Many years ago I was working in the Pepper Laboratory of Clinical Medicine at the university of Pennsylvania in the bacteriological department mainly working with crabological bacteria and doing research work on bacteria, the culture and the pathology of certain bacteria and also the handling out of cases of amoeba and amoeba infections.

All of these things involve the growth of microorganisms. While I was there, there was considerable talk about a new entity called bacteriophage which instead of growing actually disintegrated b. coli. And so I did work with bacteriophage and b. coli and what I found, in fact what I experienced, in contrast to the normal bacteriological work where bacteria grew, was to me the unique thing of a material that dissolved and broke down bacteria and this carried the name of bacteriophage.

It was strange in comparison with all the other things that we did in that it actually dissolved cells and you could not see it grow but that it was filterable. And the filterable material, that is the material from the dead bacteria that was filtered through a filter, could then be put into a living culture of bacteria and it would kill them and it could be propagated through filtration.

We passed the bacteriophage, which was a specific bacteriophage for b. coli, through a number of propagations and we finally saw that the bacteria lost its ability to propagate.

One of the strangest things about the bacteriophage is where it was located. The source was a sewer and in order to get the bacteriophage the personnel went down into the sewer, took samples of water from the sewer, and put this sewer water into a number of cultures of b. coli, and some of the sewer water dissolved the b. coli, and was in fact the bacteriophage.

I continued to work with bacteria and amoebic parasites for some time after that, but in the adjacent laboratory it was observed that cell cultures could be made and here some of the earliest cell cultures were being done and it became a striking thing to me that cells, that is cells from a human being, could be cultured the same as amoebas could be cultured.

I also observed in the hospital there that there were similar diseases in humans that were called virus diseases and one of these was polio.

Shortly after this I left the laboratory and took up considerable work on polymers which extended for many years and here I produced and synthesized and did research on a number of types of polymers particularly phenol amaldahyde polymers and, most aggressively, polymers of the polyester-type or so-called alkid polymers. The polyester-type polymer can be made into a whole variety of things. In the polymers I did considerable work with ion exchange polymers, polymers that would absorb ions from water so that this is the method used in purifying water like removing calcium and magnesium salts from water.

I continued polymer work for some time and I also observed in the literature the growth of information about the DNA and RNA and the bases for heredity were being clarified and considerable information becoming available on DNA and RNA.

As I followed this I observed, and it was quite apparent, that DNA and RNA were in fact polymers and they fit into a group of polymers that were very similar in concept to the polyester polymers. The difference was that the DNA and RNA were polymers based on the phosphoric ribose ions whereas the polymers of polyester were based on dibasic acids and polyhedric alcohols. But the variety of things that could be achieved with polyhedric alcohols and dibasic acids were just as great, and in fact greater than could be achieved with the DNA and RNA polymers.

At this time it became apparent that the DNA and RNA polymers had their own method of reproduction. The reproduction of DNA, RNA phosphate-type polymers was quite unique and differed from the polyester polymers. In fact they were similar to a cross between the polyester polymers and the ion exchange polymers.

As time passed, it became apparent that there were various DNA poisons that could get into the system and alter the DNA. Among these was thalamid and of course many aggressive poisons and there were also materials that were adjacent to the system that would withdraw magnesium from the system and magnesium and other metals are important terminators of polymers.

About this time an actual picture of the bacteriophage was available and this picture of the bacteriophage showed the chain, a protective cap and a hook at the end. Examining this picture it became apparent that the hook at the end was based on a metal terminal of the phosphogenetic chain¹ and the protective cap was really a continuation of the growth of the phosphogenetic chain that had been in a normal cell.

So it now became quite clear as to how bacteriophage actually originated, that it was a fragment of a normal phosphogenetic chain that had been broken out of a cell and moved through an external medium and acquired a metal terminal and the cap on it continued to grow. So this was why bacteriophage originated in a sewer: it was a fragment plus terminations, while the virus cap was the product. The other part of the fragment of DNA as it was fragmented developed into an interferon so that here we had an explanation as to what the origin of a virus was and what interferon was. And it became clear that placing the interferon and the virus together would inactivate both.

There were many reported works on attempts to immunize against a virus. Since a virus is simply a phosphogenetic chain this is not subject to immunization. The cap on the virus is a protein cap and this is subject to immunization testing in many cases. But since the cap is a much less complicated structure than the normal proteins produced by DNA, DNA being the production agency, the immunity tests for a virus only test for the cap.

