According to this:
Current mortality due to the Covid-19 pandemic (approximately 1.2 million by November 2020) demonstrates the lack of an effective treatment. As replication of many viruses - including MERS-CoV - is supported by enhanced aerobic glycolysis, we ...
www.ncbi.nlm.nih.gov
2.2. The Warburg effect likely sustains the replication of SARS-CoV-2 in airway cells
Many viruses alter the host cell metabolism in a similar way to the Warburg effect, enhancing glycolysis and therefore producing rapid energy and “bricks” for nucleotide replication and specific protein synthesis
Our coronavirus friend cannot replicate in our airway cells without switching the chemistry in the same way as cancer cells do. This is an old idea known as the Warburg effect.
Cell energy supply becomes dependent on breaking down glucose, outside of mitochondria, which disables most energy production and is highly inefficient. To achieve survival, it becomes necessary to make more membrane transporters to being in the sugar fast enough.
(Regular cells can run their mitochondria from fat or protein breakdown too, so a strategy to block that has been tried in cancer treatment. )
Disrupting fuel supply by interfering with glucose causes these cells to self destruct. They were going to die from viral replication anyway, but this way the virus is stopped before it divides into thousands of offspring.
Since affected cells are the ones with multiple transporters desperate for glucose, this explains why 2 Deoxy D Glucose concentrates in the infected lung.
In late stage Covid, all the virus is dead, as you know.
So the medicine is no longer useful at that stage. It is primarily effective in the middle of the cycle when the virus is established, and replicating maximally, around days 7 to 14.
Would it work in early stage disease? Sure, but as uptake would be reduced, more normal cells will pick it up, leading to off target effects. Benefit small, risk increased.
If used at the right time of disease cycle, 2DeoxyGlucose probably defends future lung damage by just reducing the dead virus load before the cytokine storm gets out of control. Another possible mechanism:
the Warburg effect is promoted in endothelial cells of lung vessels by hypoxia and this activation sustains vasoconstriction and platelet micro thrombosis. PI3K signaling and HIF-1α are activated in a feedback loop. If this cascade is not arrested, in particular by AMPK activation, it can result in extensive lung damage.
You can arrest the Warburg effect by brute forcing the absence of real glucose.
Or, block downstream targets of those pathways: mTOR activation. Curcumin would do it.
That would be tea and curry. In India, I would be a popular Doctor-ji.
Anybody looking into Curcumin? There are piles of theoretical articles.
