This is the second anti-ivermectin column that this author has written. I believe it's in the British Medical Journal, which may give it wide readership. I didn't respond to the first article, but I did respond this time. Here's my response, which I'm posting in case my response gets deleted (it's a little snotty). It's currently waiting approval.
The last line of the column is:
On pharmacokinetic grounds alone, ivermectin is unlikely to be beneficial.
%%%%%%%%%%%%%%%%%%%%
Well, thank God then that we don't have to rely on pharmacokinetic grounds.
You've recited (with expert arguments) CONCENTRATION TOO HIGH!!!
Yawn. Join the chorus. Who cares? Certainly not the researchers conducting the 45 or so clinical trials that are underway. They don't think CONCENTRATION TOO HIGH!!! is a problem. Your focus on that issue is unfortunate. I guess when one has a hammer...
The big point of your previous column was that ivermectin's theoretical blocking of the Importin α/β1 receptors, so the virus cannot penetrate the cell nucleus, proves ivermectin is useless against COVID-19 because the virus doesn't replicate in the nucleus! This overlooks the basic crucial fact that COVID-19 does penetrate the nucleus and then disables the cell's immune function. If in fact ivermectin blocks the α/β1 receptors, that is prevented, and the cell can use its defenses to fight the virus.
ivermectin is known to help with blood clotting for patients with severe malaria. Blood clotting (as you know) is a serious complication of severe COVID-19 disease. The pattern of blood clotting with malaria and COVID-19 is similar, implying that ivermectin may reduce blood clotting for COVID-19 patients.
[A]n enzyme called nsp16, which the coronavirus produces and then uses to modify its messenger RNA cap. These modifications fool the cell, as a result of which the viral messenger RNA becomes considered as part of the cell’s own code and not foreign.
finds that ivermectin has a strong binding to nsp16, implying it could interfere with the virus's use of the enzyme to hide itself from the immune system.
The molecular study also finds that ivermectin may:
Prevent entry to the cell by binding to the region where the COVID-19 spike and the ACE2 receptor interact
Impede virus replication by binding to RdRp, an enzyme that catalyzes the replication of RNA from an RNA template
Also impede replication by binding to NSP12 and CoVs N protein, also vital to replication
Prevent the virus from disguising itself to evade the immune system by binding to NSP16 and related proteins
These are just theories out of the lab, but we know (some of us) that ivermectin works; these findings could explain why.
Our results show that topical IVM improved allergic skin inflammation by reducing the priming and activation of allergen-specific T cells, as well as the production of inflammatory cytokines. While IVM had no major impact on the functions of dendritic cells in vivo and in vitro, IVM impaired T-cell activation, proliferation, and cytokine production following polyclonal and antigen-specific stimulation.
This may be a reach, since the article is about topical ivermectin, but this anti-inflammatory benefit could happen in the body too -- which would likely help with COVID-19.
Your analysis and the whole CONCENTRATION TOO HIGH!!! campaign (there must be 8-10 articles) all ignore the fact that ivermectin vs COVID-19 takes place in a complex system, namely the immune system. In my opinion, overfocus on what happens in a test tube really misses the point.
With your next ivermectin column, I'll share with you some of the remarkable results from clinical trials and other studies. 100s (1000s?) of MDs around the world are having impressive results with ivermectin, including in Broward County, Florida!
I apologize if I'm being rude. I'm a strong ivermectin advocate and get carried away sometimes.
Summarizing: Possible mechanisms for ivermectin vs COVID-19 are preventing entry to the cell, preventing entry to the nucleus so immune functions remain intact, interfering with viral replication, preventing the virus from disguising itself so the immune system attacks it effectively, reducing blood clotting and reducing inflammation.
Uh, can't you just drag the mouse across the text to select it? Then right-click, Copy?
Otherwise, if you'll send me an email address, I'll email it to you. I promise I'm not a stalker.
Edit: Worked for me just now. Left-click at the top and drag a little, so the text is selected. Then go to the bottom of the post, hold down the shift-key, and left-click at the end of the text. Then right-click, Copy. Easy!
And yet, you mention nothing of CD147. The whole nucleus importin shite is being hyped by whom? Those vids with some hack, Adam Gaertner? He can't even be interviewed without being led in biochemistry by the interviewer. That is a hack if I ever saw one. Does disgrace to anyone pursuing ivermectin research.
