Why AIDS Was Invented

AIDS is proving fantastically beneficial to cancer researchers. In this e-book the author proposes that these benefits are not coincidental and reveals that cancer researchers not only created animal immunosuppressive viruses to do exactly what HIV does but even modified them for growth in human cell cultures, shortly before the epidemic began. Moreover, published human experiments with deadly monkey cancer viruses are exposed and proposed as smaller-scale versions of the cancer experiment which culminated in the useful epidemic of immunosuppression and cancer associated with HIV. The surprising manner in which this catastrophic epidemic is systematically fulfilling the long-term goals of the cancer vaccine establishment—the very group that invented immunosuppressive viruses—is also revealed. For more information on how cancer research is related to AIDS and the Gulf War

AIDS: The “Perfect” Disease

In this study the author argues that AIDS and the associated epidemic of cancer are caused by a type of virus specifically developed and tested by cancer researchers (prior to AIDS) to increase susceptibility to cancer. Moreover, it is proposed that AIDS is the culmination of increasingly sophisticated experiments which were conducted intentionally in animals and humans to induce cancer as a means of developing and testing cancer vaccines. An eye-opening series of published experiments, including one in which immunosuppression was exploited to cause sarcoma tumors in human subjects injected with monkey cancer viruses, is revealed as a precedent for the experiment proposed to explain the explosion of immunosuppression and useful sarcomas in AIDS Evidence is also presented to support the thesis that the AIDS epidemic was deliberately started as an exercise in biowarfare conducted under the cover of an international human cancer experiment. This would explain why the HIV epidemic is selectively depopulating regions of the globe that the national security establishment had targeted for depopulation in the 1970s as a means of maintaining access to resources in the developing world. Additionally, the “cancer vaccine experiment” theory of the origin of AIDS could also explain not only why the AIDS virus selectively depopulates the exact components of the immune system that cancer researchers had been targeting for decades prior to AIDS but why homosexual populations are disproportionately infected by HIV and rare cancers. The relationship between AIDS research and the Gulf War Syndrome are also reviewed in this work.

Why AIDS Was Invented

“As disastrous as the spread of HIV is, the insights that the AIDS epidemic provides into the causes of cancer may ultimately lead to new and successful approaches to cancer prevention.” [1]

On the heels of one of medical science’s greatest triumphs—the vaccine against polio—researchers pursued the ultimate goal: a vaccine against human cancers. Unfortunately, unlike the case with the poliovirus, there were no known cancer viruses with which to make or test human cancer vaccines. Therefore, researchers engaged in a crash government program to isolate and characterize animal and human viruses capable of causing human cancer so they could manipulate them into serving as vaccines. [2] In this long-range human cancer vaccine research program, scientists consistently followed the path that had already led to cancer vaccines in animals. In the effort with animal cancer viruses, tumor cells were extracted from chemically or radiation-induced tumors and turned into so-called “cell-free filtrates.” These filtrates were then injected into other animals to see if the tumors could be “transplanted.” If transplanted tumors successfully grew, the researchers assumed that these injections had contained cancer viruses (since all other cells had been filtered out). [3] As part of this effort, researchers injected these “synthetic” cancer viruses into experimental animals with differing immune system health and genetic backgrounds. This allowed them to observe how viral cancer growth was controlled by the immune response under different host conditions. After watching how the immune system reacted to the injected cancer viruses, researchers were able to develop procedures for artificially boosting the immune system reactions they observed in the form of vaccines. By manipulating into vaccines the cancer viruses they had created, researchers now had a laboratory model for the creation and prevention of viral cancer in animals—they could give lab animals combinations of the experimental cancer viruses and vaccines (based on these or other viruses) they had created to determine the effectiveness of the cancer vaccines. In order to replicate this successful research technique in humans, [4] researchers needed a way to induce human cancer on demand. This would allow researchers to observe cancer growth from its earliest stages [5] as well as develop and test potential human cancer vaccines. As a means of reaching this lofty goal, virologists engaged in a long-running research effort to isolate human cancer viruses from cancer patients using procedures developed in animal research. [6] The cancer-causing potential of these viruses was tested by injecting them in lab animals. In some cases researchers went even further and conducted barbaric human “cancer transplant” experiments in which an array of human and animal cancer cells and viruses were isolated, combined and injected in human subjects to induce and measure tumor growth directly. This gave researchers the opportunity not only to monitor carefully the critical transition from health to cancer growth in human subjects, but also to look for natural immune responses to the initial challenge with cancer which might be artificially amplified with vaccines.

