This is the full twitter thread Murph was ref to--
Post# of 1418
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My hypothesis (note: highly speculative, not a doctor, etc):
A lot of attention has been focused on the ability of 3CL protease inhibitors to stop viral replication (see https://todosmedical.com/3cl-protease-inhibitors
). But SARS2 has more tricks up it's sleeve than viral replication, though...
The 3CL protease in SARS2 is not only responsible for viral replication but also cleaves a cell surface receptor called NEMO, which regulates cell survival.
When NEMO is cleaved, the immune system is disrupted, causing inflammation and killing endothelial cells in the brain (and possibly elsewhere). This can result in capillary loss in brain vasculature (among others). This is why SARS2 causes hypoxia, isochemia... brain fog!
The immune disruption leaves your body susceptible to not just SARS2 but any other virus kicking around, as well as bacterial and fungal infections. Your defenses are compromised. This makes diagnosis harder, because you miss the root cause when other baddies slip in.
This is where a 3CL protease inhibitor (and Tollovid in particular) come in. In principle when you stop the NEMO cleavage, you stop the immune dysfunction, allowing your body to mount an IgA response, protecting T cells and allowing them to produce IgG.
Also, in your case, you saw improvement after light exercise, which would have normally caused PEM. But with the 3CL protease inhibitor in your system, your cells got the oxygen they needed because the virus wasn't disrupting NEMO and destroying capillaries, causing hypoxia.
In summary, not only does Tollovid stop viral replication as a 3CL protease inhibitor, but it restores normal immune signaling function and stops the virus from disrupting many processes downstream. Then your immune system does its job and produces neutralizing antibodies.
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