Mechanisms of action of #ivermectin against SARS-CoV-2:
1. Inhibits binding at ACE2 an TMPRSS2 keeping the virus from entering our cells
2. Blocks alpha/beta importin (the virus cell taxi) keeping it from gettin to the nucleus
3. Blocks the viral replicase zipper (RdRp)
4. 3-Chimotrypsin protease inhibition (keeps the virus from assembling)
5. Ivermectin strengthens our natural antiviral cell activity by increasing our natural interferon
production (this Counters SARSCOV2 activity which inhibits cellular interferon)
6. Decreases IL-6 and other inflammatory cytokines through NF Kappa Beta downregulation,
taking the patient from a cytokine storm to calm.
7. Binds NSP14 necessary for viral replication and blocks it (equals less virus).
8. Most important mechanism is inhibiting binding to CD147 receptor on red cells, platelets,
lung and blood cell lining. Ivermectin keeps the virus from binding here and decreases
deadly clotting.
Now for more detail on each of the mechanisms:
1) “Ivermectin hinders binding of SARS-COV2 spike protein at the ACE2 receptor . Ivermectin
binds not only to the virus spike, but also to the ACE2 receptor (yes, more strongly than
remdesivir). ..”This is the primary receptor on our cell surface where the virus binds and then
gets gulped into the cell. If the virus can’t bind, it can’t get in. If it can’t get in, it can’t
replicate. Both the key and the lock are altered and don’t work together in the presence of
IVM.” “We have heard much about ACE2 but TMPRSS2 is a serine protease that is needed on the
cell surface to prime the Spike protein. Ivermectin inhibits this.”
https://pubmed. ncbi.nlm.nih. gov/32871846/
https://www.ncbi.nlm.nih. gov/pmc/articles/PMC7996102/
https://www.frontiersin .org/articles/10.3389/fmicb.2020.592908/full
https://www.cell. com/cell/pdf/S0092-8674(20)30229-4.pdf
2) “It binds to the alpha/beta importing and saturates it. This is the “taxi/uber” the virus
uses to ride into the cell to arrive at the area where it would replicate.”
“So ivermectin essentially takes up that “taxi/uber” seats so the virus has trouble getting a ride in to where it needs to be to copy itself.
3)Alpha/Beta importin ivermectin mechanism information we have known for almost a decade”
“Ivm binds and inhibits the viral RdRp (RNA dependent RNA polymerase). Basically
this is an enzyme the virus needs to activate to replicate itself, essentially zippering back and
forth. So ivermectin ends up being that annoying piece of fabric stuck in that zippering
mechanism.
https://pubmed.ncbi.nlm.nih .gov/22417684/
4) After the virus copies itself into its long form of all of its protein parts, enzymes clip it so
those proteins can assemble into new virions. “There are 11 sites on this long protein string that
are clipped by the enzyme 3-Chimotrypsin protease. Ivermectin inhibits this protease by
85-100% forcing the virus replication to halt, because it cannot become its constituent building
blocks.”
https://www.nature. com/articles/s42003-020-01577-x
5)”As important is the viral inhibitory mechanisms, are the immune modulation mechanisms. As
mentioned in 2 above, the virus rides into the cell on alpha/beta, arrives in the nucleus and
shuts down our interferon production.”
“Interferon of many types are produced by our body. SARS-COV2 selectively shuts down this interferon pathway and allows itself to replicate and highjack the body’s mechanisms more quickly. As in #2, ivermectin blocks the virus from getting to this point.” It does this for countless other viruses as well.
https://pubmed.ncbi.nlm.nih. gov/27973612/
https://www.nature. com/articles/s41429-020-0336-z/tables/1
6) “[Regarding] the cytokine storm, Ivermectin inhibits many inflammatory cytokines including the
prominent one IL-6. Also IL-1B, IL-10. Anti inflammatory effect by down regulating the nuclear
transcription factor Kappa-B and mitogen activated protein kinase activation pathway.” “this means it tunes down inflammatory cytokines such is IL-1beta and IL-10 as well as tumor necrosis factor alpha.” “In a nut shell it calms the immune system and decrease the cytokine storm in acute Covid patients but also shows effect in long haul patients suffering from a cytokine “trickle”.
https://link.springer. com/article/10.1007/s00011-008-8007-8
7) “Binds to NSP14 (non structural viral protein 14) ribonuclease which is necessary and critical
for SARS1 and 2 and MERS to replicate.” “….Ivermectin has a much stronger binding to this site
than remdesivir and inhibits viral replication.”
https://journals.asm. org/doi/full/10.1128/JVI.01246-20
https://www.frontiersin. org/article/10.3389/fmicb.2020.592908/full
8) CD147 is a receptor found on our red blood cell, platelets and blood cell lining, as well as
lung cell. SARS COV2 has a strong predilection for binding to this receptor. This causes
clumping and clotting. COVID is a clotting disease!!
https://www.nature .com/articles/s41392-020-00426-x
https://papers.ssrn. com/sol3/papers.cfm?abstract_id=3636557
please, no outside links