Dude dismissing IVE was such a scam. I looked at meta studies that showed it worked. I read 30 peer reviewed studies inside of that meta study that showed it worked.
It worked. Period.
The biggest evidence was the absolute lack of covid spread where it was used. Until the mega corps cracked down and made Japan and such stop with it too.
I don't think people really understand what happened with the antiviral trials, and why they were so crooked.
I've said this before, but it merits saying again; COVID-19's clinical course is such that peak viral load occurs around day 2 after symptoms emerge, and tapers off from there.
By the time someone is an inpatient, in a hospital, with severe COVID-19 sepsis, they have been symptomatic for 8 to 11 days already. The virus is
gone.
All of the antiviral trials tested the drugs on inpatients with severe COVID-19. They provided a late and futile treatment, and then claimed it didn't work. Again, this is like taking a defibrillator and only using it on someone who has been flatlined for a day or two, and claiming that it is incapable of resurrecting the dead, and therefore useless.
Antivirals work by inhibiting the mechanisms of viral replication, by altering the cellular environment or interfering with protein synthesis or gene translation machinery. If the lingering symptoms are delayed sepsis brought on by overactive immune cells, and the virus is well past its peak titers, then what the fuck is the point of dosing someone with antivirals?
Paxlovid was pretty much the only one that got a head start in the trials. They almost never tested prophylaxis or early treatment.
Any one of the antivirals could have worked. Kaletra, Remdesivir (which is toxic to the liver and kidneys and is the prodrug form of a
much cheaper gray market metabolite), HCQ, Ivermectin, any of them. But they administered them all late, and then claimed they didn't work.
After more than one year of the COVID-19 pandemic, antiviral treatment options against SARS-CoV-2 are still severely limited. High hopes that had initially been placed on antiviral drugs like remdesivir have so far not been fulfilled. While individual case reports provide striking evidence for...
www.mdpi.com
After more than one year of the COVID-19 pandemic, antiviral treatment options against SARS-CoV-2 are still severely limited. High hopes that had initially been placed on antiviral drugs like remdesivir have so far not been fulfilled. While individual case reports provide striking evidence for the clinical efficacy of remdesivir in the right clinical settings, major trials failed to demonstrate this. Here, we highlight and discuss the key findings of these studies and underlying reasons for their failure. We elaborate on how such shortcomings should be prevented in future clinical trials and pandemics. We suggest in conclusion that any novel antiviral agent that enters human trials should first be tested in a post-exposure setting to provide rapid and solid evidence for its clinical efficacy before initiating further time-consuming and costly clinical trials for more advanced disease. In the COVID-19 pandemic this might have established remdesivir early on as an efficient antiviral agent at a more suitable disease stage which would have saved many lives, in particular in large outbreaks within residential care homes.
Allow me to emphasize the important part:
We suggest in conclusion that any novel antiviral agent that enters human trials should first be tested in a post-exposure setting to provide rapid and solid evidence for its clinical efficacy before initiating further time-consuming and costly clinical trials for more advanced disease.
They recommended using antivirals as post-exposure prophylaxis, instead of doing trials on people with COVID-19 sepsis who had no viral load.
Here's another study admitting that these treatments were late and futile:
Severe COVID-19 is a biphasic illness, with an initial viral replication phase, followed by a cascade of inflammatory events. Progression to severe disease is predominantly a function of the inflammatory cascade, rather than viral replication per se. ...
www.ncbi.nlm.nih.gov
Severe COVID-19 is a biphasic illness, with an initial viral replication phase, followed by a cascade of inflammatory events. Progression to severe disease is predominantly a function of the inflammatory cascade, rather than viral replication per se. This understanding can be effectively translated to changing our approach in managing the disease. The natural course of disease offers us separate windows of specific time intervals to administer either antiviral or immunomodulatory therapy. Instituting the right attack at the right time would maximize the benefit of treatment. This concept must also be factored into studies that assess the efficacy of antivirals and immunomodulatory agents against COVID-19.
This was from 2020, so they knew even back then. Basically all studies that mention COVID-19 clinical course show some variation of this exact same chart. After 7 days of symptoms, there is next to no viral replication going on at all.
What in the hell were they doing giving patients who'd been symptomatic for 10 days Remdesivir, besides stressing their livers and kidneys and giving them organ failure?
