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link to www.sciencedirect.com (secure)]
2003 write up - read it slowly. Then read it again.
Human immunodeficiency virus type-1 (HIV-1) particles incorporate a trimeric envelope complex (Env) made of gp120 (SU) and gp41 (TM) heterodimers. It has been previously established that soluble CD4 (sCD4) interaction leads to shedding of gp120 from viral particles, and that gp120 may also be easily lost from virions during incubation or particle purification procedures.
In the design of HIV particle or pseudovirion-based HIV vaccines, it may be important to develop strategies to maximize the gp120 content of particles. We analyzed the gp120 retention of HIV-1 laboratory-adapted isolates and primary isolates following incubation with sCD4 and variations in temperature. NL4-3 shed gp120 readily in a temperature- and sCD4-dependent manner. Surprisingly, inactivation of the viral protease led to markedly reduced shedding of gp120.
Gp120 shedding was shown to vary markedly between HIV-1 strains, and was not strictly determined by whether the isolate was adapted to growth on immortalized T cell lines or was a primary isolate. Pseudovirions produced by expression of codon-optimized gag and env genes also demonstrated enhanced gp120 retention when an immature core structure was maintained. Pseudovirions of optimal stability were produced through a combination of an immature Gag protein core and a primary isolate Env.
These results support the feasibility of utilizing pseudovirion particles as immunogens for the induction of humoral responses directed against native envelope structures.UD, this is an excellent find!
I want to just recap a bit of background then take it forward a bit..
Background
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First, we know the SARS2 spike has HIV inserts, including gp120 (#PradhanWasRight).
The inserts are produced from never-before-seen RNA sequences, hence lab-origin, but the result is four HIV-replicated sections:
We also know they got HIV's DC-SIGN infection route working into Dendritic Cells, because SARS2 is creating the same class of antibodies as HIV.
What is the DC-SIGN path (it uses gp120)?
HIV infects Dendritic Cells (DC) via the DC-SIGN receptor, and 'hitches a ride' into T-Cells (DOOM!).
DC-SIGN was one of the main things Peter Daszak wanted to have in a new virus from their research proposal...
...Here - DEFUSE/EcoHealth proposal, leaked and analysed mostly by Charles Rixey, Page 17:
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link to www.researchgate.net (secure)]
18. THE PROPOSAL PLANNED TO RESEARCH ALTERNATE RECEPTORS TO ACE2
“To evaluate this, we will sequentially introduce clade 2 disrupting residues of SARS-CoV and SHCO14 and evaluate virus growth in Vero cells, non-permissive cells ectopically expressing DC-SIGN, and in human monocytes and macrophages anticipating reduced virus growth efficiency.“ (D1, p.13)
We note that while SARS-CoV was documented to use DC-SIGN as an attachment receptor (Marzi et al. 2004), L-SIGN and DC-SIGN act as entry receptors for SARS-CoV-2 (Amraei et al. 2020; Thépaut et al. 2021).
Quoting: We know the SARS-2 spike itself is toxic in many ways.
The gp120 itself (part of HIV and SARS2) causes the IgG4 class-switching of the immune response -- to 'tolerance' - like an allergy response..
I think this (gp120) is why the vaxxes have caused the class-shifting to IgG4.
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Now, moving on to your finding...
My first stand-out sentence was this:
"Surprisingly, inactivation of the viral protease led to markedly reduced shedding of gp120."--Now, we know Ivermectin is a 3CLPro inhibitor - the SARS2 viral protease is stifled by Ivm.
--Nice.
SARS2 was not an escaped HIV vaccine
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I would also just add that, in ALL HIV-vaccine research I know of, thanks to Charles again, the Furin Cleavage Site was removed, because they knew it does so much damage on its own.
Bette Korber removed FCS from all her experimental vaccines.
Dormitzer (Pfizer head vaccines) admitted polybasic cleavage sites are alywas removed.
It's a basic check that they do, SOP.
So, the conjecture that SARS2 is an escaped live 'vaccine' seems wrong to me.
Conseqences
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Right, so we know gp120 binds to nicotenic receptor...and so does SARS2.
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link to onlinelibrary.wiley.com (secure)]
"Here we report findings about the existence of a mechanism of functional molecular mimicry which could enable the binding of HIV-l gp120 to nicotinic acetylcholine receptors in muscle cells and neurons."We know HIV and SARS2 use the DC-SIGN pathway, and both induce immune class-shifting to IgG4.
We know HIV crosses the BBB
...leads to neurodegen
...thanks to gp120:
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link to www.sciencedirect.com (secure)]
"HIV-1 infects the brain and leads to AIDS dementia complex."
"The viral coat glycoprotein, gp120, may facilitate the passage of HIV-1 and HIV-infected immune cells across the blood-brain barrier (BBB)"-- I also think ^this is related to Dosha's post re Mark Crispin Miller -and vaxxes driving people crazy.
-- Vax or infection induced encephalitis or encephalopathy, brain swelling, inflammation, Prof. Bhakdi's mutifocal necropathy in the brain video....
