One more time, with feeling!

So I had this thread removed because I was an idiot and didn't read the rules about content, contribution, etc...

Sorry Mods.

Back to our regularly scheduled nightmare.

What is addressed in the following is something that came out very early in the "pandemic." That is the "HIV like Insertion" That was discovered by two different groups around the same time: One from India, and a group from Taiwan. The group from India published their findings which seemed to point to the virus being created in a lab, not naturally occurring. They were immediately laughed off the internet, and derided until the pulled it down.

The crux of the matter is this: This virus, in it's original variant form could bypass your immune system through what is know as Furin cleavage, which is how HIV evades, and disables the immune systems of those infected.

Furin enzyme chains are basically the T-cell starter mechanism. By attaching via this method, HIV has the ability to basically render the T-cells blind initially, then like a worm in a computer, destroys them all together, writes them out of existence. There are very few naturally occurring viruses that feature this means of attachment.

The thing I ask myself, having been infected with the original strain in march of 2020 (At least I think that is what it was, no tests were available, and they suck anyway) and Omicron in May of this year, is my health gonna start falling apart in a few years out of the blue because of this "HIV like Insertion?" Was it just to give the spike protein another point of entry, or was it more for long term destruction?

I guess we'll see.
jessica5b3.substack.com...

On novel inserts in SARS-nCoV-2

There’s been a lot of debate about the Pradhan paper: a paper that had a short life span on the bioRxiv pre-print server a while back - Jan. 31, 2020 - to be precise. It showed the presence of four unique inserts in the SARS-nCoV-2 genome that are not present in any other coronaviruses, including SARS-nCoV (I might refer to the original SARS as ‘original recipe chicken’ in this article, or some variation of this). “How did they get there?” was the question of the day. And “Why was the paper really withdrawn by the authors”? Will they rise to their intentions to ‘revise it in response to comments received from the research community on their technical approach and their interpretation of the results’? What does that even mean? And who exactly is this ‘research community’?

I am part of the research community and I have independently confirmed the presence of these 4 inserts in SARS-2 that are not present in the original recipe chicken SARS.

All four of these inserts had sequence similarity to motifs found in the Human Immunodeficiency Virus (HIV). It was my impression that most people bought the idea that there was no possible way that function could be ascribed to these tiny little peptides. But then again, the fact that they were all so beautifully situated on the spike protein for easy access as binding sites (potentially functional), does indeed raise some furry eyebrows. The manuscript was very rapidly withdrawn from pre-print by the authors themselves. Someone did not want this paper being read. So, please read it. It’s not long and it’s not complicated.

It was clear to me as soon as I saw the sequence alignment of SARS-nCoV-2 and SARS-nCoV (Figure 1) that something was ‘artificially’ different about this new version of SARS. My exact words (that I uttered in tears as I read the Pradhan paper) were: “They made it”. I had hoped to be wrong and I let it play on my mind while keeping an eye on supportive publications hitting the pre-print servers or heaven forbid, published with or without retraction.

Another great and informing post.

a reply to: MaxxAction

Evil Intent Never Sleeps......

originally posted by: Zanti Misfit
a reply to: MaxxAction

Evil Intent Never Sleeps......

...and his name is Bill Gates.

originally posted by: jarsue97

originally posted by: Zanti Misfit
a reply to: MaxxAction

Evil Intent Never Sleeps......

...and his name is Bill Gates.

And Klaus Anal Scwab..

a reply to: MaxxAction

One more time, with feeling!

couldn't resist,

I got I gotta do it again, wait a minute wait a minute
Hold on I'm not done. One more time. With feeling
Come on. All-right. Help me out now

HIV was a bio weapon developed in the 1970s (I read a newspaper article about it in 1978), COVID is airborne AIDS, their latest and greatest bio weapon to date. They used two HIV insertions and one SIV insertion I believe. That information came out early, spring of 2020 I think. I've got the source material in off line storage and in the cloud.

a reply to: BernnieJGato


Kinda goes with the theme...

I'll allow it.

So if this is a bioweapon, which it seems more so after reading that, what does the vaccine do in this scenario? Because if Covid gives you something like HIV, is the vaccine doubling that up, or is it helping cancel out the HIV? Are the people who were not vaccinated in more trouble than we think?

I have so many questions. Great post!

a reply to: JBHemi

No one knows JB...

The original variant really was a marvel of viral engineering.

It had four different types of cellular attachment capabilities, and was Neuroinvasive meaning it could and did infect the brain, the spinal cord, brain stem, the cardio-respiratory center in the brain, anything and everything. There's never been anything like it come out of nature that I can find.

Let's compare and contrast. HIV was different than anything that had ever been seen before because it was so sneaky.

When HIV first appeared, I was a highly "active" single guy, heterosexually so, but nonetheless, I paid a lot of attention.

Most people who contracted HIV would feel nothing but a couple days of malaise, maybe a sore throat and low grade fever within a couple weeks of infection, then do fine for months to years. Then when the virus had broken down enough of their defenses, they get something weird like shingles over 100% of their body, multiple carcinomas in a short time, or an upper respiratory infection that would never go away.