• 1 V. Beral, H. Jaffe, and R. Weiss, “Cancer Surveys: Cancer, HIV and AIDS,” Eur. J. Cancer, vol. 27, no. 8, 1991, 1058.
• 2 This program was called the Special Virus Cancer Program. The goals of this massive government research effort were outlined in its 1967 Progress Report: “The main objectives of this Program are: (1) to determine whether viruses comparable to those now known to be associated with avian and murine leukemia are etiological agents of human leukemia, and (2) to develop an effective vaccine or other means for the prevention and/or control of human leukemia and lymphoma when such etiological agents are found.” F. Rauscher and R. Reisinger, Special Virus-Leukemia Program, Progress Report #4, Program Staff, National Cancer Institute, Etiology Area, May 1967, p.1.
• 3 “Un-natural Viruses” Nature New Biology, vol. 230, March 17, 1971, 65, 66.
• 4 Virologists were anxious to extend the cancer vaccine procedures successfully developed for use in animals to man: “It has already been shown that a vaccine prepared against one particular virus will immunize mice not only against that virus but against others as well. …This is important because it shows that (a) animal leukemia can, in fact, be prevented with vaccines and that the causative viruses from which the vaccines were prepared can be attenuated and/or killed by procedures already established for the influenza, polio, and measles diseases of man… This approach may make possible more effective control of the human disease than that attained by drug therapy alone.” Special Virus-Leukemia Program, Progress Report #4, p. 14.
• 5 Cancer researchers have long coveted the ability to watch cancer grow from its earliest stages in a large number of human subjects. To this end, human victims of naturally occurring immunosuppressive disorders have been the subjects of numerous monitoring programs in which the relationship between immune system health and cancer could be correlated. By watching people predisposed to cancer, researchers could eliminate the drawbacks of epidemiological studies, in which such correlations were typically made after cancer had already been manifested. R. A. Good, “Relations between Immunity and Malignancy,” Proc. Nat. Acad. Sci. USA, vol. 69, no. 4, April 1972, 1026-1032.
• 6 Scientists affiliated with the government’s cancer virus program correctly predicted that deadly human cancer viruses would be created using the same techniques by which animal viruses had been isolated and made more potent: “Experience with animal tumor viruses suggests that it may be possible to establish and enhance the disease-inducing potency of candidate particulates from human neoplasma by use of virus passage, concentration and purification procedures. As with murine and avian tumor viruses it must be anticipated that increasing potency of candidate viruses from human and other animal neoplasms will confer on these viruses…” Special Virus-Leukemia Program, Summary Progress Report for the Period September 1964 through June 1965, p. 9. [emphasis added]

A similar procedure had been used in vaccine research for hepatitis (an alleged cancer-causing virus in humans). In this case mentally retarded children were injected with hepatitis so that vaccine researchers could watch the disease progress from its earliest stages. One government investigation described a study “from 1956 to 1972 [by] Dr. Saul Krugman of New York University [who] led a study team at the Willowbrook State School for the Retarded, on Staten Island, New York”: Noting the high incidence of hepatitis among the residents of the school, nearly all of whom were profoundly mentally impaired children and adolescents, Krugman and his colleagues injected some of them with a mild form of hepatitis serum. The researchers justified their work on the grounds that the subjects probably would have become infected anyway, and they hoped to find a prophylaxis for the virus by studying it from the earliest stages of infection.[7]

Human experiments involving vaccines against hepatitis would continue for years to come and can be tied directly to the outbreak of AIDS in homosexuals chosen for experimental hepatitis vaccine trials shortly before they began dying of previously rare cancers. Vaccines against hepatitis would also later be used in an ambitious international human cancer vaccine experiment (recently declared a success), which will be discussed shortly.

