This is an excerpt from:
Simian Virus 40 (SV40):
A Cancer Causing Monkey Virus
from FDA-Approved Vaccines
This article was originally published in the Albany Law Journal of Science & Technology, Volume 13, Number 3, 2003
The Creation and Production of the Polio Vaccines
In the 1950s, scientists like Doctors Jonas Salk and Albert Sabin had isolated the poliovirus strains to make vaccines. Dr. Salk’s strains would be inactivated with formaldehyde and injected into children. Dr. Sabin’s strains would be attenuated or weakened by transferring or passaging the live viruses through different host cells and then fed to children orally.
Because his goal was to create a live attenuated vaccine, Dr. Sabin had to isolate the poliovirus strains and then passage the strains through a myriad of host cells in order to attain the right virulence—strong enough to illicit an immune response, but weak enough so as to not cause polio in the recipient. Sabin’s oral polio vaccine (OPV) is a trivalent vaccine and was, therefore, comprised of three types – Type I, II, and III. For example, Type I has the following lineage: In 1941, Drs. Francis and Mack isolated the Mahoney poliovirus “from the pooled feces of three healthy children in Cleveland.”  Dr. Salk then subjected the strain to passages through fourteen living monkeys and two cultures of monkey testicular cultures. In 1954, the strain (now called Monk14 T2) was given to Drs. Li and Schaeffer who subjected the virus to nine more passages through monkey testicular cultures. Next, the strain (now called Monk14 T11) underwent fifteen more passages in monkey testicular cultures, eighteen passages in monkey kidney cells, two passages through the skin of living rhesus monkeys, and additional passages through African Green monkey skin and monkey kidney cell cultures. This strain was now called MS10 T43 or LS-c. In 1956, Dr. Sabin took this virus and passaged it through seven cultures of African Green Monkey kidney cells.That same year, the pharmaceutical company, Merck, Sharp & Dohme, passed the strain (now called LS-c, 2ab/KP2) through a rhesus monkey kidney cell culture. The resulting material was called Sabin Original Merck (SOM) and was provided to Lederle in 1960 as the seed material to manufacture its polio vaccine. Types II and III were created in a similar fashion.
Once their strains were isolated, pharmaceutical companies needed a method to propagate the viruses in order to produce the vast quantities of vaccine needed for nation-wide immunization campaigns. This required a substrate upon which the poliovirus could be efficiently grown and harvested. Kidney cells from rhesus monkeys were chosen because they were found to be an effective growth medium. A small quantity of poliovirus could be added to the minced kidneys surgically removed from these monkeys and within a few days, large quantities of poliovirus could then be harvested from these same monkey cells.
There was a problem, however, with using these monkey kidney cells to both create the original vaccine strains and grow the vaccine in large quantities. Monkeys contain simian viruses. When the poliovirus was passaged through the monkeys or grown on the monkey kidney cells for production, extraneous viruses became part of the final poliovirus vaccine. As early as 1953, Dr. Herald R. Cox, a scientist working at Lederle Laboratories, one of the polio vaccine manufacturers, published an article in a peer reviewed scientific journal in which he stated, “[P]oliomyelitis virus has so far been cultivated only in the tissues of certain susceptible species—namely, monkey or human tissues. Here again we would always be confronted with the potential danger of picking up other contaminating viruses or other microbic agents infectious for man.” In fact, in 1958, a scientific journal reported that “the rate of isolation of new simian viruses (from monkey kidney cells) has continued unabated.” Additionally, in 1960, the pharmaceutical company Merck & Co. wrote to the U.S. Surgeon General:
Our scientific staff have emphasized to us that there are a number of serious scientific and technical problems that must be solved before we could engage in large-scale production of live poliovirus vaccine. Most important among these is the problem of extraneous contaminating simian viruses that may be extremely difficult to eliminate and which may be difficult if not impossible to detect at the present stage of the technology.