I recuse myself. You did mention it, but still seem enamored by the quack. I believe ivermectin may act upon CD147 more than any other means. The Gaertner guy is totally a quack.
You'll be glad to know that after a brief respite, Gaertner has blocked me again on twitter. During the 2-3 weeks that I wasn't blocked, I didn't see anything from him presenting new information. I did see a couple tweets where he posted studies that others found, without attribution, if that makes sense. When @whomever brings my attention to a new paper, when I tweet about that paper I (usually) include something like "Great find by @whomever!" Seems courteous.
Uh -- As I recall, that comes up the the paper suggesting that ivermectin may have the same anti-coagulating effect with covid-19 as it does with malaria -- because of CD147, somehow. I forget the details. I didn't mention it because that's too much in the weeds, not essential to the point.
I gather that you think CD147 is important and I should have mentioned it. What would you write about CD147?
You've made me curious. ... Hmm, "ivermectin CD147" doesn't turn up any hits on PubMed. If found this but I don't discern an ivermectin connection.
The whole nucleus importin shite is being hyped by whom? Those vids with some hack, Adam Gaertner? He can't even be interviewed without being led in biochemistry by the interviewer. That is a hack if I ever saw one. Does disgrace to anyone pursuing ivermectin research.
Are you suggesting that ivermectin does not block the Importin α/β1 receptors? That theory is presented in the April 3 Monash study that found the 5000-fold reduction in covid-19 virus after 48 hours. That's probably where Adam got it, if he's been talking about it. The theory is bolstered by this paper that was published a few days ago -- though the paper doesn't address COVID-19, which isn't a good sign.
I don't know Adam's work. Maybe 3 months ago, when I was about a month into my first use of twitter, trying to get word out about ivermectin -- I ran into him there, asked him for a source or did something else annoying, I forget -- and he blocked me. He unblocked me a few days ago, so I cannot say that I'm not literally a follower. He hasn't posted much about ivermectin since I was re-instated.
I tried to watch a video of him being interviewed, that someone posted to the sub recently, but I couldn't understand the audio and gave up. Old, too many (5!) Ramones concerts, lousy hearing. Ivermectin videos in general frustrate me because I can't skim them to see if there's new information therein. I've only managed to watch a couple through.
I guess you think I should take his ivermectin stuff with a grain of salt? I pretty much regard everyone that way, especially on twitter. I need to see sources and I ask for them all the time.
If you have suggestions about how the essay can be improved, I'm interested in hearing what you have to say. Are you aware of possible mechanisms of ivermectin that I have left out? CD147-related, perhaps? Did I present bogus information (other than the Importin α/β1 thing)?
I know zip about biochemistry, by the way. Undergrad major in statistics, public policy grad school, wrote code for a living for 35 years. I can barely spell boichem (joke). Sadly, there is a ton of research that's largely incomprehensible to me. I use the browser to find ivermectin mentions and try to gather the gist. If you know biochemistry, I'll appreciate your sharing your knowledge.
Thanks in advance for your help!
- TLA
Edit: Whoops, I forgot this:
This is an RNA virus... duh
If you're making a point, I missed it. Please explain.
Being an RNA virus, Sars-Cov-2 replicates by it's mRNA being translated by the mitochondria to produce proteins that are then assembled into complete reproductions by the golgi apparatus within the cytoplasm. DNA viruses enter the nucleus to reproduce.
It is known that Sars-Cov-2 enters the nucleus, as well; however it is not to reproduce. There is conjecture that it affects the cell's nuclei to affect the innate immune system response. I would say a more insidious affect of this particular virus is that is has some similar traits to HIV, in that it can pull an antigen from the cellular membrane into the cell with it. The T cells may have no way of detecting an infected cell because of this. No one seems to be pushing this theory, as it may be scary. Chinese paper (always download or read full PDF's): https://www.biorxiv.org/content/10.1101/2020.05.24.111823v1
As for CD147, it is another receptor besides ACE-2 that the virus binds to. I agree with the following article's theory that this is part of the extraordinary method of the disease to act with it's thrombotic mechanism. The virus destroys endothelial cells, red blood cells, etc. https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3636557
In silico papers are one thing, in vitro another, and in vivo entirely different.