Unfortunately, clues to the hypothesized naturally occurring human immune response to cancer, which might be harnessed for vaccines, proved elusive. Therefore, an indirect way of determining which immune system components were critical in fighting off human cancer was investigated. This effort—which was similar to the approach used in human hepatitis research and animal cancer research—consisted of injecting cancer cells in patients with various immune system deficiencies. The hope was that if cancer cells grew more consistently in patients with immune system components that were damaged in specific ways, then these components were the keys to fighting off cancer in healthy patients. Follow-up efforts that focused on strengthening these identified components might be the key to training the human immune system to prevent cancer with vaccines. [8]Thus, it was hoped that if researchers traveled the path through “immunosuppression,” it would lead to the ultimate goal of cancer “immunocompetence” in the form of vaccines. [9] In the 1950s researchers began to use this procedure systematically in humans in the same manner it had been used in lab animals. For example, researchers deliberately induced tumors in human subjects with compromised immune systems by injecting them with cancer cells thought to contain human cancer viruses. Clues were sought as to the immune system deficiencies responsible for increased tumor transplant growth by correlating tumor rejection rates with other measures of immune system health. Chester Southam was a leading researcher who published numerous papers describing the use of this technique in human subjects. Southam described his methodology as follows: The procedure, as I explained, requires simply the hypodermic injection of a suspension of tissue-cultured cells at two sites on the anterior thigh or arm and observation of the sites at about weekly intervals for six weeks or until regression is complete. These cells are of two or more cancer cell lines. These cancer cell lines were chosen because they have the necessary growth capacity to produce a measurable reaction.[10]

• 7 Advisory Committee on Human Radiation Experiments - Final Report, Chapter 3, Section: “The Development of Human Subject Research Policy at DHEW,” http://tis.eh.doe.gov/ohre/roadmap/achre/chap3_2.html (12/31/01)
• 8 One author stated the goal: “Here, then, we have a wide possibility: if there is such a biological mechanism as a defense against cancer, then it may be possible to stimulate it either before cancer strikes or perhaps even later when the cancer has taken hold.” Earl Ubell, “Injecting Cancer Cells—the Case for the Defense,” New York Herald Tribune, January 26, 1964, 29.
• 9 It was in order to generate organisms with various immune system defects for these studies that numerous means of inducing immune system deficiencies (or immunodeficiencies), including the use of viruses designed for this purpose, were eventually developed.
• 10 Jay Katz, Experimentation with Human Beings (New York: Russel Sage Foundation, 1972), 11.

Southam injected hundreds of healthy and diseased patients [11] with “cancer transplants” so he could measure the tumor growth and correlate it with the immune system health of the cancer transplant recipient. [12] One of the results of Southam’s dangerous tests was that the tumors he transplanted in healthy human subjects seemed to regress faster with repeated implants while the implants in cancer patients showed less favorable results: In brief, normal recipients responded to implanted human cancer cells with a marked local inflammatory reaction and rapid complete regression of the implants within a maximum period of 3 to 4 weeks. . . . In striking contrast, however, those recipients that had advanced cancer showed little or no acute inflammatory response, the implanted cancer cells grew progressively for a period of 3 weeks or more before regression started, and some individuals failed to reject implanted cancer cells over periods of observation between 6 weeks and 6 months. [13]

Southam assumed that the different reactions to cancer injections were due to the differences in the test subjects’ immune systems. [14] After watching how these tumor transplants grew in healthy patients, patients with cancer, and patients with diseases other than cancer (at the Jewish Chronic Disease Hospital), Southam claimed cancer patients had an immune system defect that contributed to cancer growth: All the patients in the study undertaken at the Jewish Chronic Disease Hospital rejected the transplants as promptly as did the healthy persons. Thus it has been demonstrated that cancer patients lack an immune mechanism present in other individuals, including chronically diseased patients.

