Reverse transcriptase, or, how your body (doesn't) create dormant retroviruses
Elite Controller Chronicles XI
“A criticism which does not hit the core stabilizes the construct, unfortunately.” - Lanka
In his recent interview, Dr Stefan Lanka offered an insight regarding Covid vax damage that I think is relevant to HIV. According to Lanka, otherwise well-meaning critics of the Covid mRNA jabs get the science wrong by focusing on mythical “long term spike protein production” instead of the (real) short term damage caused by pumping liquid nanoparticles through your vascular system. By missing the core argument, these critics propagate the narrative that “mRNA” is a bioweapon.
In the case of AIDS critics there are many ways to get it wrong. The most common is to claim that HIV exists, but it doesn’t cause AIDS. Another is to acknowledge the existence of retroviruses, but claim that Montagnier’s experiments did not prove that he discovered one. A third is to concede that “reverse transcriptase” is a real thing.
In the words of Margaret Thatcher:
“No, No, No!”
There are so many clear examples of fraudulent science in the areas of virology, retrovirology, immunology, and diagnostics, that it’s impossible to limit it to one fraud in particular.
Despite that, in preparing for this article about reverse transcriptase it dawned on me that the key conceptual fraud underlying HIV—overtly appropriated from cancer research—is the idea of dormancy. Simple RNA viruses are supposed to infect you, perhaps create the symptoms of a cold within hours, and then your symptoms disappear. But a retrovirus like HIV infects you, remains dormant for an indeterminate amount of time, perhaps ten years, and then somehow “wakes up”, causes AIDS, and you die.
And what creates dormant viruses?
Reverse transcriptase.
The early “viruses-cause-sarcoma” experiments
Here’s how many experiments trying to establish viral causes of cancer were performed from the early 20th century until the 1980s:
Start with diseased tissue sample (tumour).
Grind it up and pass it through a filter to eliminate everything that’s larger than a “virus”.
Add antibiotics, enzymes, growth promoters, and radioactive tracers. Allow viruses to “replicate”.
Transfer the mixture to a centrifuge. Separate the components according to their density in a sugar solution.
Skim one layer from the centrifuge (the “purified virus”, or “viral proteins”) and reserve.
Transfer the reserve to a mixing bowl. Fold in more enzymes, bean extract, etc. Once again, allow the “virus to replicate”.
Perform additional experiments on the now super-concentrated virus mixture to see what grows and what dies off when exposed to solvents.
Conclude that this is evidence of viral infection/DNA integration/etc.
(There are variations, such as mixing the diseased tissue sample with a healthy sample to demonstrate “infectivity”.)
Let’s look at the “purification” step, #5. How do they know that the layer they’ve skimmed from the centrifuge contains only pure virus? Did they use transmission electron microscopy to image the virions?
Hahahahahahaha
They don’t know, and they don’t want to know. In “HIV — A Virus Like No Other” published by the Perth Group, one of Montagnier’s collaborators later admitted that the layer that was supposed to contain a “retrovirus”, at a density of 1.16 g/cc, actually contained random cellular debris. That fact alone should have falsified the results.
FIlter passing viruses and bacteriophages
In 1915, Frederick Twort performed a series of experiments on filter passing viruses. He believed that submicroscopic particles were responsible for infecting and killing bacteria. Because these hypothesized viruses were too small to observe with optical microscopes, he passed sera (ground up tissue) through an ultra-fine filter to eliminate cellular debris. (So he thought.) Twort discovered that if passed vaccinia, or cowpox vaccine through a filter and added that to a micrococcus culture, areas of the culture would turn “glassy” (devoid of micrococci), first where the “virus” was added, and later in adjacent areas. He suggested this was due to a replicating virus that infected and killed bacteria, and then infected new bacteria, etc.
Twort, however, admitted he had no idea what a virus was. A virus could be a “minute bacterium” or an amoeba or protoplasm, or an enzyme. It might be living, or it might be chemical. (Like antibiotics?) Twort’s experiments were repeated by a French biologist, Félix d'Hérelle, in 1917. Hérelle was responsible for coining the word “bacteriophage” to describe any biological entity that kills bacteria.