I am very interested in Ivermectin. I have my own supply. I try to stay away from Twitter and social media for information. Here I am, though.
A mechanism initially proposed for activity of IVM against SARS-CoV-2 is inhibition of nuclear transport by importin α/β proteins.8,19,117 But the applicability of this effect at clinical tissue levels has been questioned,74,118 as has whether the SARS-CoV-2 nucleocapsid protein localizes to the nucleus or nucleolus of an infected cell.119,120
Being an RNA virus, Sars-Cov-2 replicates by it's mRNA being translated by the mitochondria to produce proteins that are then assembled into complete reproductions by the golgi apparatus within the cytoplasm. DNA viruses enter the nucleus to reproduce.
It is known that Sars-Cov-2 enters the nucleus, as well; however it is not to reproduce. There is conjecture that it affects the cell's nuclei to affect the innate immune system response. I would say a more insidious affect of this particular virus is that is has some similar traits to HIV, in that it can pull an antigen from the cellular membrane into the cell with it. The T cells may have no way of detecting an infected cell because of this. No one seems to be pushing this theory, as it may be scary. Chinese paper (always download or read full PDF's): https://www.biorxiv.org/content/10.1101/2020.05.24.111823v1
As for CD147, it is another receptor besides ACE-2 that the virus binds to. I agree with the following article's theory that this is part of the extraordinary method of the disease to act with it's thrombotic mechanism. The virus destroys endothelial cells, red blood cells, etc. https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3636557
In silico papers are one thing, in vitro another, and in vivo entirely different.
I am very interested in Ivermectin. I have my own supply. I try to stay away from Twitter and social media for information. Here I am, though.
https://www.google.com/search?q=cd147+coronavirus&rlz=1C1PRFI_enUS797US797&oq=cd147&aqs=chrome.0.69i59j69i57j0l2j69i61l2j69i65j69i61.4330j0j9&sourceid=chrome&ie=UTF-8
[-] TrumpLyftAlles | 4 points | Aug 12 2020 14:55:28
This is the second anti-ivermectin column that this author has written. I believe it's in the British Medical Journal, which may give it wide readership. I didn't respond to the first article, but I did respond this time. Here's my response, which I'm posting in case my response gets deleted (it's a little snotty). It's currently waiting approval.
The last line of the column is:
On pharmacokinetic grounds alone, ivermectin is unlikely to be beneficial.
%%%%%%%%%%%%%%%%%%%%
Well, thank God then that we don't have to rely on pharmacokinetic grounds.
You've recited (with expert arguments) CONCENTRATION TOO HIGH!!!
Yawn. Join the chorus. Who cares? Certainly not the researchers conducting the 45 or so clinical trials that are underway. They don't think CONCENTRATION TOO HIGH!!! is a problem. Your focus on that issue is unfortunate. I guess when one has a hammer...
The big point of your previous column was that ivermectin's theoretical blocking of the Importin α/β1 receptors, so the virus cannot penetrate the cell nucleus, proves ivermectin is useless against COVID-19 because the virus doesn't replicate in the nucleus! This overlooks the basic crucial fact that COVID-19 does penetrate the nucleus and then disables the cell's immune function. If in fact ivermectin blocks the α/β1 receptors, that is prevented, and the cell can use its defenses to fight the virus.
Ivermectin may help with COVID-19 in other ways.
As discussed in this paper:
https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3636557
ivermectin is known to help with blood clotting for patients with severe malaria. Blood clotting (as you know) is a serious complication of severe COVID-19 disease. The pattern of blood clotting with malaria and COVID-19 is similar, implying that ivermectin may reduce blood clotting for COVID-19 patients.
This paper:
https://www.hospimedica.com/covid-19/articles/294783685/understanding-how-coronavirus-disguises-itself-to-hide-inside-host-cells-and-replicate-may-help-develop-covid-19-treatment.html
says that:
[A]n enzyme called nsp16, which the coronavirus produces and then uses to modify its messenger RNA cap. These modifications fool the cell, as a result of which the viral messenger RNA becomes considered as part of the cell’s own code and not foreign.
So the RNA is not attacked by the immune system.
What does that have to do with ivermectin?
This molecular study:
https://chemrxiv.org/articles/preprint/A_Combination_of_Ivermectin_and_Doxycycline_Possibly_Blocks_the_Viral_Entry_and_Modulate_the_Innate_Immune_Response_in_COVID-19_Patients/12630539
finds that ivermectin has a strong binding to nsp16, implying it could interfere with the virus's use of the enzyme to hide itself from the immune system.
