What I meant was even if sars-cov-2 does bond to carbonic anhydrase (and I haven't seen anything that lets me believe that it does), it would still be premature to advise against following mainstream scientific recommendations on mask wearing. Let me alter your quote of mine to see if you still agree:
"...it's hard to know how much of a factor
increasing levels of breathed CO2 would be in the real world (if it would be a factor at all), what levels of CO2 would need to be reached, etc."
Georgia Hunter said...
The room CO2 has to do with transmissibility and that would be similar to TB
.. because it strongly correlates with airborne pathogens, right? ..which masks help to reduce?? I still can't tell if you've accepted this or not as the primary explanation.
Georgia Hunter said...
More carbonic anhydrase activity, IMO, would increase binding sites for the virus and increase viral load. It would just make it easier for them to reproduce.
A few things...
1 - I don't see how viruses can use RBCs to reproduce:
"Without ribosomes or a genome, mammalian erythrocytes are incapable of signal transduction, gene transcript
ion, or new protein synthesis..."
https://www.ncbi.nlm.nih.gov/pmc/articles/pmc6108441/2 - Wouldn't replication in (or somehow involving) these cells be delayed until days after initial exposure? ...thinking nose-->throat-->lungs before major progression into RBCs.
3 - I'm not sure why you've zeroed in on carbonic anhydrase for attachment. I have seen others suggesting CD147 leads to RBC damage (without involving viral replication).. CD147 has actually been proven as a route for sars-cov-2 infection, and it is expressed in RBCs (also endothelial, brain, lung, et al). It is also the route of RBC infection by the malaria parasite.
This was recently published (Dec. 4):
"CD147-spike protein is a novel route for SARS-CoV-2 infection to host cells"
https://pubmed.ncbi.nlm.nih.gov/33277466/I guess this is one reason why melatonin has been recommended by some for treatment:
"Role of melatonin in the treatment of COVID-19; as an adjuvant through cluster differentiation 147 (CD147)."
https://europepmc.org/article/med/32920757Stephen Buhner talked about
CD147 in May on page 27 of his sars-cov-2 write up.. says scutellaria baicalensis downregulates CD147 expression. Also very interesting is how cyclophilin A's "affinity" for CD147 receptors leads to substantial increase in viral load..
https://www.stephenharrodbuhner.com/wp-content/uploads/2020/05/coronavirus-1.pdfGeorgia Hunter said...
Big molecules like Ivermectin that have a lot of stereochemistry may block the viral binding to carbonic anhydrase and stop replication. There are now multiple peer reviewed double blind placebo controlled studies showing the benefits of Ivermectin. Its antiviral activity hasn't been explained but my explanation makes perfect sense.
Ivermectin may prevent the spike protein from attaching to CD147, as well as ACE-2, the other
known route of infection. Here is a computational model showing... "Ivermectin docked in the region of leucine 91 of the spike and histidine 378 of the ACE2 receptor. The binding energy of ivermectin to the spike-ACE2 complex was -18 kcal/mol and binding constant was 5.8 e-08. Conclusion: The ivermectin docking we identified may interfere with the attachment of the spike to the human cell membrane."
https://iiar-anticancer.org/wp-content/uploads/2020/04/5093lehrer.pdf...I haven't really dived into the studies that show benefit of ivermectin in covid-19, so I can't confirm any real world implications of the above.
Post Edited (potsnpans) : 12/22/2020 2:53:57 AM (GMT-7)