A few years earlier in 1911, Peyton Rous (after whom the famous Rous sarcoma virus was named) had also performed experiments on “filter passing viruses”. Rous extracted a sarcoma (tumor) from a dead chicken, passed it though a filter, and injected the filtered sarcoma juice into other chickens. This caused the other chickens to develop sarcomas.
Or did they?
Here’s a description of Rous’ experiment by Harry Rubin (a collaborator of Howard Temin) writing in 2011:
“When the filtrate of the tumor [i.e. “sarcoma juice”] was injected alone, only a small proportion of the chickens developed a minute growth and did so in the track of the needle. [Bold italics mine] When it was injected in the form of dried and powdered tumor tissue, the sarcoma appeared as a diffuse mass... It seemed that the filterable causative agent required […] cell derangement or proliferation, such as the needle prick or the presence of dried tissue. When powdered diatomaceous earth known as Kieselguhr…was added to the filtrate, a local reaction occurred and the resultant tumor appeared in more sites, at an earlier time with faster expansion than in its absence. It was therefore added in most cases...]
Tumors were seen to grow only in a “small proportion” of chickens, and “in the track of the needle” or “in the presence of dried tissue”. Tumors could also be encouraged to grow more widely and faster by adding powdered sedimentary rock (Kieselguhr) to the sarcoma juice.
Well, I’m convinced! Those sarcomas were definitely caused by the injected virus and not by chemicals or metal toxins or wounds.
Rous’s claim that “lysis” (cell disintegration due to rupture of the cell walls) was caused by invading viruses was controversial for many years. Some believed that lysis was caused by bacteriophages that were already present in bacteria and could be activated at any time.
The issue of whether lysis was due to a virus or an internal “sleeper” phage was “resolved” several decades later by Andre Lwoff. Lwoff proposed that bacteria have non-infectious “prophages” that result in lysogeny. These are dormant, non-infectious viruses that reproduce with the dividing bacteria, and are usually really quiet, until they get angry and start killing their host. Lwoff’s concept of prophages became widely accepted.
In my opinion, Lwoff’s theory was nothing more than a compromise designed to rescue virology by combining two equally unfounded theories. The prophage had characteristics of a virus, but unlike an infectious virus, it also formed part of the genetic makeup of the bacterium. It could reproduce with its host for a long time until something activated it and caused the host cell to die.
Is this starting to sound like the HIV retrovirus?
Guess which discoverer of retroviruses (originally called “proviruses”) fell under the influence of Lwoff?
Howard Temin, of course.
Blatant Inhibitionism
The 1950s and early 1960s saw a series of experiments using the antibiotic actinomycin D. According to the theory, actinomycin D was able to bind to DNA and thereby inhibited DNA synthesis. This antibiotic was show to inhibit the growth of cowpox vaccine (vaccinia), but not other small viruses such as “picornaviruses” (pico-rna-virus— GEDDIT??).
How did they know back in the 1960s before PCR that vaccinia was a double stranded DNA virus rather than the usual single stranded RNA virus?
It’s a good question. I don’t have the answer. Perhaps they used a similar method to the one used to discover reverse transcriptase (see below).
In the 1960s, Howard Temin developed an idee fixe: “proviruses”. Drawing on Lwoff’s prophages, Temin believed that proviruses were dormant and inheritable (meaning they were part of your DNA). Temin conducted several experiments in the 1960s using actinomycin D as an inhibitor. However, as David Baltimore himself pointed out much later, Temin’s inhibition experiments to demonstrate proviruses were “inconclusive”.
The discovery of reverse transcriptase provided conclusive evidence of that theory. Allegedly.
In the interest of keeping this article to a reasonable length, I will only discuss Baltimore’s famous experiment published in Nature in 1970 proving the existence of reverse transcriptase.
The 1970 Nature article
Baltimore states “The formation of virions by RNA tumour viruses is sensitive to actinomycin D, and therefore seems to involve DNA-dependent RNA synthesis.”
As RNA viruses are not supposed to respond to actinomycin D (only DNA responds), the “formation of virions” must somehow involve DNA. (Note: no one looked for the formation of virions in this experiment.)
Baltimore used the Rous sarcoma virus as well a mouse virus called R-MLK.