The molecular study also finds that ivermectin may:
Prevent entry to the cell by binding to the region where the COVID-19 spike and the ACE2 receptor interact
Impede virus replication by binding to RdRp, an enzyme that catalyzes the replication of RNA from an RNA template
Also impede replication by binding to NSP12 and CoVs N protein, also vital to replication
Prevent the virus from disguising itself to evade the immune system by binding to NSP16 and related proteins
These are just theories out of the lab, but we know (some of us) that ivermectin works; these findings could explain why.
And this study:
https://pubmed.ncbi.nlm.nih.gov/28052336/#:~:text=Results%3A%20Our%20results%20show%20that,the%20production%20of%20inflammatory%20cytokines.
Our results show that topical IVM improved allergic skin inflammation by reducing the priming and activation of allergen-specific T cells, as well as the production of inflammatory cytokines. While IVM had no major impact on the functions of dendritic cells in vivo and in vitro, IVM impaired T-cell activation, proliferation, and cytokine production following polyclonal and antigen-specific stimulation.
This may be a reach, since the article is about topical ivermectin, but this anti-inflammatory benefit could happen in the body too -- which would likely help with COVID-19.
Your analysis and the whole CONCENTRATION TOO HIGH!!! campaign (there must be 8-10 articles) all ignore the fact that ivermectin vs COVID-19 takes place in a complex system, namely the immune system. In my opinion, overfocus on what happens in a test tube really misses the point.
With your next ivermectin column, I'll share with you some of the remarkable results from clinical trials and other studies. 100s (1000s?) of MDs around the world are having impressive results with ivermectin, including in Broward County, Florida!
I apologize if I'm being rude. I'm a strong ivermectin advocate and get carried away sometimes.
Summarizing: Possible mechanisms for ivermectin vs COVID-19 are preventing entry to the cell, preventing entry to the nucleus so immune functions remain intact, interfering with viral replication, preventing the virus from disguising itself so the immune system attacks it effectively, reducing blood clotting and reducing inflammation.
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[-] foggynotion | 5 points | Aug 12 2020 19:08:33
great response, the aspect of ivermectin helping with blood clotting is new to me.
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[-] TrumpLyftAlles | 1 points | Aug 12 2020 21:09:33
Thanks!
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[-] Murky-Lengthiness | 2 points | Aug 13 2020 13:04:14
Very good arguments! Is there a way to copy the text, I want to repost your answer in Dr. Covid’s forum
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[-] TrumpLyftAlles | 1 points | Aug 13 2020 20:57:57
Uh, can't you just drag the mouse across the text to select it? Then right-click, Copy?
Otherwise, if you'll send me an email address, I'll email it to you. I promise I'm not a stalker.
Edit: Worked for me just now. Left-click at the top and drag a little, so the text is selected. Then go to the bottom of the post, hold down the shift-key, and left-click at the end of the text. Then right-click, Copy. Easy!
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[-] No-Sandwich-777 | 1 points | Aug 13 2020 02:27:58
And yet, you mention nothing of CD147. The whole nucleus importin shite is being hyped by whom? Those vids with some hack, Adam Gaertner? He can't even be interviewed without being led in biochemistry by the interviewer. That is a hack if I ever saw one. Does disgrace to anyone pursuing ivermectin research.
This is an RNA virus... duh
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[-] No-Sandwich-777 | 2 points | Aug 13 2020 03:04:20
I recuse myself. You did mention it, but still seem enamored by the quack. I believe ivermectin may act upon CD147 more than any other means. The Gaertner guy is totally a quack.
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[-] TrumpLyftAlles | 1 points | Aug 13 2020 16:19:26
I believe ivermectin may act upon CD147 more than any other means.
Please elaborate. What is the importance of CD147?
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[-] TrumpLyftAlles | 1 points | Aug 29 2020 03:31:06
You'll be glad to know that after a brief respite, Gaertner has blocked me again on twitter. During the 2-3 weeks that I wasn't blocked, I didn't see anything from him presenting new information. I did see a couple tweets where he posted studies that others found, without attribution, if that makes sense. When @whomever brings my attention to a new paper, when I tweet about that paper I (usually) include something like "Great find by @whomever!" Seems courteous.
