https://insight.jci.org/articles/view/150111#.YNXPiWM1AVs.twitter
https://pubmed.ncbi.nlm.nih.gov/23939536/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5295168/
I am highlighting everything he is late to on this board.
For instance, with Bidoli….
Ok inactivated vaccines have the benefit of creating antibodies to more than just the spike protein (3 more proteins including the nucleocapsid…)
But if the virulence of the new variants have dropped drastically and the mortality is near minimal AND we have EFFECTIVE treatment, why the push for inactivated vaccines?
What I don't understand is that if PCR looks for genetic material you would think they would choose a sequence to be able to differentiate SARS-COv-2 from the FLU….
I might be completely wrong but my mind drives me to want to verify if mRNA vaccines themselves can be shed.
We know that they distribute widely throughout the body and endogenous reverse transcriptase can help them make low levels of protein sequence coded a lengthy amount of time after initial infection and resolution…. hence positive PCR's down the line.
Also if you look at the life cycle of SARS- COV-2, Q is most certainly correct in stating that flu medications would be effective. I will recheck the studies performed, but up until 2-3 months ago when I checked influenza meds effectiveness on corona, they claimed it wasn't effective.
Everything seems to be falsified and corrupt.
Virus Entry
SARS-CoV-2 can hijack the cell in two ways, either via endosomes or via plasma membrane fusion. (In both ways) Spike proteins (S1, S2) of SARS-CoV-2 mediate attachment to the membrane of a host cell and engage angiotensin-converting enzyme 2 (ACE2) as the entry receptor.1 Inhibitors like Griffithsin (Inhibitor III) bind to the spike glycoprotein, thus preventing viral entry. Cell surface vimentin (VIM) acts as a critical co-receptor and is essential for successful ACE-2 binding.2 Binding of heparan sulfate (HS) to the receptor binding domain (RBD) enhances binding to ACE2 as well. Viral adhesion may be inhibited by by exogenous heparin. Heparin competes with HS for binding of the SARS-CoV-2 S protein.
When virions are taken up into endosomes, cathepsin L activates the spike protein. The pH dependent cysteine protease can be blocked by lysosomotropic agents, like bafilomycin A1 or ammonium chloride (Inhibitor Classes IV,V). Alternatively, the spike protein can be cleaved between the S1 and S2 domains by the cellular serine protease TMPRSS2 in close proximity to the ACE2 receptor, which initiates fusion of the viral membrane with the plasma membrane (Inhibitor II: Camostat). 1 The plasma membrane fusion entry is less likely to trigger host cell antiviral immunity and therefore more efficient for viral replication.
Translation of Viral Replication Machinery and Replication
After the viral RNA is released into the host cell, polyproteins are translated. The coronavirus genomic RNA encodes nonstructural proteins (NSPs) that have a critical role in viral RNA synthesis, and structural proteins which are important for virion assembly. First, polyproteins pp1a and pp1ab, are translated which are cleaved by the Papain-like protease (Pl pro ) and 3C-like protease(3CL pro ) (Inhibitor VIII) to form functional NSPs as Helicase or the RNA replicase–transcriptase complex (RdRp). 5 RdRp especially can be inhibited by virostatica like Favipiravir or Penciclovir (Inhibitor VI); the replication of viral RNA in general by kinase signaling pathway inhibitors like Saracatinib (Inhibitor VII). 6 Expression level of N protein can be decreased by resveratrol (Inhibitor X).
Translation of Viral Structure Proteins (4) and Virion Assembly (5)
RdRp is responsible for replication of structural protein RNA. Structural proteins S1, S2, Envelope (E), Membrane (M) are translated by ribosomes that are bound to the endoplasmic reticulum (ER) and presented on its surface as preparation of viron assembly. The nucleocapsids (N) remain in cytoplasm and are assembled from genomic RNA. They fuse with the virion precursor which is then transported from the ER through the Golgi Apparatus to the cell surface via small vesicles.
Release of Virus
Virions are then released from the infected cell through exocytosis and search another host cell. Oseltamivir inhibits cleavage of sialic acids by neuroamidase from the cell receptors thus preventing release of newly formed virions from the cell surface (Inhibitor XI)
https://www.nature.com/articles/s41598-021-85227-0
https://www.documentcloud.org/documents/20793561-leopold-nih-foia-anthony-fauci-emails