The Discovery of Simian Virus 40 (SV40)
Between 1959 and 1960, Bernice Eddy, Ph.D., of the National Institute of Health (NIH) examined minced rhesus monkey kidney cells under a microscope. These were the cells of the same species of monkeys used to create and produce the oral polio vaccine. Dr. Eddy discovered that the cells would die without any apparent cause. She then took suspensions of the cellular material from these kidney cell cultures and injected them into hamsters. Cancers grew in the hamsters. Shortly thereafter, scientists at the pharmaceutical company Merck & Co. discovered what would later be determined to be the same virus identified by Eddy. This virus was named Simian Virus 40 or SV40 because it was the 40th simian virus found in monkey kidney cells.
In 1960, Doctors Benjamin Sweet and Maurice Hilleman, the Merck scientists who named the virus SV40, published their findings:
Viruses are commonly carried by monkeys and may appear as contaminants in cell cultures of their tissues, especially the kidney . . . . The discovery of this new virus, the vacuolating agent, represents the detection for the first time of a hitherto “non-detectable” simian virus of monkey renal cultures and raises the important question of the existence of other such viruses . . . . As shown in this report, all 3 types of Sabin’s live poliovirus vaccine, now fed to millions of persons of all ages, were contaminated with vacuolating virus.
The vacuolating virus was another name for SV40.
In 1962, Dr. Bernice Eddy published her findings in the journal produced by the Federation of American Societies for Experimental Biology. She wrote:
There is now an impressive list of oncogenic (cancer causing) viruses—the rabbit papilloma, polyoma, Rous sarcoma, the leukemia viruses . . . . It has been known for a number of years that monkeys harbor latent viruses . . . . The (SV40) virus was injected at once into 13 newborn hamsters and 10 newborn mice. Subcutaneous neoplasms indistinguishable from those induced by the rhesus monkey kidney extracts developed in 11 of the 13 hamsters between 156 and 380 days . . . .
Subsequent studies performed in the early 1960s demonstrated that SV40 caused braintumors in animals and that SV40 could transform or turn cancerous normal human tissuein vitro. A disturbing experiment performed during this era also suggested that SV40 could cause human cancers in man in vivo. In 1964, Fred Jensen and his colleagues took tissue from patients who were terminally ill with cancer. They exposed the tissue to SV40 and then after it was transformed, they implanted the tissue back into the patient.These implants grew into tumors in their human hosts. This suggested the possibility that SV40 could cause cancers in man.
New Regulations are Implemented
By 1960, the Salk injectable polio vaccine (IPV) had been administered to about 98 million American children and adults, and Sabin’s OPV had been administered to about 10,000 Americans and millions in the USSR where the clinical trials had been conducted. It was estimated that 10% to 30% of the vaccines contained live SV40. The federal agency in charge of vaccine licensing and safety at the time was the Division of Biologics Standards (DBS) of the National Institute of Health (NIH). Incredibly, this agency did not order a recall of any of the SV40-contaminated vaccines. The tainted vaccines continued to be administered until 1963 when they were all used and replaced by allegedly SV40-free vaccines as required by the new federal regulations promulgated in 1961.
On March 25, 1961, the federal regulations that controlled the production of oral poliovirus vaccine were amended. These new regulations did not require the vaccine manufacturers to discard their SV40-contaminated poliovirus seeds which were the source for all subsequent polio vaccines. Instead, the rules required that “[e]ach seed virus used in manufacture shall be demonstrated to be free of extraneous microbial agents.”The new regulations also required that each pair of monkey kidneys removed from a monkey for vaccine production “shall be examined microscopically for evidence of cell degeneration.” Furthermore, fluid from the monkey kidney cells had to be combined with other tissue cultures in order to detect if there was any contaminating virus. The regulations required that “[t]he cultures shall be observed for at least 14 days.”