• 11 Southam summarized this procedure: “During the past 10 years, as we have seen, cancer cells have been implanted in almost 600 well persons and cancer patients. . . . The technique for measuring immune reactions is now standardized and the results are predictable.”
• 12 Southam explained, “Other than the two hypodermic injections and observation of the reaction, the only other procedure would be drawing serum for study of antibody reactions to the transplanted [cancer] cells at approximately two-week intervals during the observation period.”
• 13 C. M. Southam and A. E. Moore, “Induced Immunity to Cancer Cell Homografts in Man,” Annals of New York Academy of Sciences, vol. 73, 1958, 635.
• 14 “The tumor inoculums survived for longer periods in patients with more advanced cancer. These observations could be explained by variations in the immunological responses of the hosts.” [emphasis added] C. M. Southam, “Homotransplantation of Human Cell Lines,” Bull. N.Y. Acad. Med., vol. 34, no. 6, June 1958, pp. 416-23.

More specifically, Southam postulated that the reason the cancer patients were more susceptible to tumor growth was due to defective cellular-based immune reactions. [15] Southam also assumed that the reason healthy patients seemed to reject the repeated tumor cell implants with greater efficiency was that they had a natural mechanism for preventing cancer that he was stimulating through injections of controlled amounts of cancer—resulting in an induced immunity. Southam wrote: The growth of a repeat implant of the same cell type has been studied in normal recipients. The repeated implants formed smaller nodules and regressed more rapidly as judged by gross and microscopic examination. This accelerated rejection of a second implant is presumably the result of an induced immunity.[16]

Southam hoped that the defense mechanisms against cancer he claimed to be monitoring in these studies might be further manipulated to control cancer growth: The studies also demonstrated a correlation between the rate of rejection of homotransplanted cancer cells and the patient’s apparent ability to restrain his own disease, thus providing additional direct evidence that patients may have immunological (defense) mechanisms to restrain their own cancer. These results, of course, give hope that, through further clinical research, methods of stimulating such mechanisms to greater efficacy can be developed. [17]

The question was how to make such human cancer vaccines. One of the goals of these tumor transplant studies was to identify potential human cancer viruses in the tumor transplant cells so that these viruses could be tested as vaccines. Chester Southam summarized, “If and when a causative virus of human cancers is found, it may provide a source of antigen for cancer prophylaxis, but this is merely a hope for the future.”[18]

• 15 “The immunologic derangement responsible for the comparative slowness of rejection in patients with cancer is still unidentified, but the search is narrowing down and an impairment of cell-associated immune mechanisms now seems probable.”
• 16 Ibid.; C. M. Southam, et al.
• 17 Katz, 37.
• 18 C. M. Southam, “Studies of Host Defense Against Human Cancer,” Indian J Cancer, vol. 4, no. 1, March 1967, 3-15.

While Southam and other researchers were able to induce tumor growth in human subjects using human tumor transplants,[19] they were not able to identify human cancer viruses in these studies.[20] Researchers had considered the possibility that animal cancer viruses that had acquired the ability to jump the species barrier—like the flu virus—might be responsible for human cancer. If it were true that animal cancer viruses could cause human cancer, then existing animal cancer vaccines might be directly applicable to humans.

As a means of examining this intriguing hypothesis, researchers began to study how cancer viruses from one species could cause cancer in other species. Cancer researchers also began to join cancer viruses from various species and grow them in human cell cultures. [21] They also began to study how animal cancer viruses might cause cancer directly in humans—by injecting human subjects with the animal cancer viruses they grew in cell cultures.

In one of these tests, researchers used a procedure similar to the one that Southam and his colleagues had used in human guinea pigs. However, in addition to injecting subjects with human cancer cell growths (such as the cancer cell line known as HeLa), they also injected a monkey cancer virus known as SV40.

