By Ken Biegeleisen, M.D., Ph.D
Ken Biegeleisen, M.D., Ph.D., explains why he believes Johnson & Johnson cannot guarantee its COVID vaccine won’t alter your genetic code.
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EDITOR’S NOTE: As The Defender reported this morning, U.S. health officials paused vaccinations with the Johnson & Johnson vaccine following multiple reports of people who developed blood clots after receiving the vaccine. Health officials said the pause is immediate but temporary. The article below was written before J&J vaccinations were paused.
Everyone is talking about DNA/RNA vaccines. Can they alter our own genetic codes?
The vaccine lobby says “Never!” I, however — laboring beneath the weight of a Ph.D. in virology — would instead quote Gilbert and Sullivan: “Well, hardly ever.”
Most people don’t know very much about DNA or RNA, so I’ll start with a 30-second chemistry discussion. DNA and RNA are both polymers, long strings (in this case, very long strings) composed of seemingly endless repetitions of a single basic chemical building block, called a nucleotide.Ask Congress to Investigate COVID Origins – Take Action
The resulting structure is often likened to a string of pearls, or to the rungs of a very, very long ladder. A single human cell contains some 6 billion nucleotide building blocks in its chromosomes.
In the picture below, the DNA basic building block is on the left, and the RNA building block is on the right. Take a look and see whether or not you can discern the difference:
Don’t see much difference? That’s because there isn’t much. The red asterisk (*) shows the primary difference. RNA has an extra “O” (the abbreviation for an Oxygen atom). That’s about it.
Viruses have no lives of their own. They can grow only in host cells, such as, for example, your cells. In order for a virus to infect you, it needs to recognize a “receptor” on your cell surfaces. If — and only if — the virus can recognize such a receptor, then it has its own clever way of attaching itself to that receptor and sneaking its DNA (or RNA — viruses can have either one) into your cells.
Once inside, the DNA (or RNA) virus chromosome proceeds to reproduce itself, giving rise to hundreds or thousands of exact copies. These are then turned into complete virus particles by being covered with a protective protein coat. Next, the cell is broken open and the new progeny viruses disperse, infecting hundreds or thousands of other cells.
It’s easy to see how a viral infection can spread like wildfire in your body.
Even though the chemical differences between DNA and RNA are relatively small, the cell is smart enough to instantly recognize those small differences and act accordingly.
DNA is replicated in our cells by means of an enzyme called “DNA polymerase.” RNA, however, will not ordinarily be replicated by our cells because that’s simply not the way things work. So how does the RNA virus reproduce?
Some RNA viruses have an enzyme called “reverse transcriptase,” which begins each new viral life cycle by converting the virus’ RNA chromosome into DNA. This DNA copy can then be replicated by the cell’s own DNA polymerase-based system.
But other RNA viruses, including the COVID-19 strain of coronavirus, bring in their own special reproductive enzyme called “RNA polymerase,” which has the ability to directly produce numerous copies of the virus’ own RNA chromosome without any help from the cell’s native DNA polymerase system.
Now let’s speak for a moment about alteration of our genetic code. The interaction between a virus and the host cell is generally classified as being one of two distinct types of interaction.
Historically, the first type of interaction (discovered in the late 19th and early 20th centuries) was what we now call, in retrospect, a “productive infection.” Here the virus reproduces and kills the cell, releasing the many progeny as described above.
It was only in the later years of the 20th century that it became clear that there is a second sort of interaction, very different in nature, known as a “transforming” interaction (also called a “latent” infection). In a transforming interaction there is no virus growth at all. Instead, the single chromosome of the virus uses its bag of genetic tricks to insert itself into one of the 46 chromosomes of the host cell. There the viral DNA remains, sometimes forever.
In some species, such as herpesviruses, the virus’ chromosome just sits there, inside the host chromosome, apparently doing nothing — unless and until some sort of stimulus causes it to “pop out” again and begin growing. This produces a “cold sore” of the lips (herpesvirus type 1) or genitalia (herpesvirus type 2).