In essence these regulations required an SV40 test that was comprised of taking the monkey kidney cells upon which the vaccine would be grown and: 1) Looking at them through a microscope to see if they demonstrated SV40; 2) Taking fluids from them; 3) Introducing those fluids into other cell cultures; 4) Waiting 14 days; and 5) Seeing whether the other cell cultures were changed as a result of the presence of SV40. These tests werenot designed to detect the contaminating viruses themselves. One cannot see SV40 or any virus with a standard light microscope or the naked eye. Instead, the government’s SV40 test relied on the observation of the presumed effect of an SV40 infection on certain tissue cells to demonstrate the presence of the virus.
On November 8, 1961, after the new regulations were in force, an internal Lederle Laboratories memo stated that three lots of OPV that had been released for clinical trials were probably contaminated with SV40. The memo states, “The decision by Dr. Murray to allow SV40 to be present at the PCB-2 level was the basis for our allowing these lots to pass.” The PCB-2 level comprised one set of fluids taken from the monkey kidney cells and introduced into other cell cultures to detect SV40. It was used to perform the 14-day observation tests for the presence of SV40 and had indicated that these particular polio harvests were SV40 contaminated. “Dr. Murray” referred to above is Dr. Roderick Murray who was the director of the Division of Biologics Standards (DBS) of the National Institute of Health (NIH) from 1955 to 1972. It is unknown why, according to this internal memorandum, the DBS would allow polio vaccines to be released when the very tests designed to find SV40 produced positive results of SV40 infection.
A. The Scientific Rationale for the New Regulations
In 1962, an article received for publication on September 29, 1961, appeared in the Journal of Immunology; entitled, Studies on Simian Virus 40, it was written by scientists from the DBS of the NIH. This article presented the rationale for the new SV40 safety regulations that would remain in place, ostensibly unchanged, for the next four decades. The article’s lead author was Harry M. Meyer, Jr. Dr. Meyer would succeed Dr. Murray as the director of the DBS and would hold this post from 1972 to 1987.
This article discussed some of the challenges with SV40 and polio vaccine production including the fact that the time required for SV40 to show itself in tissue culture tests was “directly related” to the amount of SV40 present. In other words, the testing required by the federal regulations for SV40 detection was dependent on the amount of SV40 present.
The authors also pointed out that it could take up to thirty-five days for SV40 detection when the virus was removed from the blood of an infected monkey. Interestingly, however, the authors also stated that it took only eleven days for low doses of SV40 to be detected when it was removed from monkey kidney cells. This was reportedly based on a single experiment. The eleven-day result was significant because the regulations only required fourteen days of observation. If low doses of SV40 could be detected in eleven days then the fourteen-day observation period would be sufficient. A close reading of this article, however, reveals that this crucial study was at best incomplete.
B. A Critique of the Scientific Basis of the New Regulations
The authors of the Journal of Immunology article stated that 10 to 100 TCID50 or “Tissue Culture Infective Dose” of SV40 was detected in eleven days. TCID50 is defined as that dilution of virus required to infect 50% of a given batch of inoculated cell cultures.Therefore, a titer of 10 to 100 TCID50 represents a substantial amount of SV40 because one-half of the cells are infected. In other words, if it took a certain sized dose to infect 50% of the cells in eleven days, it would probably take a substantially smaller dose to infect 1% of the cells in the same period. This smaller dose would then take longer to infect 50% of the cell cultures. Therefore, this article left out the important fact that very low doses of SV40 would most likely not be detected in eleven days.
Second, the government scientists used pure SV40 as a surrogate for SV40-contaminated monkey kidney cells. There is no study that demonstrates the validity of this. During vaccine production, polio seed virus is inoculated into monkey kidney cells in order to grow the vaccine. Samples of these cells are set aside and fluids are drawn off and injected into other cell cultures to test for the presence of SV40. Since these fluids are drawn from monkey kidney cells, they contain a variety of viruses, cellular components, growth medium, and other debris. The sensitivity of the SV40 test for detection of SV40 from this amalgam was the important public health question. The Division of Biologics Standards, however, did not perform this test, or if they did, they did not report their findings. Instead, they used pure SV40 without any other ingredients to determine that eleven days was sufficient.
