Update: I found what I’m looking for and might be reading this shit for days. I’ll update a few items below.
The telomeres are the cap at the end of your chromosomes , telomeres being lengthened is indeed a function of disease process and or free radicals, making them much longer than they should be. However abnormal shortening happens with aging and that is bad too. DNA sequences get whacked off or sliced somewhat as I theorized below and this is officially “the end replication problem” but I found a better explanation or two.
https://www.sciencedaily.com/releases/2016/11/161108111356.htm
https://royalsocietypublishing.org/doi/10.1098/rsbl.2017.0463
tl;dr what i am even getting at is that it may be worth looking into , not just whether genetic sequences of HIV are present , but where on the chain they even are.
— snip — original post:
Someone asked me what the consequences of using a n1 nuclear import inhibitor could be.
Im wondering if they already know the answer or are just curious. But here goes:
It would arrest the cell cycle at the g2 phase.
However in the case of HIV, vpr1 already blocks this. That’s one of the reasons HIV is a problem.
HIV is framed as this .. almost somehow sentient virus that intelligently “evades your defenses” but it is in fact something that your body regards just as equally catastrophic as a dna strand break, which will arrest the cell cycle at the g2 phase or halt mitosis / replication of cd4 cells.
You would do the same thing as part of a repair/checkpoint process if you encountered a broken dna strand or something equally catastrophic.
That is part of the puzzle for why some theorize it might be beneficial for cancer, like “no we actually WANT to throw up a red flag and initiate this checkpoint and repair process” and I am not saying I know whether that is accurate or not, just that this is my tl;dr understanding of the theory behind that.
Ivermectin alone would not stop the accumulation of TRF (telómeric terminal restriction fragment), wherein the telomeres of t-cells are abnormally long.
When the telomeres are abnormally short, you write random TTTGGG sequences to “pad” them.
So what do you do with the abnormally long telomere sequences seen in hiv?
Continue encoding them, would be my guess.
Is it “bad” that the TRF accumulation cannot be stopped?
Where they are encoded , is probably significant.
If they’re somewhere in the middle of a chain, they might serve as padding— sort of like TTTGGG sequences — even though they would be isolated or detected as unique “HIV” genetic sequences just as surely as TTTGGG would be isolated , detected, and/or considered junk or padding.
These can only be a certain length, so at what point is there an offset that breaks this process and renders these sequences inherently incapable of replication?
Even though they would still be identified as “HIV” due to their specific genetic sequence.
I have been responsible for some train wreck code where timers eventually crash into each other and conflict with each other and cause a cascading failure of interdependent tasks that have executed out of order.
Maybe this process does a similar thing in some people, chopping the telemeres off at the correct/desired length but interrupting or relocating these genetic sequences for HIV to somewhere they are just “padding” in the process.
Hopefully your actual genetic code takes precedence in assembling your telemeres . And the rest of this is just an aberrant process that tacks this garbage onto the end of it, or pads it if something is broken or missing.
It’s like saying that I have to write a chain of text strings that are of identical length and content, like so:
AAAAAAAAAAAAAAAA
Being a meaningful string.
But i have some extra space to pad. Call that O:
AAAAAAAAAAAAAAAAOOOOOOOOO
AAAAAAAAAAAAAAAAOOOOOOOOO
Suppose one of them is … incomplete for some reason.
AAAAAAAAA
Fuck, where’s the rest?
And so i have a built in checkpoint process to halt what i am doing and pad it with more meaningless O’s to preserve the correct string length:
AAAAAAAAAOOOOOOOOOOOOOOOO
And then continue writing:
AAAAAAAAAAAAAAAAOOOOOOOOO
So let’s say I have something really bad called ZEZE that I can no longer knock off of the end of this chain:
AAAAAAAAAAAAZEZEOOOOOOOOOO
AAAAAAAAA has “permanently” become :
AAAAAAAAAZEZE
But okay, due to timing or assembly errors , somewhere along the way this turns into:
AAAAAAAAAOOOOZEZE
And ZEZE isn’t … exactly behaving the way it was in the previous offset.
But my PCR looks for a genetic signature of “ZEZE” and goes “oh no, you still have ZEZE.”
And you do.
And it still does not belong there.
But it might not be .. behaving in line with your assumptions about what ZEZE does or what the implications are.
Fuck, maybe it’s even worse!
I have been reading about a couple of people in whom HIV appears to have spontaneously resolved. Okay. Their host/integral DNA has .. survived their infection intact.
There is an explanation for that and Im not sure if anyone knows what it is yet.
I am wondering if their ZEZE got offset or knocked so far to the end of the chain, it got snipped at the point where the telemere had the expected amount or length of data and it became ZE at the end of the last string.
Now you can find no trace of ZEZE in this person.
So for fun, instead of looking for the full genetic signature for HIV in those people, look for smaller blocks of it.
Like ZEZ or ZE.
Gross oversimplification, if you know what I’m talking about you are probably seething at my layman’s ignorance.
This isn’t for you 😀
HIV is more complicated than that:
“HIV has a 9.2kb unspliced genomic transcript which encodes for gag and pol precursors; a singly spliced, 4.5 kb encoding for env, Vif, Vpr and Vpu and a multiply spliced, 2 kb mRNA encoding for Tat, Rev and Nef.”
Out of these 9, it’s thought that 6 are not that important and that you have to break one of three gene (gag, pol, env) products to disrupt HIV. The other 6 vary due to mutation.
What if we have it wrong , and there is an overlooked / favorable mutation in one of the other six?
Take this big ass string and cut it up into blocks and say, does this person have “ QANFLREDLAFLQC “ ? Or any other random portion of it?
I would say that there are .. implications .. for initiating this “checkpoint” or halting the cell cycle.
What they are, and whether they’re helpful or harmful, is not something I can answer to.
The reason they use things like coronavirus (cold virus) or adenovirus , among others, in vaccines as a “passenger” virus , “delivery vector “ or whatever you want to call it.
It is because these particular viruses enter and replicate in cell nuclei, rather than in , say , cytoplasm.
They can sort of re-write your genetic code this way.
Viruses that enter and replicate in the nucleus of your cells, are the ONLY away they can do this.
So we’re all tripping that “omg mrna rewrites your dna” and well, here’s some bad news. So do “vaccines” and bioweapons and whatever the fuck else they deign to use one of these viral vectors to tamper with your body with.
Contrasted with what we traditionally understood to be a vaccine, ie an attenuated/deactivated/whole virus.
It is almost impossible for these bio weapons — aids, covid, etc — to just fortuitously be attached to such a delivery vector in nature by sheer coincidence.
They are intentionally selected in a laboratory because these are the only delivery vectors that behave this way.
Is it an accident no one will fess up to? Or worse?
There is only a limited number and or subset of known or useful virii that can achieve this “safely” and every single variation of these currently to known, or theorized, to exist is either patented or hotly in dispute.
Hence, intellectual property holders are eating into the profitability of the vaccine market.
And furthermore; market desperation and or speculation for the introduction of competitive or novel delivery vectors such as mRNA which will be profitable beyond anyone’s wildest dreams … if the manufacturer just so happens to own the intellectual property/patents for the delivery vector.
Now you know why they do this “gain of function research.”
So the NIH can investigate new delivery vectors for their god damned vaccines to patent or license out.
This shit is risky.
And this isn’t about superiority of one over the other.
We have plenty of them that already “work.”
This is about intellectual property, patent rights, and profitability.
Patenting viruses and vector viruses should be illegal IMO.
