Just read this and your subsequent articles on Paxlovid. I can't thank you enough for these. I'm a physicist, not a biologist. I actually loathe molecular biology and find something chilling about it. But God bless you for going there. And then putting together your lockpicker sequences for those of us who can't bear to break life down into molecular steps!
A friend had been told by her doctor that this drug would protect her from hospitalization and death. I've offered her ivermectin; her doctor has told her it's elephant tranquilizer or something. She said she'd heard of the fails of Paxlovid but still ...says it's still better than hospitalization and death. Not sure if she'd appreciate your commentaries here but I sure do. Thank you, and thanks to Igor too.
What does this proposed mechanism tell us about the much-touted efficacy of ivermectin therapy for Covid-19? I thought one of Ivermectin's therapeutic pathways was supposed to be interference with nsp5.
Apr 16, 2022·edited Apr 16, 2022Liked by Brian Mowrey
I just sat down with a cup of turmeric tea, just to see if there is anything new on Substack, and...
... drumroll...
OMG: THE MOST AMAZING POST showed up! Incredible.
I linked your post to mine and the interplay between them is most interesting and worthy of anyone's close attention.
Just FYI: I did NOT, in any way, selectively choose those reddit paxlovid posts. There is not that many on that subreddit. I always read all paxlovid posts on /r/COVID19Positive because I thought I would find something worth reporting, given Pfizer's reputation, and two things jumped to my attention
1) Horrible taste in mouth, which did not seem newsworthy enough
and
2) The story of Paxlovid NOT helping end the infection, which seemed extremely newsworthy to me, even if it seemed anecdotal and premature.
I am glad this got your interest and there is a cellular mechanism for this sort of turn of events.
I hope that someone very important, besides the two of us of course :-) notices this and tests the Paxlovid recipients more closely.
Interesting, but do we know these anecdotal results are real?
- PCR tests should not be used unless in controlled ways where we know the PCR rounds. They are known to detect old infections for weeks after infection. Also they can simply signal re-exposure (as opposed to re-infection), which is likely in the omicron era.
- Symptoms alone are useless too, as we have countless respiratory illnesses giving the exact same symptoms. We also know co-infection of 2 or more of such 'bugs' is common (~5% according to two recent studies).
My point you can hence test PCR positive and have symptoms and not actually have COVID (again).
So I would only trust a [antigen+ plus symptoms+] to [antigen- plus symptoms-] to [antigen+ plus symptoms+] transition, especially in such a short interval. And even then antigen tests are also notoriously easy to mess up.
And even more so, since we do not know the baseline re-infection rates of COVID-19, let alone the "I have Delta and now Omiron" or "BA.1 vs BA.2", we won't even know if these are then just re-infections within the normal bounds.
Social media is a horrible way to conduct measurements...
It's very interesting. In some regards I suppose we are entering into new waters with just the administration of a protease inhibitor. Usually these drugs are used in conjunction with a nucleoside analogue to bump of the antiviral effects. For some reason I did not take into account the effects of cellular proteases when examining SARS-COV2 but it does require an initial proteolysis by host proteases unless some intact nsp5 comes along for the ride during assembly and escape.
It is actually quite interesting that we never take into account the factor of tropism as it applies to viruses and to therapeutics. We ingest these drugs, we take blood samples for antibodies, and we swab noses for the presence of virus. All different sites that take into account different scenarios, and yet we treat each of them all the same.
Also, I may be remiss in stating that your speculations are a hypothesis rather than a theory. I think that term gets misused a lot but who am I to talk about misusing terms? I guess I'll blame Game Theory on YouTube for misappropriating the term!
Dr Fauci confirmed what you and I were saying about Paxlovid being a PAUSE button, not a STOP button.
https://twitter.com/ichudov/status/1535425707693813765
Just read this and your subsequent articles on Paxlovid. I can't thank you enough for these. I'm a physicist, not a biologist. I actually loathe molecular biology and find something chilling about it. But God bless you for going there. And then putting together your lockpicker sequences for those of us who can't bear to break life down into molecular steps!
A friend had been told by her doctor that this drug would protect her from hospitalization and death. I've offered her ivermectin; her doctor has told her it's elephant tranquilizer or something. She said she'd heard of the fails of Paxlovid but still ...says it's still better than hospitalization and death. Not sure if she'd appreciate your commentaries here but I sure do. Thank you, and thanks to Igor too.
What does this proposed mechanism tell us about the much-touted efficacy of ivermectin therapy for Covid-19? I thought one of Ivermectin's therapeutic pathways was supposed to be interference with nsp5.
I just sat down with a cup of turmeric tea, just to see if there is anything new on Substack, and...
... drumroll...
OMG: THE MOST AMAZING POST showed up! Incredible.
I linked your post to mine and the interplay between them is most interesting and worthy of anyone's close attention.
Just FYI: I did NOT, in any way, selectively choose those reddit paxlovid posts. There is not that many on that subreddit. I always read all paxlovid posts on /r/COVID19Positive because I thought I would find something worth reporting, given Pfizer's reputation, and two things jumped to my attention
1) Horrible taste in mouth, which did not seem newsworthy enough
and
2) The story of Paxlovid NOT helping end the infection, which seemed extremely newsworthy to me, even if it seemed anecdotal and premature.
I am glad this got your interest and there is a cellular mechanism for this sort of turn of events.
I hope that someone very important, besides the two of us of course :-) notices this and tests the Paxlovid recipients more closely.
Interesting, but do we know these anecdotal results are real?
- PCR tests should not be used unless in controlled ways where we know the PCR rounds. They are known to detect old infections for weeks after infection. Also they can simply signal re-exposure (as opposed to re-infection), which is likely in the omicron era.
- Symptoms alone are useless too, as we have countless respiratory illnesses giving the exact same symptoms. We also know co-infection of 2 or more of such 'bugs' is common (~5% according to two recent studies).
My point you can hence test PCR positive and have symptoms and not actually have COVID (again).
So I would only trust a [antigen+ plus symptoms+] to [antigen- plus symptoms-] to [antigen+ plus symptoms+] transition, especially in such a short interval. And even then antigen tests are also notoriously easy to mess up.
And even more so, since we do not know the baseline re-infection rates of COVID-19, let alone the "I have Delta and now Omiron" or "BA.1 vs BA.2", we won't even know if these are then just re-infections within the normal bounds.
Social media is a horrible way to conduct measurements...
It's very interesting. In some regards I suppose we are entering into new waters with just the administration of a protease inhibitor. Usually these drugs are used in conjunction with a nucleoside analogue to bump of the antiviral effects. For some reason I did not take into account the effects of cellular proteases when examining SARS-COV2 but it does require an initial proteolysis by host proteases unless some intact nsp5 comes along for the ride during assembly and escape.
It is actually quite interesting that we never take into account the factor of tropism as it applies to viruses and to therapeutics. We ingest these drugs, we take blood samples for antibodies, and we swab noses for the presence of virus. All different sites that take into account different scenarios, and yet we treat each of them all the same.
Also, I may be remiss in stating that your speculations are a hypothesis rather than a theory. I think that term gets misused a lot but who am I to talk about misusing terms? I guess I'll blame Game Theory on YouTube for misappropriating the term!
Last week's Walgreens COVID-19 test data from the USA: https://www.walgreens.com/businesssolutions/covid-19-index.jsp
https://i.redd.it/0h26yrziljt81.png
https://i.redd.it/baa8pwscint81.png
I love the subtitle, the totally reckless theory. 😄👍🏽
I understood till you got to Chesteron’s Fence and then I was overwhelmed.