This flaw in the methodology was demonstrated when the authors discussed the fact that after three weeks of observation, SV40 did not appear from the kidneys of four monkeys that were known to carry SV40 antibodies in their blood. The government scientists stated, “[T]he failure to demonstrate virus in the renal tissue of an appreciable number of rhesus monkeys that had been infected some time earlier was of interest.” This is an admission that even after three weeks of observation (one week longer than the federally mandated two-week observation period) the SV40 from the kidneys of SV40 contaminated monkeys (not pure SV40) did not reveal itself in culture. Unfortunately, the government scientists did not act on this important observation other than to note that it “was of interest.”
By 1965, it was well established in the scientific literature that there were several problems with the SV40 tests mandated by the Code of Federal Regulations. First, the fourteen-day SV40 tests were not long enough to detect the virus. In fact, numerous experiments by leading virologists (all non-governmental scientists) found that it took from two to five weeks for the detection of low doses of SV40. Second, there were more sophisticated microbiological tools available that could detect SV40 with greater accuracy. These tests were all widely used and accepted virological techniques. Third, there were several more sophisticated measures available to eliminate SV40 from cultures used to make the poliovirus vaccine. Nonetheless, despite the mounting scientific evidence that the SV40 tests were crude and unreliable, the regulations were not changed and oral polio vaccine manufacturers did not voluntarily adopt any technical improvements to ensure that SV40 was detected and eliminated from their products.
The Flawed Epidemiology
After SV40 was originally detected in the Salk and Sabin vaccines that had been administered to millions of children around the world, the scientific community held its breath and wondered if these children would be stricken with cancer. Indeed, the pediatric cancer rate continued to climb through the 1960’s, 70’s, 80’s and 90’s. But, the few epidemiological studies that looked for a direct link between SV40 and human cancer provided inconsistent conclusions. Some reports found that there was an increased risk of cancer from SV40 exposure and others found that there was no risk. Each of these studies suffered from major flaws including the fact that no one knew who actually received the SV40-contaminated vaccines and who did not, so it was impossible to compare an SV40-exposed group with a non-exposed group.
SV40—A Human Carcinogen
By 1999, numerous pathologists, microbiologists, and virologists throughout the world had detected SV40 in a variety of human cancers such as brain tumors including medulloblastomas, bone cancers, and mesotheliomas a fatal lung cancer. These were the very same cancers that were created when SV40 was introduced into animals.The advent of Polymerase Chain Reaction (PCR) technology that could identify the genetic code of specific strands of DNA demonstrated with precision that it was this monkey virus that was being detected in human cancers and no other. Moreover, the rates of these particular cancers had steadily increased over the last few decades. The question that had been left unanswered for almost four decades now faced scientists again—was SV40 responsible for causing or contributing to human cancers?
Over the last forty years since its discovery, SV40 had become one of the most widely studied and best understood viruses in microbiology. It was routinely used to create human cancers in the laboratory in order to test cancer therapies. In addition, it is now known how this virus caused cancer on a molecular level. After careful study documented in peer reviewed publications, leaders in SV40 research announced that SV40 was a class 2A human carcinogen.
The Government’s Response
Nonetheless, the various United States government agencies such as the Centers for Disease Control (CDC) and National Cancer Institute (NCI) disputed these conclusions. According to the CDC, “SV40 virus has been found in certain types of cancer in humans, but it has not been determined that SV40 causes these cancers.” According to the National Intsitutes of Health (NIH), “the NCI is continuing to evaluate the possible link between SV40 infection and human cancers.” A question has been raised whether this continuing evaluation is being performed with complete scientific integrity. One article written by an attorney and published in a peer reviewed scientific journal describes how the NCI deliberately compromised a study that would have demonstrated the association between SV40 and mesothelioma.