But HIV is not it's own agent of infection like Covid is. HIV has one way of attacking the body, or type of attachment:

HIV enters macrophages and CD4-positive T cells (CD4 is a glycoprotein receptor found on cells) by the adsorption of glycoproteins on its surface to receptors on the target cell, followed by fusion of the viral envelope with the cell membrane and the release of the HIV capsid into the cell.

Which means that HIV doesn't actually kill you, it just unlocks the door to let all the other killers in. The original variant of Covid19 replicated thousands of times faster than HIV.

There was a group of researchers in taiwan that were decoding this thing in astonishing time, what they found is that Covid-19, like HIV could bypass the immune system's first line of defense, and carried with it a cache of weapons with which to wipe you out once it had taken out the guards.

ACE-2 Receptors
The first is via the ACE2 receptors found on human cell membranes and it’s a typical mode of most coronaviruses. (The original variant, SARS-CoV-2 coronavirus had a plus 80 percent genomic matching to the previous SARS virus, hence it explains this property that it possesses)

Furin Enyme Cleavage
As the findings of the new study indicates that the new SARS-CoV-2 coronavirus has a mutated gene similarly found on the HIV virus, it is also able to attack human cells via the target called furyn, which is an enzyme that works as a protein activator in the human body. Typically many proteins are inactive or dormant when they are produced and have to be “cut” at specific points to activate their various functions which furyn does in the human cellular pathways. So Covid had the ability to splice itself into the enzyme activation of T-cells and shut down the initial immune response.


GRP78 Receptors
Another, which was at the time non-peer reviewed study that was released by the researchers from the University of Cairo, Egypt which ,came to the same conclusion as the Taiwanese group indicating that the spike proteins in the SARS-CoV-2 coronavirus is also able to bind to the GRP78 receptors (Glucose Regulated Protein 78) on human cells

(from another source explaining GRP78 Receptors)
www.ncbi.nlm.nih.gov...

Cell surface GRP78 (csGRP78, glucose-regulated protein 78 kDa) is preferentially overexpressed in aggressive, metastatic, and chemo-resistant cancers. GRP78 is best studied as a chaperone protein in the lumen of endoplasmic reticulum (ER), facilitating folding and secretion of the newly synthesized proteins and regulating protein degradation as an ER stress sensor in the unfolded protein pathway. As a cell surface signal receptor, multiple csGRP78 ligands have been discovered to date, and they trigger various downstream cell signaling pathways including pro-proliferative, pro-survival, and pro-apoptotic pathways. In this perspective, we evaluate csGRP78 as a cell surface death receptor and its prospect as an anticancer drug target. The pro-apoptotic ligands of csGRP78 discovered so far include natural proteins, monoclonal antibodies, and synthetic peptides. Even the secreted GRP78 itself was recently found to function as a pro-apoptotic ligand for csGRP78, mediating pancreatic β-cell death.

GRP78 when activated signals pancreatic cells to die, couple that with the occurence of severe pancreatitis observed in covid patients, very stong possibility that this research is accurate.

CD147 Receptors
The latest study shows that SARS-CoV-2can invade human host cells via a novel route of CD147-spike protein (SP). SP bound to CD147, a receptor on the host cells, thereby mediating the viral invasion.

Past studies have shown that CoVs are non-segmented positive sense RNA viruses, which primarily cause enzootic infections typically in birds and mammals and have demonstrated strong lethality in humans.

These coronaviruses are known to have four structural proteins, including E, M, N and S protein. The primary determinant of CoVs tropism is the S protein, which binds to the membrane receptor on the host cells, mediating the viral and cellular membrane fusion.

CD147, also known as Basigin or EMMPRIN, is a transmembrane glycoprotein that belongs to the immunoglobulin superfamily, which is involved in tumor development, plasmodium invasion and virus infection.

Past researches show that CD147 plays a functional role in facilitating SARS-CoV invasion for host cells, and CD147-antagonistic peptide-9 has a high binding rate to HEK293 cells and an inhibitory effect on SARS-CoV. These researches affirm the importance of CD147 in virus invasion for host cells.

As a result of the similar characteristics of SARS-CoV and SARS-CoV-2, the researchers decided to conduct the new study to investigate the possible function of CD147 in invasion for host cells by SARS-CoV-2.

Their study confirmed that the SARS-CoV-2 invaded host cells via a novel route of CD147-SP.

The last one, I suspect, is why it has been reported that people had clotting issues when they are in the final stages of succumbing to this virus, it destroys red blood cells by shredding the cell membrane causing dams of parts of platelets in the small capillaries.

A nurse friend of ours who was a traveling covid nurse during the worst of the pandemic backs this up. She said that the worst of the cases she had, late in progression and close to death, their blood was more like water than blood.

Thankfully, as viruses always do, in it's drive to survive, it evolved to be less deadly.

As to what could happen down the road with the virus or the vaxx, ever watch the walking dead??

a reply to: MaxxAction

None of that made me feel any better about this Fingers crossed we come out of this alive.

The simplicity of being a zombie does seems peaceful. No more over thinking everything, no shelter needed, just food. The vax makes me think about the beginning of I Am Legend movie.