My reading on ivermectin is that the concentrations required to be effective outside of in vitro would be extremely high. For what it’s worth, here are a few articles. Science is an evolving understanding of complex systems. Time and testing will tell.
“Laboratory studies using monkey cells in a test tube (as opposed to clinical studies in human patients) have shown ivermectin can shut down the replication of SARS-CoV-2, the coronavirus that causes COVID-19, within 24-48 hours of exposure to the drug.
Ivermectin is thought to inhibit the virus by preventing viral proteins moving in and out of the host cell’s nucleus, which is essential for replication of the coronavirus.
The problem is this process requires very high concentrations of ivermectin – well above the recommended dose for humans. This means ivermectin’s virus-killing powers would be unlikely to be harnessed inside the human body.”
(there are several linked references from within the article as well)
This next link is excellent—it delves into the molecular science w/out becoming incomprehensibly dense and there are three updates appended to the end showing promise.
The mechanisms stopping growth in vitro at obscene concentrations I agree are probably not operative in vivo, or at the very best not in the same way. However there are other bits of data regarding the drug as an immunomodulator in other viral infections, and this virus in particular has much of its pathogenesis having to do with badly regulated immune reactions.
Basically I am at the awkward position where I think the risk to potential reward ratio is favorable and that good research is needed while thinking most of the existing research is super shoddy.
One other thing to consider is that even small differences in replication rate might actually matter. Consider that it takes a week for the virus to really ramp up, and that’s a large number of doubling periods. Even just getting a larger or smaller initial dose seems linked to how sick people get. Even a few percent difference may allow the immune system to stay ahead in the arms race, and result in a nonlinear change in death rate.
Note that I’m not saying this happens; I’m saying that because this is an exponential growth attacker (the virus) versus and exponential growth responder (the immune system), even small differences in growth rates might have a large impact.
My reading on ivermectin is that the concentrations required to be effective outside of in vitro would be extremely high. For what it’s worth, here are a few articles. Science is an evolving understanding of complex systems. Time and testing will tell.
“Laboratory studies using monkey cells in a test tube (as opposed to clinical studies in human patients) have shown ivermectin can shut down the replication of SARS-CoV-2, the coronavirus that causes COVID-19, within 24-48 hours of exposure to the drug.
Ivermectin is thought to inhibit the virus by preventing viral proteins moving in and out of the host cell’s nucleus, which is essential for replication of the coronavirus.
The problem is this process requires very high concentrations of ivermectin – well above the recommended dose for humans. This means ivermectin’s virus-killing powers would be unlikely to be harnessed inside the human body.”
(there are several linked references from within the article as well)
https://theconversation.com/amp/ivermectin-is-still-not-a-miracle-cure-for-covid-19-despite-what-you-may-have-read-144569
This next link is excellent—it delves into the molecular science w/out becoming incomprehensibly dense and there are three updates appended to the end showing promise.
https://blogs.sciencemag.org/pipeline/archives/2020/05/11/whats-up-with-ivermectin
Another very useful article:
https://www.isglobal.org/en/healthisglobal/-/custom-blog-portlet/questions-and-answers-about-ivermectin-and-covid-19/2877257/0
mng
The mechanisms stopping growth in vitro at obscene concentrations I agree are probably not operative in vivo, or at the very best not in the same way. However there are other bits of data regarding the drug as an immunomodulator in other viral infections, and this virus in particular has much of its pathogenesis having to do with badly regulated immune reactions.
Basically I am at the awkward position where I think the risk to potential reward ratio is favorable and that good research is needed while thinking most of the existing research is super shoddy.
One other thing to consider is that even small differences in replication rate might actually matter. Consider that it takes a week for the virus to really ramp up, and that’s a large number of doubling periods. Even just getting a larger or smaller initial dose seems linked to how sick people get. Even a few percent difference may allow the immune system to stay ahead in the arms race, and result in a nonlinear change in death rate.
Note that I’m not saying this happens; I’m saying that because this is an exponential growth attacker (the virus) versus and exponential growth responder (the immune system), even small differences in growth rates might have a large impact.