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[-] No-Sandwich-777 | 2 points | Aug 29 2020 04:04:06
I would drop Gaertner like a wet rag.
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[-] TrumpLyftAlles | 1 points | Aug 13 2020 03:25:54
And yet, you mention nothing of CD147.
Uh -- As I recall, that comes up the the paper suggesting that ivermectin may have the same anti-coagulating effect with covid-19 as it does with malaria -- because of CD147, somehow. I forget the details. I didn't mention it because that's too much in the weeds, not essential to the point.
I gather that you think CD147 is important and I should have mentioned it. What would you write about CD147?
You've made me curious. ... Hmm, "ivermectin CD147" doesn't turn up any hits on PubMed. If found this but I don't discern an ivermectin connection.
The whole nucleus importin shite is being hyped by whom? Those vids with some hack, Adam Gaertner? He can't even be interviewed without being led in biochemistry by the interviewer. That is a hack if I ever saw one. Does disgrace to anyone pursuing ivermectin research.
Are you suggesting that ivermectin does not block the Importin α/β1 receptors? That theory is presented in the April 3 Monash study that found the 5000-fold reduction in covid-19 virus after 48 hours. That's probably where Adam got it, if he's been talking about it. The theory is bolstered by this paper that was published a few days ago -- though the paper doesn't address COVID-19, which isn't a good sign.
I don't know Adam's work. Maybe 3 months ago, when I was about a month into my first use of twitter, trying to get word out about ivermectin -- I ran into him there, asked him for a source or did something else annoying, I forget -- and he blocked me. He unblocked me a few days ago, so I cannot say that I'm not literally a follower. He hasn't posted much about ivermectin since I was re-instated.
I tried to watch a video of him being interviewed, that someone posted to the sub recently, but I couldn't understand the audio and gave up. Old, too many (5!) Ramones concerts, lousy hearing. Ivermectin videos in general frustrate me because I can't skim them to see if there's new information therein. I've only managed to watch a couple through.
I guess you think I should take his ivermectin stuff with a grain of salt? I pretty much regard everyone that way, especially on twitter. I need to see sources and I ask for them all the time.
If you have suggestions about how the essay can be improved, I'm interested in hearing what you have to say. Are you aware of possible mechanisms of ivermectin that I have left out? CD147-related, perhaps? Did I present bogus information (other than the Importin α/β1 thing)?
I know zip about biochemistry, by the way. Undergrad major in statistics, public policy grad school, wrote code for a living for 35 years. I can barely spell boichem (joke). Sadly, there is a ton of research that's largely incomprehensible to me. I use the browser to find ivermectin mentions and try to gather the gist. If you know biochemistry, I'll appreciate your sharing your knowledge.
Thanks in advance for your help!
- TLA
Edit: Whoops, I forgot this:
This is an RNA virus... duh
If you're making a point, I missed it. Please explain.
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[-] No-Sandwich-777 | 1 points | Aug 14 2020 02:10:17
Being an RNA virus, Sars-Cov-2 replicates by it's mRNA being translated by the mitochondria to produce proteins that are then assembled into complete reproductions by the golgi apparatus within the cytoplasm. DNA viruses enter the nucleus to reproduce.
It is known that Sars-Cov-2 enters the nucleus, as well; however it is not to reproduce. There is conjecture that it affects the cell's nuclei to affect the innate immune system response. I would say a more insidious affect of this particular virus is that is has some similar traits to HIV, in that it can pull an antigen from the cellular membrane into the cell with it. The T cells may have no way of detecting an infected cell because of this. No one seems to be pushing this theory, as it may be scary. Chinese paper (always download or read full PDF's): https://www.biorxiv.org/content/10.1101/2020.05.24.111823v1
As for CD147, it is another receptor besides ACE-2 that the virus binds to. I agree with the following article's theory that this is part of the extraordinary method of the disease to act with it's thrombotic mechanism. The virus destroys endothelial cells, red blood cells, etc. https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3636557
In silico papers are one thing, in vitro another, and in vivo entirely different.
