Introduction: Past broadcasts have dealt with the subject of cancer as a weapon of assassination, as well as the contamination of vaccines with SV40, a deadly cancer-causing simian virus . This program details the mechanisms through which SV40 causes cancer. It is important to remember that this virus has, in all probability, been “weaponized” through the research detailed by Ed Haslam in Dr. Mary’s Monkey .
To understand how a virus can cause cancer, it is helpful to understand how the body and its cells defend themselves against becoming cancerous. There are mechanisms which function as cellular brakes, working to prevent the propagation of damaged and potentially cancerous cells and others that act as “accelerators,” working to produce virtually unlimited and pathological cell growth.
SV40 neutralizes the Rb and p53 genes, two of the body’s most important defenses against cells becoming cancerous. Neutralizing the Rb proteins and p53 gene is essential to cause a cell to become cancerous. Acting in tandem, they assure that a cell that undergoes abnormal reproduction will die, rather than reproduce and pass on the developmental abnormality and any associated risk for cancer.
In addition to neutralizing p53 and the Rbs, SV40 and its T‑antigen protein scramble the nuclei of infected cells. With P53 and the Rb proteins neutralized by large T‑antigen, the resulting abnormal cells are free to reproduce.
In addition to neutralizing the P53 gene and the Rb proteins–the cellular “brakes”–SV40 activates two “oncogenes”–Met and Notch‑1, which function as cellular accelerators permitting the uncontrolled growth characterizing cancer cells.
In yet another fashion, SV40 facilitates oncogenesis by preventing the progressive shortening of the telomeres as cells repeatedly divide. A spindle of fibers at the end of each chromosome, the telomeres are essential for cellular reproduction and they shorten progressively as cells reproduce. Eventually, they shorten to the point where cellular reproduction becomes impossible and the cell line perishes. SV40 prevents this progressive shortening, facilitating the formation of cancer cells.
Yet another remarkable and deadly feature of SV40 is its “stealth” ability to cause cancer, infecting cells, transforming them and then disappearing, thus escaping the immune system’s natural mechanisms for attacking large T‑antigen. With the now malignant cells no longer manifesting large T‑antigen, those cells can escape neutralization by the immune system.
On top of the other cancer-causing mechanisms that SV40 manifests, the virus stimulates the production of VEGF, which causes the growth of blood vessels that nourish tumors.
Yet another devastating aspect of SV40 is the fact that there are two major varieties–”slow growth” and “fast growth” SV40. Slow growth SV40 takes 19 days to mature, evading the screening process which evaluates cell cultures after the fourteen days that the faster growing variant of the virus takes to reach maturity and damage cells in such a way as to become evident to the screening procedures of the time.
Program Highlights Include: An overview of the molecular simplicity of SV40’s structure; review of the apparent weaponization of SV40 discussed by Ed Haslam ; review of the apparent soft-tissue cancer-epidemic  stemming from SV40 vaccine contamination; discussion of the interaction of environmental carcinogens with SV40 to produce mesothelioma and other cancers.
1. The SV40 is as simple as it is deadly.
Magnified fifty thousand times under an electron microscope, SV40 doesn’t seem particularly menacing. In contrast to the portentous, wormlike shape of some more notorious viruses, such as Ebola, SV40 looks almost pretty–bluish snowflakes against a field of white. It owes its delicate appearance to its isosahedral triangular scaffolding, a geometric, twenty-sided protein skin that surrounds its lone circular double strand of DNA. Compact and efficient, the DNA strand contains only 5,243 base pairs–a lean life form compared to the four million base pairs of DNA contained in even a simple bacterium. SV40 is as simple as it is small. The human genome codes for 150,000 proteins while SV40 codes for just six (although some scientists believe they have recently discovered a seventh), three of which make up its protein skin. Of the remaining proteins, one regulates the virus’s growth and the two others are the virus’s tumor-causing proteins, hence the name: T‑antigen, for tumor-causing antigen. The large T‑antigen, distinguished by its capital T, is about 700 amino acids in length, while its sister protein, the small t‑antigen, designated with a lower-case t, embodies 174 amino acids. Scientists often refer to these two tumor-causing proteins by shorthand designations of “Tag,” for the large T‑antigen and “tag” for the small t‑antigen. These tumor antigens, particularly the large T‑antigen are highly oncogenic. [Pioneer SV40 researcher Dr. Michele] Carbone describes large T‑antigen as “the most oncogenic protein ever discovered. It is unique”, he says, “in its ability to cause cancer when set loose inside certain cells.”