While the United States government continues to evaluate whether or not SV40 represents a public health threat and whether SV40 is a human carcinogen, several scientists at the NCI concluded that SV40 contributed to the formation of mesotheliomas. In fact, the federal government has licensed technology to target SV40 in the treatment of human mesotheliomas.
SV40 and the Public Health
Despite the government’s foot dragging, in the last several years, scientists from around the world have made startling and disturbing discoveries. They have found SV40 antibodies in a significant percentage of people including children who were too young to receive the SV40 contaminated vaccines of the early 1960’s. They have also discovered that cancers with SV40 are less likely to be responsive to chemotherapy and radiation because SV40 interferes with the genes necessary for cancer cells to die when they are exposed to chemo or radiation therapy.
The Institute of Medicine Report
In July 2002, the National Academy of Science Institute of Medicine (IOM) Immunization Safety Committee convened a study into SV40 and cancer which culminated in a report published in October 2002. According to the IOM report “SV40 Contamination of Polio Vaccine and Cancer”:
The committee concludes that the biological evidence is strong that SV40 is a transforming [i.e., cancer-causing] virus, . . . that the biological evidence is of moderate strength that SV40 exposure could lead to cancer in humans under natural conditions, [and] that the biological evidence is of moderate strength that SV40 exposure from the polio vaccine is related to SV40 infection in humans.
* Mr. Michael Horwin, M.A., J.D. and his wife Raphaele Horwin, M.A., M.F.S. testified in front of the U.S. Congress on June 7, 2000 in hearings entitled Cancer Care For The New Millenium – Integrative Oncology. Mr. Horwin is a magna cum laude law school graduate and winner of the National Scribes Award for article “War on Cancer”: Why Does the FDA Deny Access to Alternative Cancer Treatments?, 38 Cal. W. L. Rev. 189 (2001). He has written a number of articles on pediatric vaccines and health freedom that have been published in law and health publications. The Horwin’s lawsuit as described in this article is the first case alleging that Simian Virus 40 (SV40) was responsible for the cancer and death of a child, in this case, their son Alexander. As they do in all their writings, the Horwin’s dedicate this article to their son Alexander and to other children who have been injured or killed by the very vaccines designed to protect them. For more information, see the Horwins website:www.ouralexander.org.
 A.B. Sabin, A.B. & L. Boulger, History of Sabin Attenuated Poliovirus Oral Live Vaccine Strains. 1 J. Biol. Stand. 115, 115–18 (1973). The Mahoney virus was isolated in 1941 by Drs. Fancis and Mack.
 M.R. Hilleman, Discovery of Simian Virus (SV40) and its Relationship to Poliomyelitis Virus Vaccines, in Simian Virus 40 (SV40): A Possible Human Polyomavirus, 94 Dev. Biol. Stand. 183–90 (F. Brown & A.M. Lewis eds., 1998).
 Bernice E. Eddy, Tumors Produced in Hamsters by SV40, 21 Fed’n Proc 930, 930–35 (1962) [hereinafter Eddy I]; Bernice E. Eddy et al., Identification of the Oncogenic Substance in Rhesus Monkey Kidney Cell Cultures as Simian Virus 40, 17 Virology 65–75 (1962) [hereinafter Eddy et al. II]; Edward Shorter, The Health Century 195–99 (1987).
 In vitro means outside a living body. Webster’s New Collegiate Dictionary 609 (1977). Harvey M. Shein & John F. Enders, Transformation Induced By Simian Virus 40 in Human Renal Cell Cultures, I. Morphology and Growth Characteristics, 48 Proceedings of the National Academy of Sciences, 1164, 1164 (1962); Hilary Koprowski et al., Transformation of Cultures of Human Tissue Infected with Simian Virus SV40, 59 J. Cellular & Comp. Physiology 281, 281–92 (1962).
 Institute of Medicine of the National Academies, Immunization Safety Review: SV40 Contamination of Polio Vaccine and Cancer 4, 21 (Kathleen Stratton et al. eds., 2002), www.nap.edu/books/0309086108/html (last visited May 26, 2003) [hereinafter Immunization Safety Review].