• 19 It was determined after much of this type of human cancer transplant experimentation had been completed, that Southam and his colleagues had conducted many of his experiments on cancer patients at Sloan-Kettering and the Jewish Chronic Disease Hospital in Brooklyn without their consent. The prestigious journal Science published a scathing review of the controversy which ensued (along with an inset of the Nuremberg Code) in which it was revealed that many of the patients involved in the cancer transplant experiments were told only that they would be involved in “skin tests” or that they were to receive “some cells.” (Some of these patients were senile and some didn’t even speak English.) As the Attorney General of the State of New York noted during an investigation into Southam’s experiments in 1964/65: “An analysis of the patients selected amply illustrates that a substantial number of them had not sufficient mental or physical ability to comprehend what was being told to them or what was being done to them; and those who may have had the capacity to understand were not given the full and true nature of the experiment.” Louis J. Lefkowitz, Attorney General of the State of New York, Petitioner’s Post-Hearing Memorandum, published in: Jay Katz, Experimentation with Human Beings, (N.Y., New York, Russel Sage Foundation, 1972), 45; E. Langer, “Human Experimentation: Cancer Studies at Sloan-Kettering Stir Public Debate on Medical Ethics,” Science, vol. 143, 551-553.
• 20 The New York Times summarized the overall situation in 1975 as follows: “[M]ore than 100 different viruses have been proved capable of causing some kind of cancers in some animal species under some circumstances. Many viruses have been suggested as possible causative factors of some cancers in man, but no such case has been proved to date.” Harold M. Schmeck Jr., “Scientists Find Virus Linked to Human Leukemia; Diagnostic Value Seen,” New York Times, January 9, 1975.
• 21 One example is particularly noteworthy. In this example a rat sarcoma virus (Kirsten sarcoma virus) adapted for human cell growth was combined with a noncancerous baboon virus (a virus known as M7). This pseudotype murine/baboon combination virus proved to have extraordinary characteristics. In addition to being capable of infecting human cell cultures, this pseudotype virus was capable of inducing tumors in a wide range of primates including dogs and monkeys. Since the virus proved so infectious, researchers thought it would readily cause cancer in man. S. S. Kalter and R. L. Heberling, “Primate Endogenous Viruses: Their Role in Oncogenesis and as Biohazards,” Joint WHO/IABS Symposium on the standardization of cell substrates for the production of virus vaccines, Geneva, December 1976. Develop. biol. Standard., vol. 37, 219-228.

In a twenty-page paper in the Journal of the National Cancer Institute, researchers published table after table of the results of their attempts to induce tumors with a monkey virus in human subjects (cancer patients) of various ages and in various disease states. They began by using separate injections of human cancer cells and animal cancer viruses in different regions of the same subject’s body. Because initially only the human cancer cell implants resulted in tumors while the SV40 implants did not, researchers began to investigate systematically the mechanism by which the monkey virus SV40 could be made to cause human tumors. Experimental parameters investigated included: the length of time the SV40 was cultured in human cells, the type of human cancer cells the SV40 cancer virus was cultured with, the length of time the recipient subject had been on immunosuppressive drugs, and the dose of cancer virus cells injected. [22] The experimentation with human subjects using the human cancer cell/monkey cancer virus cultures eventually paid off. Researchers found that by using the right mixture of human cancer cells and the SV40 virus (cultured for the proper length of time and given in sufficient quantities), the SV40 monkey cancer virus could not only reproducibly cause tumors (referred to as “nodules”) in human subjects but could also be retrieved in cells removed from induced cancer growths. [23] The authors summarized: The formation of nodules after . . . implantation of cells from simian virus 40 (SV40) transformed human tissue culture could be correlated with the stages of the transformation process, number of cells implanted, and possibly the presence of infectious virus in the implants.

While initially the researchers had more difficulty inducing human tumors with the SV40 virus than they did with just human cancer cells (such as HeLa cancer cells), eventually they found the SV40 monkey virus, when mixed and cultured properly, could produce human tumors (characterized as sarcomas) with comparable ease: Judging by the results of homologous implantation, HeLa cells and late passage, virus-free SV40-transformed cells had a comparable neoplastic potential. Histologically, nodules produced by SV40-transformed human cells were sarcomas.

• 22 The caption of Table 5 read: “Growth of nodules after homologous implantations of SV40-transformed cultures related to cell dosage and length of time spent in tissue culture after exposure to SV40.” The subheading read: “Ratios represent number of sites showing growth of nodules over number of sites inoculated.” F. Jensen, H. Koprowski, J. S. Pagano, J. Ponten, and R. G. Ravdin, “Autologous and Homologous Implantation of Human Cells Transformed In Vitro by Simian Virus 40,” Journal of the National Cancer Institute, vol. 32, no. 4, April 1964, 922-937.
• 23 In this manner researchers attempted to verify experimentally that the SV40 monkey virus fulfilled Koch’s postulates in human cancer growth. This meant that for an agent to be responsible for a disease, 1) it had to be present in all cases of the disease, 2) it had to cause the disease when intentionally placed in healthy subjects, and 3) it had to be present in the intentionally infected subject. J. Cohen, “Fulfilling Koch’s Postulates,” Nature, vol. 266, 1994, 1647.