The picture of the virus at this point became clear that the virus was part of the normal phosphogenetic chain that had left the cell, passed through an external fluid, acquired a metal terminal and attachments to the metal terminal, and developed a protein cap or sheath, and that in affecting the normal cell the virus approached the normal cell, lost the cap, was oriented through the metal terminal, passed through to a phosphogenetic chain of similar characteristics, split the phosphoric chain, developed a picture of itself, broke off the phosphogenetic chain and there became then two viruses and the remaining part of the phosphogenetic chain that was not used and converted to viruses converted to interferon. And infection of the body then consisted of the virus breaking up cells and multiplying in cells in cells using the phosphogenetic material of the cell to produce a copy of itself and this continued.

The question came up, and apparently nobody had understood virus diseases enough to ask the question, of how does the body handle virus and recover. The possibilities are that the virus exhausts itself, that it loses its aggressive metallic termination after many passes and that there’s not enough metallic termination to continue the production of new viruses. An alternative is that the virus precipitates because the caps are affected by immunity and the virus cannot get into the cell. And the other thing is that the chemicals in the media or in the cell affect the virus terminating material.

It then developed that there were a number of viruses and now the growth of new viruses became widespread information – that there was an AIDS virus and that there were special characteristics of the AIDS virus. Some of the special characteristics that became clear were that there was a limited cell affect, that is, that it affected only certain cells and these were the cells aggressively producing antibodies. That it had a secondary effect and that certain viruses could stay in a cell and not cause pathogenic material.

The importance of this is that when a cell breaks and the cell phosphogenetic material gets into the external fluid, if that phosphogenetic material does not contain all the components necessary for an aggressive virus it will produce a sub-virus or zypoid and the corresponding interferon would be much greater because the short length of the zypoid would leave a longer length for the interferon so that there is a specific length in the AIDS virus that has an effect. But, as the AIDS virus is produced and the conditions for producing it produce a number of sub-viruses, that do get into the cell but do not have all the capability of reproducing – these are called zypoids. And these are specifically determined in length.

Now as to the chemicals that will affect the virus, a number of chemicals that have been suggested to affect the virus are chemicals that block the cycloamines on the phosphogenetic chain of the virus. The phosphogenetic chain simply consists of phosphorus ribose as a chain with side groups of cycloamines. It is the position and spacing of these cycloamines that give the characteristic capability of the phosphogenetic chain to produce and direct the production of proteins. It is possible to interfere with some of the cycloamines. When this is done, the phosphogenetic chain, which is of course the basic reproductive chain of the gene, then cannot function, or functions in such a way that it doesn’t produce anything useful.

There are a number of chemicals that will affect the cycloamines on the phosphogenetic chain. When this happens, and some of these exist very well in plants and these are the so-called plant hormones, some of these are in animals and one of the treatments for AIDS for instance has been hydrobyzaradine. What this does is that it is a cycloamine and it replaces the normal byzaradine so that the DNA cannot reproduce.

This happens in and out of the cell so that while the AIDS virus can be attacked by the hydrobyzaradine on the outside of the cell it can also be attacked inside of the cell and therefore it affects both the normal cell and the pathogenic virus.

In order to compensate for this, it occurred to me that if the materials that would affect the side chains, or the chain of the phosphogenetic chain, was attached to a polymer that was long enough not to get into the cell and was flexible enough and soluble enough and workable enough to attack the phosphogenetic material of the viruses outside the cell, that we would have a material that would interfere with the virus in the extra-cellular fluid and not penetrate into the cell and affect it, that we would have effective stopping material for viruses. And this is the way that the recent work that I’ve carried forward has occurred. So that what seems the most suitable way to handle virus is to have a long chain polymer – polyester, polyamid, or some other type – terminated in an aggressive chemical that will attack the cycloamine polymer. It will be large enough so that it will not penetrate the cell and we will then prevent further propagation of the virus. In doing so as the virus leaves the cell it will be effectively stopped and the patient or the animal involved will be free of virus completely.

Note:

1. The term "phosphogenetic chain" used in this document refers to DNA or RNA and other gene carrying polymers. Phosphogenetic indicates a phosphorus-organic-nitrogenous polymer having genetic, reproduction or synthesis directing features.