 National Institutes of Health (NIH) Division of Biologics Standards (DBS) was a forerunner of today’s Center for Biologics Evaluation and Research (CBER). Paul Parkman, Harry Meyer, Jr., MD Lecture, CBER Centennial—Slide Presentation(Sept. 23–24, 2002), at www.fda.gov/cber/summaries/cent092302pp.htm (last visited May 26, 2003). “The transfer of DBS to the Food and Drug Administration took place in 1972.” Id. The DBS became the FDA’s Bureau of Biologics (BoB). Id. “Later incarnations of this organization included the Center for Drugs and Biologics (CDB) and finally, the present day Center for Biologics Evaluation and Research (CBER).” Id.
Under federal law, a manufacturer must receive a product license prior to marketing a brand of live oral polio vaccine. In order to become eligible for such a license, a manufacturer must first make a sample of the vaccine product. This process begins with the selection of an original virus strain. The manufacturer grows a seed virus from this strain; the seed virus is then used to produce monopools, portions of which are combined to form the consumer-level product. Federal regulations set forth safety criteria for the original strain, . . . the seed virus, . . . and the vaccine monopools, . . . . Under the regulations, the manufacturer must conduct a variety of tests to measure the safety of the product at each stage of the manufacturing process. Upon completion of the manufacturing process and the required testing, the manufacturer is required to submit an application for a product license to the DBS. In addition to this application, the manufacturer must submit data from the tests performed and a sample of the finished product.
Id. (citations omitted); see also Kops, supra note 15, at 4745–49.
 Id. According to Lederle Laboratories, they also perform a 14-day subculture. A subculture, however, is like starting new because fluids are drawn from the original culture and infected into a new tissue culture. See B. Brock et al., Product Quality Control Testing for the Oral Polio Vaccine, in Simian Virus 40 (SV40): A Possible Human Polyomavirus, supra note 28, at 217–19.
 Memorandum from Dr. James L. Biddle, to Dr. I.S. Danielson (Nov. 8, 1961), at www.sv40cancer.com/doc2.asp (last visited May 15, 2003).
 In the early 1960’s, the Laboratory of Biologics Control was reorganized, and elevated to Division level, becoming the Division of Biologics Standards. See Parkman, supra note 47. It was given a separate new building, more research and regulatory staff, and a new Director, Dr. Roderick Murray. Id. One of the first major products the new organization was called upon to approve was the live oral poliovirus vaccines. See id.
 See Parkman, supra note 47. “In 1972, Hank became responsible for directing the research and regulatory programs for all biologicals in the newly formed Bureau of Biologics and in 1982, became Director of the combined Center for Drugs and Biologics.” Id.
 It also discussed other problems with SV40 detection, including: 1) CPE was dose dependent; 2) One could not tell clinically or by autopsy whether a monkey is contaminated with SV40; 3) Some SV40-contaminated monkeys do not demonstrate antibodies; and 4) The key tissue culture test may not be reliable because it could contain SV40 itself. Meyer et al., supra note 61, at 796–806.
 Meyer et al., supra note 61, at 796–806, 797, 799. SV40 Seed Pool A was passaged from SV40 strain 776. Id. at 797. At a concentration of 105 or 106 SV40 Seed Pool A demonstrated CPE in Cercopithecus kidney cells by the 3rd day.See id. at 799. At a concentration of 103 it demonstrated CPE in Cercopithecus kidney cells by the 7th day. See id. at 798–99. At a concentration of 10 or 100, it demonstrated CPE in Cercopithecus kidney cells by the 11th day. See id. at 799.
