology and the virus itself and suggest that both the LA binding pocket within the S protein and the multi-nodal LA signaling axis, represent excellent therapeutic intervention points against SARS-CoV-2 infections."
I think it was Puddleg who made a very reasonable comment about what, should he find himself in the ITU and someone tried to hook him up to a linoleic acid based intravenous emulsion, he would try to do. I think strangling them was involved.
The virus is looking to help the virus to make more virus, not to kill the host. A good plan to generate anabolic substrate might be activating peroxisomes to get all of that peroxisomal acetyl-CoA and cytoplasmic malonyl-CoA. Like this:
and if we wanted to be a bit more specific we could take a lesson from Cytomegalovirus:
Cytomegalovirus Infection Triggers the Secretion of the PPARγ Agonists 15-Hydroxyeicosatetraenoic Acid (15-HETE) and 13-Hydroxyoctadecadienoic Acid (13-HODE) in Human Cytotrophoblasts and Placental Cultures
which uses good old 13-HODE derived from linoleic acid as well as 15-HETE from arachidonic acid to get what it needs. Both are potent peroxisome proliferation stimuli and are being used, probably also by most other enveloped viruses, to generate the lipid precursors needed to build more envelope. Hence their love affair with linoleic acid.
The fact that your cardiologist made you obese and diabetic as you become elderly (what ever your age) as a result of promoting hearthealthypolyunsaturates ties in neatly with the probability that linoleic acid might also markedly assisted viral replication in addition to triggering a cytokine storm.
The lipid hypothesis just never stops giving.