According to Baltimore, if DNA is present in the RNA tumour virus sample—as proven by the inhibition mechanism of actinomycin D on viral replication—the only way that DNA could have appeared is if the RNA virus made a DNA copy of itself. There is an enzyme DNA polymerase which allows for the copying of DNA to mRNA or DNA. Therefore, there must be another enzyme, reverse transcriptase, which enables an RNA virus to make a DNA copy of itself.
“A preparation of purified R-MLK was incubated in DNA polymerase.”
How did he purify R-MLK? Centrifugation and extraction at a density of 1.16 g/cc.
“The preparation incorporated radioactivity from 3H-TTP".” [3H-thymidine]
This is the radioactive tracer which is supposed to measure DNA synthesis.
(Here is the title of a 2002 paper by Valerie Hu, et al, about this radioactive tracer.
“3H-thymidine is a defective tool with which to measure rates of DNA synthesis”
Apparently radioactivity destroys DNA as well as cells. Luckily they didn’t know that in 1970.)
“The reaction product could be rendered acid-soluble by deoxyribonuclease [DNAse], but not by ribonuclease [RNAse].”
Deoxyribonuclease was first isolated in 1950 from a beef pancreas by M. Kunitz. DNAse has a molecular weight of 60,000 (similar size to immunoglobulins). DNAse breaks down DNA, while ribonuclease only breaks down RNA. Since the reaction product that was first mixed with DNAse dissolved in acid, but the reaction product mixed with RNAse did not, the reaction product must contain DNA.
That’s it.
Recapping the experiment.
Strain blended mouse sarcoma though a very fine sieve to remove unwanted particles. Add DNA polymerase. Garnish with 3H-TTP. Allow to cool on stove for 5 hours and let it rise. Spin the resuling mixture in a centrifuge. Skim off the layer corresponding to the virion density of 1.16 g/cc. Take part of this layer and mix with DNAse, and another part and mix with RNAse. The DNAse/virion mixture dissolves in acid, but RNAse/virion mixture doesn’t. Therefore DNA must be present in what was previously a pure RNA mixture. The only way that could have happened is that it was copied from RNA. The DNA now has the genetic information of the original RNA virus and can use that to make more “retroviruses”.
When Eleni Papadopoulos-Eliopoulos refers to Montagnier having observed reverse transcriptase activity in “The Emperor’s New Virus”, I assume that this is what she means. Reverse transcriptase activity is observed when in a sample “known” to initially contain only RNA viruses, demonstrates that DNA is present in this sample after the procedures described above.
On the other hand, as mentioned in the previous article (“OMG! Kidney Beans Literally Cause AIDS!”), simply adding PHA to other virus samples than HIV can generate reverse transcriptase activity — or expressing it more accurately, it causes something to dissolve in acid when mixed with DNAse but not with RNAse. So if kidney beans don’t cause AIDS, do they contain DNA?
Summary
There is no reason to believe that reverse transcriptase makes DNA copies of RNA any more than DNA polymerase makes DNA copies of DNA. (Nevertheless, the discovery of reverse transcriptase has given rise to the field of “transcriptomics”.)
What was novel in Baltimore and Temin’s papers compared to the prior inconclusive actinomycin D inhibition research was the isolation of the virus in the centrifuge, and the use of DNAse to demonstrate the presence of DNA. But all they really did was to show that mixing something with something else dissolved in acid. Everything else is interpretation.
One final question.
(Thanks for Swapnil Nikumbh for providing links to the research papers.)




😁I always get a kick out of watching Nobel Laureate Dr. David Baltimore as he fails to articulate basics of isolation / purification of "the virus":
"NOBEL LAUREATE DAVID BALTIMORE [tries and fails to] EXPLAIN VIRUS ISOLATION"
(Excerpted from "The Emperor's New Virus")
https://www.youtube.com/watch?v=xTZWv-Xb-uI
1m 11s
😆😂🤣😭
Kevin, if you’re going to the goal of getting the gay community to stop antiviral meds from your scientific background expertise, this ain’t it. Yes, I know what you’re talking about because I’ve been a dissident for decades that can read studies. There’s no way the normie gay community can understand this stuff.
You literally need to explain stuff like they are 5 years old.
I see you’re very enamored with lanka & Celia etc.
That’s a one way ticket to the abyss and none of my gay friends can understand this stuff.
My 2 cents