PSA: Being prescribed certain antibiotics for illness (or STDs) wrecks bacteria in your gut and intestines that produce biotin.
This makes you more susceptible to malaria and/or “hiv.”
I have seen numerous people on 4chan postulate that promiscuity and repeat antibacterial treatment increase your susceptibility to “hiv.”
If true, this is the apparent mechanism: Biotene decimation.
Without biotene, liver stages of malaria can’t develop.
So they stay latent forever.
With biotene, they hatch into blood stages.
Which “protease inhibitors,” ivermectin, and CQ/HCQ/others can treat.
A normal daily intake for someone without deficiency is 8-80mcg/day.
It’s not enough if you’re eating for two. (you and malaria) ๐
While zithromax is a zinc ionophore, it’s not the best one for malaria, because biotene decimation makes you more susceptible to malaria.
I previously endorsed Zelenko’s protocol. I can’t with this information.
Ivermectin and HCQ are both zinc ionophores that don’t destroy biotin.
Unrelated correction: “siRNA” is short interfering RNA, which blocks viral (and viral vector “vaccine”) access to nucleotides as previously described. It is not “silicon” and i’m not sure where I got that from.
Searching for whether biotene availability facilitates siRNA synthesis came up with next to no information on that. Another time. where I’m going with that, is wondering 1) whether biotene depletion is responsible for unresolved/unrepaired/unencoded “telomeres” and 2) do you give up on attempting to encode that stuff after awhile? I’m thinking that it could be a non-productive exhaustion of biotene.
Uptake is almost exclusively in the hSMVT system if I have that right.
What that might portend, is that “siRNA” is isolated to attempts at repairing or having an autoimmune reaction against liver stages.
What is “insertional octogenesis” ? I am not qualified to evaluate or comment on the bulk of this article while we use different terminology and concepts here, I only want to go into this authors section “2: linearized plasmid dna” .
I want to remind you that the “circular plasmid dna” applies to the apicoplast in falciparum. It has its own dna, separate from the host.
Here’s what Dr. Syed says about the process:
What the “GAG envelope” (gp120) supposedly even is, is a dna repair checkpoint, it’s not even pathological – it’s a valid shortcut on the dna wheel. Some people make this nucleotide substitution (see: “g6pd”) and others don’t. That does not mean that it is pathological: I might make a nucleotide substitution when I put nutrasweet in my tea, that you don’t when you put nutrasweet in your tea. Because of conditions such as g6pd which cause nucleotide substitutions, you cannot say that a vaccine or gene therapy targeting nucleotides will behave the same in two different people, whether due to g6pd or other genetic adaptations that produce as yet undiscovered nucleotide substitution.
Follow the encoding for GAG , it’s GLU(E) , its glutamic acid. It stimulates DNA repair and neuron resiliency. That is gp120/gp41.
A full 1/3 of what they call “hiv” isn’t even infectious or a “virus.”
GAG is an analog shortcut that is identical to GAA.
GAG and GAA are invoked when there is repeat instability.
GAA is implicated in transfection via cDNA:
These sequences represent the protein coding region of the gaa cDNA ORF which is encoded by the open reading frame (ORF) sequence. ORF sequences can be delivered in our standard vector, pcDNA3.1+/C-(K)DYK or the vector of your choice as an expression/transfection-ready ORF clone.
https://www.genscript.com/gene/oryzias-latipes/101161640/gaa.html
To say that “hiv” is somehow intelligent and “evades your immune or surveilance system” is false. If GAG/GAA are invoked, your dna checkpoint process is well aware that its encoding is unstable.
A person with the condition you call “hiv” could just as easily be expressing GAA rather than GAG due to nucleotide substituion (GAA and GAG are functional analogs) – and you’d call them “hiv negative.”
GAA, which is a functional analog of GAG, has been observed in (ORF-8) “covid” which they called a “nonsense mutation.”
Well, it’s not “nonsense” I am explaining to you plain as day what GAG/GAA are.
I previously wrote that the discovery of these extraneous ORFs in 2019 (they thought there were two ORFs prior to 2019. There are ten.) proves that “stop/superstop” isn’t always at the “end” of the payload and that sometimes it could even be in the middle. In other words, “stop” means “stop,” unless it doesn’t.
GAG observed alone — by itself — in conditions that are not “hiv,” which is why it’s not part of the “hiv test.”
GAA, being the same thing as GAG, is not considered “hiv.”
But it’s in “covid.” Under “N1” it’s in the “forward primer” (acute infection/exposure) and then under “N2” it’s in the reverse primer and then ultimately the probe (seroconversion/latent infection).
This is supposed to be where “interfering rna” is in place to block nucleotide access to “rna viruses” and even “rna vaccine” access to the nucleus of your cells.
Go back to Dr Syed:
That is what the “siRNA” does in this checkpoint/repair process.
Your body creates cells from copies of your chromosomes.
It knows that these “fragments” are foreign and not in your host chromosome and so, it invokes GAG/Glutamic Acid/DNA repair to create siRNAs to block nucleotide access. It needs biotene for this.
That’s why it’s attempting to interfere/block nucleotide access to things that don’t belong there. Treating viruses and vaccines equally.
This whole idea with “mRNA” is to bypass that and force it to encode.
I’d go on but this is already speculative enough and needs more work.
But off hand, I would implicate the human liver as being responsible for the nucleotide substitution in question.
It is after all the liver that metabolizes and converts “analogs” – such as when you enjoy a nice, refreshing cup of industrial floor cleaner at a circuit party and your liver metabolizes GBL into GHB.
Or if you’re hanging around with some friends, and someone’s like “Hey! I have an idea. Let’s drink some circuit board cleaner” and your liver converts 1,4-butenediol to GHB.
They’re “different chemicals” going into your liver, but they’re the same after they’re metabolized and thats what “drug analogs” are.
It’s just science, bitches.