2. As stated by the authors, to understand how a virus can cause cancer, it is helpful to understand how the body and its cells defend themselves against becoming cancerous. There are mechanisms which functions as cellular brakes, working to prevent the propagation of damaged and potentially cancerous cells and others that act as “accelerators,” working to produce virtually unlimited and pathological cell growth.
To understand how a cell becomes cancerous, it helps to know something about the multilayered protections bequeathed by nature to help prevent cells from becoming cancerous. It is only when these protective mechanisms are breached that the cell takes its deadly turn toward immortality.
Simply put, for a cell to become cancerous three things have to happen. The first is that the cell has to lose the function of those genes that restrain cell growth and prevent malignancy–the cellular “brakes,” so to speak. Secondly, the cell has to receive a stimulating signal from those genes–called oncogenes–that cause tumor cells to grow. Finally, the cell’s normal limit on now many times it can divide must be overcome.
Ibid.; p.205. 
3. SV40 neutralizes the Rb and p53 genes, two of the body’s most important defenses against cells becoming cancerous.
The first of these protections involve a series of tumor suppressor genes known as p53 and the Rb genes. Whenever a cell begins to divide, in the process known as mitosis, a small army of quality control agents goes to work. Running up and down the cell’s DNA, like a band of frenetic electricians looking for loose wiring in an apartment complex, these genes and proteins work together in a succession of intricately linked mechanisms to scrutinize the DNA’s integrity. If at any stage of cell division they detect DNA abnormalities, mitosis is halted and the damage is repaired. If the damage cannot be repaired, another set of genes is activated and the cell undergoes “apoptosis,” the term for programmed cell death–the cell essentially commits suicide.
4. Neutralizing the Rb proteins and p53 gene is essential to cause a cell to become cancerous. More about how p53 and the Rbs work and their role in maintaining normal cellular reproduction:
The principal in this elaborate regulatory ance is called p53. Arnold J. Levine, former president of Rockefeller University, in New York City, and one of the discoverers of p53, says that 60 percent of all cancers involve some sort of damage, mutation, or inactivation of the gene. “The p53 gene is central to human cancers,” he explains, describing it is “the first line of defense against cancer formation.” If p53 is not functioning properly, a cell with altered DNA may undergo mitosis instead of dying as it should. If the DNA alterations are such that the cell continues to reproduce wildly, that is the beginning of a cancer.
In July 1997, in two groundbreaking papers published in the journal Nature Medicine, Carbone and his collaborators examined how SV40’s large T‑antigen is able to strangle p53 and other crucial tumor suppressor genes in human mesothelial cells. one of the paradoxes about mesothelioma is that human mesotheliomas are rich in normal p53, yet they are one of the most deadly human cancers. Why, if there is an abundance of this cancer-suppressing gene, is the cancer so aggressive? Carbone’s experiments showed that in human mesotheliomas, large T‑antigen attacks p53, binding to it so that it cannot function properly even though the gene is present in large quantities. In effect, it doesn’t matter how much p53 is present in the mesotheliomas; SV40 produces enough T‑antigen to disable all of it. In the companion Nature Medicine study, Antonio Giordano, then at the Kimmel Cancer Cancer in Philadelphia, described how large T‑antigen inhibits a second series of anticancer proteins called Rbs, which together serve as the final gatekeepers in cellular division they thus serve as a second layer of cellular protection against against cancer. If p53 fails, the Rbs can step in and stop genetically defective cells from dividing. Giordano found that in mesotheliomas, SV40 T‑antigen was crippling the Rbs.
Together, the Carbone and Giordano studies established that SV40 is uniquely oncogenic in human mesotheliomas. Using a single protein–large T‑antigen–SV0 can disable the body’s most important cancer suppressing systems simultaneously. No other cancer-causing virus has that capacity. For example, human papilloma virus, which causes cervical cancer, must produce two proteins, E6 and E7, to inactivate p53 and the Rbs respectively. SV40 needs only one–large
T‑antigen. For this reason, Arnold Levine calls large T‑antigen “a remarkable protein.” . . .
Ibid.; p. 206. 