 Sara Stinebaugh & Joseph L. Melnick, Plaque Formation by Vacuolating Virus SV40, 16 Virology 348, 348 (1962). “[A]t the end point, the amount of CPE is variable and limited to portions of the culture, so that a good deal of time must be spent meticulously examining the cultures under the microscope. Furthermore the cultures must be held for 2-3 weeks to arrive at an end point . . . .” Id. (emphasis added); see also Harvey M. Shein & Jeana D. Levinthal, Fluorescent Antibody and Complement Fixation Tests for Detection of SV40 Virus in Cell Cultures, 17 Virology 595, 595 (1962). “In this laboratory in [Green Monkey Kidney] GMK cultures inoculated with small quantities of virus [(SV40)] (i.e., <100 TCID50), changes were not observed until five or six weeks after inoculation. Therefore to attain maximal accuracy with this method, a long period of observation is required.” Id. “Finally the demonstration that SV40 can multiply in cultures derived from [African Green Monkey Kidney] AGMK Cells without exhibiting any cytopathic effect detectable under non-stained, direct light microscope observations suggests that as far as this agent is concerned more attention should be given to the present safety tests used concerning vaccines prepared in monkey cells.” Mario V. Fernandes & Paul S. Moorhead, Transformation of African Green Monkey Kidney Cultures Infected with Simian Vacuolating Virus (SV40), 23 Tex. Rep. on Biology & Med., 242–57 (1965).
 See Jack van Hoff et al., Trends in the Incidence of Childhood and Adolescent Cancer in Connecticut, 1935–1979, 16 Med. & Pediatric Oncology 78, 78–87 (1988); W. Archie Bleyer, What can be Learned about Childhood Cancer from “Cancer Statistics Review 1973–1988”, 15 Cancer 3229, 3229–36 (Supp. 1993); James G. Gurney et al., The Influence of Subsequent Neoplasms on Incidence Trends in Childhood Cancer, 3 Cancer Epidemiology Biomarkers & Prevention 349, 349–51 (1994); Greta R. Bunin et al., Increasing Incidence of Childhood Cancer: Report of 20 Years Experience From the Greater Delaware Valley Pediatric Tumor Registry, 10 Paediatric & Perinatal Epidemiology 319, 319–38 (1996); J.G. Gurney et. al., Trends in Cancer Incidence Among Children in the U.S., 78 Cancer 532, 532–41 (1996); Andrine R. Swensen & Sally A. Bushhouse, Childhood Cancer Incidence and Trends in Minnesota, 1988-1994, 81 Minn. Med. 27, 27–32 (1988),www.mnmed.org/publications/MnMed1998/December/Swenson-Bushhouse.cfm (last visited May 26, 2003); Martha S. Linet et al., Cancer Surveillance Series: Recent Trends in Childhood Cancer Incidence and Mortality in the United States, 91 J. Nat’l Cancer Inst. 1051, 1051–58 (1999); Joseph J. Mangano, A Rise in the Incidence of Childhood Cancer in the United States, 29 Int’l J. Health Servs. 393, 393–408 (1999).
 M.D. Innis, Oncogenesis and Poliomyelitis Vaccine, Nature, Aug. 31, 1968, at 972–73; Jacqueline R. Farwell et al., Effect of SV40-Virus Contaminated Polio Vaccine on the Incidence and Type of CNS Neoplasms in Children: A Population-Based Study, 104 Transactions Am. Neurological Ass’n 261, 261–64 (1979); Jacqueline R. Farwell et al., Medulloblastoma in Childhood: An Epidemiological Study, 61 J. Neurosurgery 657, 657–64 (1984) [hereinafter Farwell et al. II]; Olli P. Heinonen, et al.Immunization During Pregnancy Against Poliomyelitis and Influenza in Relation to Childhood Malignancy, 2 Int’l J. Epidemiology 229, 229–35 (1973).
 Joseph F. Fraumeni, Jr. et al., Simian Virus 40 in Polio Vaccine: Follow-Up of Newborn Recipients, Science, Jan. 1970, at 59–60; Edward A. Motimer, Jr., Long-term Follow-Up of Persons Inadvertently Inoculated with SV40 as Neonates, 305 New Eng. J. Med. 1517, 1517–18 (1981).