Researchers now had a model for inducing cancer in humans using animal cancer viruses. This model allowed them to watch such cancers grow from the earliest stages under laboratory conditions. [24] They also had a model for testing vaccines for this virus, which had already been tested in animals. [25] In yet another series of experiments of this type, but published by different authors, both human cancer patients and test monkeys were injected with a monkey tumor virus known as the Yaba virus. The Yaba virus had been tested in monkeys with the following result: Intravenous inoculation of virus in the rhesus monkey produces widespread tumors in the subcutaneous tissues, skeletal muscle, lungs, and heart and occasionally results in the death of the monkey. [26]

Nevertheless, the virus was injected in human test subjects so that the induced tumors and immune system reactions to the virus could be measured—hopefully identifying an immune response that might be manipulated for use in human cancer vaccines. Following these virus injections, the researchers observed that “the humans developed lesions quite similar to those of the monkeys” and that “inoculation of virus produces only local tumors in the monkey and human.” [27]

• 24 One researcher summarized the importance of such a model in developing immunological means of fighting cancer: “We needed to know more about the earliest transforming events if we were ever to be able to make meaningful determinations of specific changes in cells which reflected their conversion to transformed and subsequently to malignant cells. This basic information about early tumor cells is essential also if we are to ever ‘unravel’ the mystery of the very complex immunologic responses which occur in the host experiencing the cancer event.” Joseph H. Coggin Jr., University of South Alabama, Annual Progress Report Contract EE-77-S-05-5601, Report Number ORO-5601-034, Period: August 1, 1978 to May 1, 1979, Project Title: Radiation and Chemical Effects on Viral Transformation and Tumor Antigen Expression.
• 25 Declassified documents from the government’s human radiation experiments reveal that researchers had developed methods for inducing “transplantation resistance” to SV40 in animals. One researcher reported, “We could reproducibly detect transplantation resistance and a significant inhibition of tumor development in animals sensitized to an intermediate level of the tumor extract and given a relatively large tumor cell challenge.” Human cells infected with SV40 were also tested as vaccines in hamsters. One report stated, “We are able to readily confirm that human cells transformed by SV40 in vitro were capable of interrupting oncogenesis in the hamsters.” Were such anticancer measures tested in humans following the development of transplantable SV40 tumors? Report titled: Induction of Transplantation Resistance with Soluble SV40 Induced Hamster TSTA, Joseph Coggin Jr., University of South Alabama College of Medicine. Declassified by the Department of Energy: Internet location: http://tis.eh.doe.gov/ohre/ (12/31/01)
• 26 J. T. Grace and E. A. Mirand, “Human Susceptibility to a Simian Tumor Virus,” Annals of the New York Academy of Sciences, v. 108, 1963, 1128.
• 27 Ibid., 1123-1128.

The depraved nature of these experiments is compounded by the fact that the researchers used human beings as walking tissue cultures for the monkey tumor virus they were studying—alternately inducing human tumors through injection of the monkey virus, removing tissue from the induced tumors, re-injecting the virus removed from the human tumors induced, and finally inducing more tumors in other human subjects with the transplanted and processed virus. The authors summarized this process: A cell-free filtrate of a monkey tumor was injected into three sites on the left forearm, and a tumor suspension into three sites on the right forearm of Patients 1, 2, and 3. Tumors developed at all sites. A single site was excised from the left forearm of Patient 2 at 17 days and from Patient 3 at 10 days. A suspension of each of these tumors was then injected into patient 5. . . . By this method, replication of the virus in the human was established. [28]