A large number of publications have documented that many — perhaps most — human beings have, within their nervous systems, cells which quietly harbor latent herpesvirus infections, even though the majority of humans will never get a cold sore. It is a known fact that herpes type I, in the latent state, resides in the trigeminal ganglion, inside the skull near the spinal cord. It is believed to be perfectly harmless in this latent state.
Other viruses, however, are not harmless in the latent state. A good example is SV-40, a DNA virus which is known to be capable of causing cancer in many mammalian species. SV-40 infects cells, but it usually doesn’t grow. Instead, it inserts its own chromosome into one of the cell’s chromosomes (a process called “integration”), and from that new base of operations it converts the cell from a normal cell, which is subject to normal forms of growth control, to a malignant cell which respects none of the host organism’s growth controls, and thereby causes cancer. This alteration, from normal to cancerous, is referred to as a “malignant transformation.”
But the term “transformation” does not automatically connote malignancy. Although a “transformation” may be harmful in any number of ways (and not solely limited to cancer), it might in other cases be entirely inconsequential (as far as the eye can see). In special cases, it might even be beneficial.
Curiously, however, even now — 68 years after the publication of the “Watson-Crick double-helix” structure for DNA — the dream of curing disease via human genetic re-engineering, employing custom-made viruses, remains in its infancy.
On the other hand, certain questionable forms of hastily-contrived human genetic experimentation, empowered by “executive orders,” and facilitated by “fast-track” bypassing of safety protocols, have become alarmingly commonplace.
Can a DNA-based vaccine ‘transform’ a human cell into something genetically different?
With all this in mind, we can now ask the question of whether or not a DNA-based vaccine might “transform” a human cell into something genetically different.
This is no small question, because if the answer is “yes,” and if the transformation proves to be harmful, then that harm may be passed to every subsequent generation — forever.
From 1972-1978, I was an M.D. – Ph.D. student at the New York University School of Medicine. Our lab addressed a question which was current at that time: In “productive infections,” where a virus replicates in cells and ultimately destroys them, might there nevertheless be integration of viral DNA into the host cell chromosomes?
We asked that question because, at that time in virological history, it had become abundantly clear that many different types of viruses could transform many different types of cells into malignant cancer cells. Those cells, if transplanted into animal hosts, would then form cancerous growths which would quickly kill the animal.
This sort of virus-mediated malignant transformation always began with the insertion (i.e., integration) of viral DNA into the chromosomes of the host cells. (Yes, I’m talking about that which the vaccine companies “assure” us will not follow vaccination with their “fast-tracked” new products).
Once these viral genes take up residence in host cell chromosomes, they are thereby empowered to seize control of the cell’s metabolism, perverting it to their own purposes.
So the question virologists were asking in the 1970s was this: Is the insertion of viral genes into host cell chromosomes a process uniquely associated with cancerous transformations? Or might the insertion of viral genes into host cell chromosomes take place in any and every sort of viral infection, whether it was a “productive” infection leading to virus multiplication and cell death, or whether it was a “transforming” infection where there was no virus multiplication at all?
We looked into this question by studying the infection of mammalian cells by herpesviruses. In the end, we published three papers, all in leading virology journals. These papers, listed below, are very difficult reading for anyone not familiar with the peculiar jargon of the field. But for those who are interested, here are the three references:
- Rush MJ & Biegeleisen K. Association of Herpes simplex virus DNA with host chromosomal DNA during productive infection. Virology, 69:246-257 (1976). https://doi.org/10.1016/0042-6822(76)90211-7.
- Rush MJ, Yanagi K & Biegeleisen K. Further studies on the association of Herpes simplex virus DNA and host DNA during productive infection. Virology, 83:221-225 (1977). DOI: 10.1016/0042-6822(77)90227-6.
- Yanagi K; Rush MG; Biegeleisen K. Integration of herpes simplex virus type 1 DNA into the DNA of growth-arrested BHK-21 cells. Journal Of General Virology, 44(3):657-667 (1979). DOI: 10.1099/0022-1317-44-3-657.
The first paper proved that herpesvirus genes are integrated into host cell chromosomes, but left some important questions unanswered concerning the physico-chemical nature of the linkage between viral and host DNA.
By the third paper, however, all reasonable doubt about the integration of viral DNA into host chromosomes had been laid to rest.