 Huato Huang et al., Identification in Human Brain Tumors of DNA Sequences Specific for SV40 Large T Antigen, 9 Brain Pathology 33, 33–42 (1999); Hai N. Zhen et al., Expression of the Simian Virus 40 Large Tumor Antigen (Tag) and Formation of Tag-p53 and Tag-pRb Complexes in Human Brain Tumors, 86 Cancer 2124, 2124–32 (1999); F. Martini et al., Simian Virus 40 Footprints in Normal Human Tissues, Brain and Bone Tumours of Different Histotypes; in Simian Virus 40 (SV40): A Possible Human Polyomavirus, supra note 28, at 55–56; J. Wang et al., Simian Virus 40 DNA Sequences in Human Brain and Bone Tumours, in Simian Virus 40 (SV40): A Possible Human Polyomavirus, supra note 28, at 13–21.
 Paul Rizzo et al., Simian Virus 40 is Present in Most United States Human Mesotheliomas, but it is Rarely Present in Non-Hodgkin’s Lymphoma, 116 Chest 470S, 470S–473S (1999); Narayan Shivapurkar et al., Presence of Simian Virus 40 Sequences in Malignant Mesotheliomas and Mesothelial Cell Proliferations, 76 J. Cellular Biochemistry 181, 181–88 (1999).
 Paul Gerber & Ruth L. Kirschstein, SV40-Induced Ependymomas in Newborn Hamsters, 18 Virology 582, 582–88 (1962); Alan S. Rabson et al., Papillary Ependymomas Produced in Rattus (Mastomys) Natalensis Inoculated with Vacuolating Virus (SV40), 29 J. Nat’l Cancer Inst. 765, 765–87 (1962); Ralph L. Brinster et al., Transgenic Mice Harboring SV40 T-antigen Genes Develop Characteristic Brain Tumors, 37 Cell 367, 367–79 (1984); Robert H. Eibl et al., A Model for Primitive Neuroectodermal Tumors in Transgenic Neural Transplants Harboring the SV40 Large T Antigen, 144 Am. J. Pathology 556, 556–64 (1994); Claudia Cicala et al., SV40 Induces Mesotheliomas in Hamsters, 142 Am. J. Pathology 1524, 1524–33 (1993); Matker et al.,supra note 86, at 193–97.
 Bharat Jasani et al., Simian Virus 40 Detection in Human Mesothelioma: Reliability and Significance of the Available Molecular Evidence, 6 Frontiers Bioscience e12, e12–22 (2001); J.S. Butel et al., Detection of Authentic SV40 DNA Sequences in Human Brain and Bone Tumours, in Simian Virus 40 (SV40): A Possible Human Polyomavirus, supra note 28, at 23–32.
 Alicia Ault, Monkey Virus in Humans may Trigger Cancer: Experts, Reuters Heath, July 2002, atwww.upmccancercenters.com/news/reuters/reuters.cfm?article=711 (last visited May 15, 2003).
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 All cells in the human body have various tumor suppressor genes and these genes tell individual cells to die when the cells become damaged and mutated. See The Chemotherapy Source Book 4 (Michael C. Perry ed., 3d ed. 2001). One tumor gene in particular, p53 is designed to kill cells through apoptosis or “cell suicide” so that mutated cells to not lead to cancer through uncontrolled multiplication and metastasis. Chemotherapy and radiation depend, to a large degree, on p53. Id. Chemotherapy and radiation create damage to cells which, in turn, leads to p53 being triggered which ultimately leads to apoptosis. Id. Without p53, cytotoxic therapies would simply create more mutations in already damaged cells. Id. Such cells would not die, and would likely become only more aggressive. Id. It is now known that SV40 binds to and inactivates the functioning of p53 so that the cells do not commit suicide even after they are damaged by chemotherapy or radiation. Id. This suggests that in cancers in which SV40 is present, radiation and chemotherapy will likely not be of any benefit. See id.