I am very interested in Ivermectin. I have my own supply. I try to stay away from Twitter and social media for information. Here I am, though.
https://www.google.com/search?q=cd147+coronavirus&rlz=1C1PRFI_enUS797US797&oq=cd147&aqs=chrome.0.69i59j69i57j0l2j69i61l2j69i65j69i61.4330j0j9&sourceid=chrome&ie=UTF-8
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[-] TrumpLyftAlles | 1 points | Aug 14 2020 04:00:12
Thanks for an already very informative reply, when I haven't yet looked at the links. Very much!
TLATODO: Links!
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[-] No-Sandwich-777 | 2 points | Aug 14 2020 05:11:58
And yes, take everything with a heaping helping of salt.
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[-] No-Sandwich-777 | 1 points | Aug 15 2020 02:14:53
https://poseidon01.ssrn.com/delivery.php?ID=582114003071119098106001081029114081029032054004040066067031091028071096106091014096122097062099041113051097030081117077115096126050004093022000022111088067080009019002077080118076100067024007022099111081109119097121118001022018000113075096066081124111&EXT=pdf
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[-] No-Sandwich-777 | 1 points | Aug 15 2020 02:19:17
A mechanism initially proposed for activity of IVM against SARS-CoV-2 is inhibition of nuclear transport by importin α/β proteins.8,19,117 But the applicability of this effect at clinical tissue levels has been questioned,74,118 as has whether the SARS-CoV-2 nucleocapsid protein localizes to the nucleus or nucleolus of an infected cell.119,120
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[-] TrumpLyftAlles | 1 points | Aug 15 2020 02:25:10
This study was posted to the sub about a month ago. Do I seem like an ungrateful wretch now? I do appreciate your work, finding things.
AND I'm going to reread that study. This stuff is really hard for me to understand. Maybe I'll pick up more if I go through it again.
Thanks!
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[-] No-Sandwich-777 | 2 points | Aug 15 2020 02:41:45
You should see my bookmarks on the whole thing. It's hard for me to keep up myself. Novel virus, constantly changing science and treatment.
When this thing first came out it was intubate, intubate, intubate. Wow, how that has changed.
I also thought that steroid treatment was under appreciated, and whoa and behold.
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[-] No-Sandwich-777 | 1 points | Aug 15 2020 02:28:25
https://osf.io/8dseq/
"
Ivermectin exerts its antiviral activity at the
onset of viral RNA replication, the only phase when helicase is active. The former mechanism
of action is less likely in SARS
-
CoVs as its nucleocapsid protein was demonstrated to be
predominantly cytoplasmic
(Wulan, et al. 2015)
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[-] TrumpLyftAlles | 1 points | Aug 15 2020 02:31:59
Wow, what a weird path!?!?!
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[-] No-Sandwich-777 | 1 points | Aug 16 2020 02:33:27
https://erj.ersjournals.com/content/early/2020/07/06/13993003.01123-2020
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[-] TrumpLyftAlles | 1 points | Aug 29 2020 04:32:03
So this post won't be deleted.
Being an RNA virus, Sars-Cov-2 replicates by it's mRNA being translated by the mitochondria to produce proteins that are then assembled into complete reproductions by the golgi apparatus within the cytoplasm. DNA viruses enter the nucleus to reproduce. It is known that Sars-Cov-2 enters the nucleus, as well; however it is not to reproduce. There is conjecture that it affects the cell's nuclei to affect the innate immune system response. I would say a more insidious affect of this particular virus is that is has some similar traits to HIV, in that it can pull an antigen from the cellular membrane into the cell with it. The T cells may have no way of detecting an infected cell because of this. No one seems to be pushing this theory, as it may be scary. Chinese paper (always download or read full PDF's): https://www.biorxiv.org/content/10.1101/2020.05.24.111823v1 As for CD147, it is another receptor besides ACE-2 that the virus binds to. I agree with the following article's theory that this is part of the extraordinary method of the disease to act with it's thrombotic mechanism. The virus destroys endothelial cells, red blood cells, etc. https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3636557 In silico papers are one thing, in vitro another, and in vivo entirely different. I am very interested in Ivermectin. I have my own supply. I try to stay away from Twitter and social media for information. Here I am, though. https://www.google.com/search?q=cd147+coronavirus&rlz=1C1PRFI_enUS797US797&oq=cd147&aqs=chrome.0.69i59j69i57j0l2j69i61l2j69i65j69i61.4330j0j9&sourceid=chrome&ie=UTF-8
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