5. In addition to neutralizing p53 and the Rbs, SV40 and T‑antigen scramble the nuclei of infected cells.
. . . What makes a cell malignant? Once again, SV40 can serve as the source of the actual genetic changes that make normal cells cancerous. Again, the virus can do it in more than one way. One is through human chromosome damage–by adding or deleting whole sections of DNA or reshuffling the genes on the twenty-three pairs of chromosomes contained in the cell’s nucleus. Joseph R. Tesra, director of the Human Genetics Program at Fox Chase Cancer Center in Philadelphia, says that once SV40 is finished with a cell, “it looks like somebody set off a bomb inside the cell’s nucleus, because of all these chromosome rearrangements.”
6. In addition, SV40 accelerates cell growth, another condition for cancer-formation. SV40 activates two “oncogenes” or cancer-causing genes, Met and Notch‑1.
Another way SV40 induces malignancy is to accelerate cell growth. An Italian team of scientists discovered that T‑antigen triggers an “activation” signal (or oncogene) in the cell called Met that stimulates growth factors. This causes the mesotheolial cell to go from a resting phase to a replicating phase–essentially flipping the switch for cellular growth to fast forward. And just as cells have more than one brake (p53 and Rbs), they also have more than one accelerator. Carbone’s colleague, Bocchetta, discovered that SV40 can also activate a gene called Notch‑1 that pushes the cell divide. SV40 thus can inactivate two key cellular brakes and activate two key accelerators, all by itself.
Ibid.; p. 208. 
7. In yet another fashion, SV40 facilitates oncogenesis by preventing the progressive shortening of the telomeres as cells repeatedly divide. A spindle of fibers at the end of each chromosome, the telomeres are essential for cellular reproduction and they shorten progressively as cells reproduce. Eventually, they shorten to the point where cellular reproduction becomes impossible and the cell line perishes. SV40 prevents this progressive shortening, facilitating the formation of cancer cells.
Knocking out a cell’s brakes and kicking on its accelerator is still not sufficient to produce unchecked tumor growth. Nature blessed the body with an additional anticancer feature: cells have a limited life span. A healthy cell will reproduce itself only a finite number of times before dying. That is because each time a cell divides, the telomeres, a spindle of microfibers on the ends of each chromosome, shorten a little bit. In classical mythology, three goddesses–the Fates–wove together the fabric of a person’s life, determining how long he or she would live. Telomeres are literally the threads of life; they determine the natural life span of all cells. Each time a cell divides, a little piece of the thread gets used up, and the telomeres get shorter. Once they have shortened beyond a certain point, the cell–and all the daughter cells, which derived from it–have used up all their allotted thread. They cannot divide any longer, and they die. This is why most scientists believe that all human beings, no matter how healthy have an upper limit to their life spans. . . .
. . . Carbone and Rudy Foddis, a postdoctoral student in his laboratory, found that SV40 activates telomerase, an enzyme that allows the telomeres to be changed every time the cell divides instead of becoming shortened–in effect, allowing the mesothelial cells to divide endlessly. Ironically, it was the virus’s contamination of the polio vaccine that led to the search for an alternative substrate by Hayflick, which in turn led to the discovery of the importance of telomeres. Now it turns out that it is SV40’s interference with the natural behavior of telomeres that allows malignant cells to become immortal, instead of dying as they should. . . .
8. Yet another remarkable and deadly feature of SV40 is its “stealth” ability to cause cancer.
. . . . Meanwhile, other research shows that SV40 has additional cancer-causing tricks. Sometimes the virus sets off the chain reaction that leads to tumor formation, yet manages to leave no trace that it was ever present. In virology, this is described as a hit-and-run mechanism: The virus can cause so much damage that the cell perpetuates its own malignant growth long after the virus has disappeared.
A team of scientists from Bonn has demonstrated this mechanism in rats, showing that SV40 is able to inflict damage in cells and then vanish completely. The German team injected fetal rat brain cells that had been rendered cancerous by large T‑antigen into the brains of adult rats. Eighty percent of the adult rats developed a brain cancer that is the rodent equivalent of human medulloblastoma, one of the pediatric brain cancers with which SV40 has been associated and the same type that afflicted Alexander Horwin. When the Bonn researchers searched for large T‑antigen in the tumors, it was no longer present in some of the cells. Yet these particular sets of transformed (or malignant) cells appeared to be even more malignant than those that were still expressing the T‑antigen–evidently because without the presence of T‑antigen, the immune system could no longer recognize them as a threat. Thanks to SV40, and perhaps other viruses, can induce cancer and yet not be readily detectable once tumor start proliferating rapidly. Without the presence of an immunogenic protein like T‑antigen, cancer cels are less prone to immune system attack. Thus, after a certain point in tumorogenesis, cancer cells that have rid themselves of the virus have higher survival rates than those that still contain SV40, eventually replacing SV40-infected cells as the dominant subset in some expanding tumors. Yet the ultimate source for the aggressive, “stealth” cancer was still SV40.
