When I say that this works like the data bus on a Daktronics , I am correct.

let’s just say you have 16 bits and the first two bits are the home team score, “00” , and the second two bits are the away team score , “01”.

Finding a 00 or a 01 in the data stream doesn’t mean its the home score or the away score – they could both be 00 00 or 01 01. Their placement on the bus — that is to say – the presence of 00 only means “home score” if “00” is present on the first two bits.

If “00” is present on the next two bits, then it means it’s the “away score.”

Additional bits could mean “inning”, “clock,” etc and they’re always in a specific position in the packet.

I had tried to explain it already :

Okay, in genetics or virology this is called a “codon” (one type of codon says this is where the chain of amino acids begins, AUG) and then three other types of codons (UAA, UAG, or UGA) are “stop codons” that say “this is where this chain of amino acids ends.”

Unstable RNA could cause a sequence of GAG. In HIV it’s a supposedly ratio of about 20:1 of being GAG:GAG/POL, if this condition exists , it’s “HIV.”

The problem with that is that 19:1 of it is “not infectious” because it’s not GAG/POL (“hiv”), it’s just a fucking amino chain with a specific molecular weight (p43), and guess what, frame shifting it -1 reduces the molecular weight of the amino chain to 42 and now it’s “Epstein Barr virus” or whatever on a western blot and everyone fucking has it, which is why you’re not allowed to use PCR to diagnose HIV– because tons of “hiv negative” people who aren’t ELISA reactive on 24 will show up as being “hiv positive” with a detectable “viral load.”

The same way these girls were getting bottles of soda to test positive for covid. The same way the president of Tanzania complained that a goat and a papaya tested positive for covid.

This is what your “viral load” is measuring. The current PCR test we have cannot tell if the “virus” is frameshifted or even infectious. it’s so fragile that a frameshift of even one byte determines whether it is intact or infectious but it’s still picked up as “viral load.”

The University of Washington has known this since at least 2021 – I keep mentioning it.

Current tests are complicated, expensive, and sometimes give inaccurate readings of viral load, said Hladik.  The two existing tests are done through sequencing the viral DNA from patient cells or inducing functional viral outgrowth in vitro from patient cell cultures. Both are time-consuming and expensive and do not lend themselves easily to the testing of new drug candidates to cure HIV.

Here’s some more from them from February 4, 2022: https://www.cell.com/cell/fulltext/S0092-8674(22)00071-X

That test won’t be used until it proves that their vaccine works.

I bet my left fucking nut it’s Moderna who will clear the bar using a new test no one else can have. Why? Because that’s who DARPA favors and works with and punished me for retweeting their gushing breathless excited tweets about fucking around with that shit from May 2019.

??? Right. The mRNA tech discovered in 1961 that no one wants to take credit for, “oh, look at that, it accidentally discovered itself!” And they were testing it 8 months before the White House would pretend they had ever even heard of covid, but lo! Three manufacturers already have it ready to go!

Trump is a lying fucking asshole. And as he tries blaming “pfizer” and “fauci” as I’ve been reading this week all I can say is if you are that god damned fucking gullible you can’t be president, we may as well have Biden if you’re that dumb.

A frameshift signal of +1 or -1 could render it completely non-infective or even replication incompetent and the tests being used right now would still say it’s positive or that there’s a detectable viral load. Does it make a little more sense, why I might suggest that making people resistant to a generic drug with NO money in it that can cause a frameshift or a stop codon (like etfak and others in its class) is a REALLY bad idea?

This initiates transcriptional termination because one does not want DNA or RNA strands building up in their bodies.

note: that is exactly what occurs on NRTIs like Truvada, it’s shattering peoples bones and destroying their organs – this whole business model of “keep them on it forever” is not sustainable for patients if it’s killing and crippling them and it’s going to be a really big problem soon, the lawsuits are already all over the news – greed and medical malpractice is the only reason they’re still selling that shit to people.


The HIV-1 virus requires a programmed -1 ribosomal frameshift signal (the HIV-1 Ribosomal Frameshift Signal) for the expression of the Pol gene, which is an example of a cis-acting element of gene regulation. In HIV-1, the gag ORF that encodes the 55 kDa Gag protein, the major viral structural protein, is located at the 5′ end of the full-length viral mRNA.[3] Translation of the 160 kDa Gag-Pol polyprotein is contingent on a -1 ribosomal frameshift event revealing the pol ORF.[4]The pol ORF is located 3′ to the gag ORF and encodes the Pol polyprotein, which is eventually cleaved into the viral enzymatic proteins (proteasereverse transcriptase, and integrase).

As a result, the HIV-1 ribosomal frameshift signal is highly regulated, as it modulates the expression levels of the Gag protein relative to the Gag-Pol polyprotein. The efficiency of the HIV-1 ribosomal frameshift signal determines the ratio of the Gag to Gag-Pol proteins synthesized, with a frameshift event occurring in approximately 5% of the total translation events, resulting in a roughly 20:1 Gag/Gag-Pol ratio.[1]Preservation of this ratio has been shown to be essential to HIV-1 infectivity and structure, as even small changes in the efficiency of the frameshift lead to inhibition of viral propagation.[3] The dependence of the HIV-1 virus on this ribosomal frameshift signal has generated interest in the frameshift as a target for novel antiviral therapeutics.[4][5]


Hidden stops are non-stop codons that would be read as stop codons if they were frameshifted +1 or −1. These prematurely terminate translation if the corresponding frame-shift (such as due to a ribosomal RNA slip) occurs before the hidden stop. It is hypothesised that this decreases resource wastage on nonfunctional proteins and the production of potential cytotoxins. Researchers at Louisiana State Universitypropose the ambush hypothesis, that hidden stops are selected for. Codons that can form hidden stops are used in genomes more frequently compared to synonymous codons that would otherwise code for the same amino acid. Unstable rRNA in an organism correlates with a higher frequency of hidden stops.[25]