- Joined
- Mar 1, 2020
@borsabil @Lichen Bark
I've just been thinking; SARS-CoV-2 Spike is thought to bind integrins.
pubmed.ncbi.nlm.nih.gov
www.ncbi.nlm.nih.gov
COVID-19 is known to cause come very unusual reductions in CD4+ and CD8+ cell counts.
pubmed.ncbi.nlm.nih.gov
www.ncbi.nlm.nih.gov
What if the Spike in the vaccines is somehow directly affecting T and B lymphocytes through their integrins? It shouldn't, if it's locked in the prefusion conformation, but what if it is, somehow?

All antivirals for COVID-19 have the same exact problem; most people who aren't hospitalized don't need them, because their symptoms will resolve without incident. Practically all people who are hospitalized for COVID-19 have been symptomatic for 5+ days and are well beyond the point where antivirals are no longer effective at all, because there's no more virus.
The best time to take antivirals is immediately after suspected exposure, or immediately after symptoms develop, whichever is recognized first.
Again, the reason why Ivermectin, HCQ, Kaletra, and Remdesivir were never shown conclusively to work is because the majority of the trials enrolled people who were already 8 to 10 days post-exposure, at the bottom of the viral replication curve. That is, the treatment was futile.
Basically any antiviral should provide at least modest effectiveness if taken prophylactically. These patented antivirals are all rip-offs. This is generally reflected by the data, which makes a strong case for early treatment:
c19early.com
I think there's a strong case to be made for a COVID-19 therapy cocktail that achieves the following things:
I've just been thinking; SARS-CoV-2 Spike is thought to bind integrins.

The Spike Glycoprotein of SARS-CoV-2 Binds to β1 Integrins Expressed on the Surface of Lung Epithelial Cells - PubMed
The spike glycoprotein attached to the envelope of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) binds to and exploits angiotensin-converting enzyme 2 (ACE2) as an entry receptor to infect pulmonary epithelial cells. A subset of integrins that recognize the arginyl-glycyl-aspartic...


A potential role for integrins in host cell entry by SARS-CoV-2
COVID-19 is known to cause come very unusual reductions in CD4+ and CD8+ cell counts.

Apoptosis-induced T-cell lymphopenia is related to COVID-19 severity - PubMed
Increased levels of acute-phase reactants and lymphopenia are predictors of disease severity in coronavirus disease 2019 (COVID-19). This study aimed to investigate the role of apoptosis in the etiology of lymphopenia in patients with COVID-19. This multicentered, prospective, and case-control...


CD4+T, CD8+T counts and severe COVID-19: A meta-analysis
What if the Spike in the vaccines is somehow directly affecting T and B lymphocytes through their integrins? It shouldn't, if it's locked in the prefusion conformation, but what if it is, somehow?

Basically all true, except for the cancer part. Not sure about that.![]()
First oral antiviral for COVID-19, Lagevrio (molnupiravir), approved by MHRA
The antiviral was found to be safe and effective following a stringent review of the available evidence.www.gov.uk
Comments on Twitter claiming thats ivermectin plus some crap to get to charge 1000 dollars per pill
@Drain Todger
How much is true please senpai enlighten me. Because last time i checked it was dangerous mutagen that increases chances for cancer
All antivirals for COVID-19 have the same exact problem; most people who aren't hospitalized don't need them, because their symptoms will resolve without incident. Practically all people who are hospitalized for COVID-19 have been symptomatic for 5+ days and are well beyond the point where antivirals are no longer effective at all, because there's no more virus.
The best time to take antivirals is immediately after suspected exposure, or immediately after symptoms develop, whichever is recognized first.
Again, the reason why Ivermectin, HCQ, Kaletra, and Remdesivir were never shown conclusively to work is because the majority of the trials enrolled people who were already 8 to 10 days post-exposure, at the bottom of the viral replication curve. That is, the treatment was futile.
Basically any antiviral should provide at least modest effectiveness if taken prophylactically. These patented antivirals are all rip-offs. This is generally reflected by the data, which makes a strong case for early treatment:

COVID-19 early treatment: real-time analysis of 1,475 studies
COVID-19 early treatment: real-time analysis of 1,475 studies
I think there's a strong case to be made for a COVID-19 therapy cocktail that achieves the following things:
- Block calcium ion channels.
- Block histamine.
- Chelate iron.
- Inhibit xanthine oxidase.
- Inhibit NADPH oxidase.
- Inhibit MPO.
- Inhibit oxidation of arachidonic acid into isoprostanes.
- Inhibit cytokines.
- Scavenge ROS.
- Activate Nrf2.
- Raise nitric oxide levels.