Studies from Italy support this novel hypothesis: SV40 is dangerous as long as it is in the right tissue, even if it is not actually present in every, or even most cells. A team led by Luciano Mutti and Giovanni Gaudino discovered that a small number of SV40-infected mesothelial cells can induce malignancy in much larger numbers of nearby noninfected cells. Mutti and Gaudino found that once SV40 invades the mesothelial cells, the virus not only turns on the Met oncogene within the cells it has infected, it also stimulates those cells to send chemical signals to their neighbors, forcing them to turn on Met. Now these neighboring, uninfected cells have also been artificially switched on from a resting phase into an unnatural, hyperactive growth phase. Thus, even if only a few tumor cells contain SV40, growth factors produced by these cells will spur the malignant growth of nearby cells that do not contain the virus.
9. On top of the other cancer-causing mechanisms that SV40 manifests, the virus stimulates the production of VEGF, which causes the growth of blood vessels that nourish tumors.
Mutti also found that once tumor formation is under way, SV40 subverts one more cellular regulatory system in order to ensure that the tumor continues to grow. SV40, Mutti discovered, stimulates mesothelioma cells to produce vascular epithelial growth factor or VEGF. VEGF is a chemical that promotes blood vessel growth. Mutti found that in mesothelioma biopsies that tested negative for the presence of SV40, little VEGF is produced, while tumor cells that contained SV40 manufacture high levels of the growth factor. In this way, SV40, by encouraging blood vessels to grow toward the tumor, helps secure for the burgeoning cancer an ample supply of blood and nutrients. . . .
10. Yet another devastating aspect of SV40 is the fact that there are two major varieties–“slow growth” and “fast growth” SV40. Slow growth SV40 takes 19 days to mature, evading the screening process which evaluates cell cultures after the fourteen days that the faster growing variant of the virus takes to reach maturity and damage cells in such a way as to become evident to the screening procedures of the time.
. . . In 1999, when Carbone tested his vials of 1955 vaccine for SV40 and realized he had detected slow-growing SV40 variants that were present in the oral vaccine, he became curious. Suppose a slow-growing SV40 variant were present in the oral vaccine? Were current FDA regulations, which required only fourteen-day cell culture cycles, adequate to detect all SV40 types, including SV40 that was slow growing? Carbone conducted his own test. He discovered that the slow-growing strain of SV40 that he had recovered from Herbert Ratner’s 1955 vaccine took nineteen days to grow out–or become apparent in tissue cultures. That means FDA-mandated tests as likely as not would have failed to detect it or other slow-growing variants present in a vaccine.
Using the FDA’s testing protocol, here’s what might have happened in the case of the slow-growing variant of SV40 such as the type Carbone found in his 1955 vaccine vials: A sample of a lot from which the final trivalent vaccine batch was derived would have been inoculated into a test culture and held for fourteen days. Because the virus contained in the lot was Carbone’s nineteen-day, slow-growing type, after fourteen days, little, if any, of the virus would have infected cells and replicated to the point where it would burst the cells and release SV40 into the fluids that surround the tissue culture cells. There would be no apparent sign of viral growth and this primary culture, therefore, would be regarded as negative. On the fourteenth day, the fluids that surround the cell culture would be inoculated into a second culture, the subculture. But these fluids from the first culture (primary culture) still contained either no SV40 or only a very small amount of the virus. If there were no SV40 in the fluids from the first culture, this second subculture, too, would be negative. In the event that some SV40 actually was in the fluids of the primary culture, the subculture would still appear to be negative, even after fourteen days of observation, since this particular slow-growing SV40 variant takes nineteen days to grow out. Thus, an SV40-contaminated lot would pass the one safety test designed to catch the virus, and it would be released.
Slow-growing SV40 happens to be the type most often found in brain and bone cell tumors–tumor types that often afflict children, including the brain cancer that killed Alexander Horwin. (Faster-growing variants of SV40 have been found in these tumor types as well.) Carbone’s tests on his vintage vaccine support the theory that if slower-growing SV40 was present in the lots used to make the oral polio vaccine administered to Alexander, it might not have been detected following the test protocols required by the FDA. It is certainly scientifically possible, therefore, that Alexander’s dose of oral vaccine was a possible source for the SV40 in his medulloblastoma.