This experimentation in which animal viruses were passaged and tested in human subjects in vaccine research is reminiscent of the Nazi concentration camp studies with typhus. In these experiments “inmates of the camp were infected with typhus for the purpose of procuring a continuing supply of fresh blood taken from persons suffering from typhus.” Having a fresh supply of such contaminated blood allowed Nazi doctors to inject patients with disease-causing blood to test vaccines. Some of these vaccines, subsequently tested directly in humans deliberately infected with the pathogenic virus to be vaccinated against, were developed using mouse viruses. As described in the Nuremburg Trials: “Other inmates, some previously immunized and some not, were infected with typhus to demonstrate the efficacy of the vaccines.” [29] Active ImmunosuppressionWhile researchers developed ways of causing cancer in animals—and extended these techniques to humans, the specific immune system dysfunctions which supposedly aided cancer growth still eluded them. In addition to injecting cancer cells and viruses into subjects with naturally occurring immune system defects, there was another, more sophisticated way of determining which defects of the immune system resulted in increased cancer growth. This involved developing ways of deliberately inducing such defects so that the immune system damage could be correlated with cancer growth due to cancer transplants. Once again, if certain viruses damaged the immune system and resulted in increased cancer growth, researchers might assume that by boosting the damaged components through vaccines, cancer could be prevented. [30] The procedure for inducing controlled immunodeficiencies allowed researchers the ability to create immune system defects on demand in the laboratory and then measure the transplantability of the cancer viruses they had developed. In addition to allowing them the flexibility of not having to find animals with natural immune system defects, it also allowed them to watch cancer grow from its earliest stages under controlled conditions.

• 28 R. S. Metzgar, J. T. Grace Jr., and E. E. Sproul, “Immunological Studies of Subcutaneous Virus-Induced Histiocytomas In Primates,” Ann. N. Y. Acad. Sci., vol. 101, 192-202.
• 29 Trials of War Criminals before the Nuremberg Military Tribunals, Vol. II, (Washington, D.C.: U.S. Government Printing Office, October 1946-April 1949), 267-269. Hereafter Trials of War Criminals.
• 30 Additionally, if there were naturally occurring immunosuppressive viruses that aided cancer growth in this manner, cancer might be immediately reduced by reducing exposure to such cofactors.

This procedure essentially represented a four-step process in cancer vaccine research. The first step would be to inject test subjects with both immunosuppressive agents and cancer agents. The second step would be to determine which induced immune system deficiencies resulted in greater cancer growth. The third step would be to develop means of stimulating these immune system mechanisms. The fourth step would be to test these immune system-stimulating procedures in the presence of cancer injections as a means of evaluating their effectiveness as cancer vaccines. [31] Thus, by carefully inducing immunodeficiency, researchers might ultimately develop immunoproficiency against cancer.

By injecting animals with different immune system-damaging viruses along with different cancer viruses, researchers hoped to identify combinations of immunosuppressive and cancer viruses which might be occurring naturally to cause cancer in humans. [32] Thus, animal immunosuppressive and cancer viruses provided a laboratory model for cancer creation that allowed researchers to mimic processes that they suspected were causing cancer naturally in man.

As part of this research, immunosuppressive viruses with properties amazingly similar to AIDS [33] were created and tested extensively in mice throughout the 1960s.

In these experiments, researchers would inject mice with both sarcoma viruses and immunosuppressive leukemia viruses. [34] Once the leukemia viruses damaged the immune systems of the experimental mice, researchers measured the resulting cancer susceptibility (due to the sarcoma viruses) in the leukemia virus-impaired test subjects. [35]

• 31 This branch of research is actively and successfully pursued in animal cancer research today.
• 32 Similarly, it had been suspected that malaria created an immunosuppressive state in humans, which aided the growth of cancer allegedly caused by the Epstein-Barr virus. To test this hypothesis, researchers injected primates with combinations of a virus capable of inducing Burkitt’s lymphoma and agents capable of inducing malaria. The 1967 report of the Special Virus-Leukemia Program noted that such studies were being conducted in monkeys: “A special project in progress involves induction of malaria in the recipient prior to inoculation with Burkitt virus.” Special Virus-Leukemia Program, Progress Report #4, p. 21. See also: D. P. Burkitt, “Etiology of Burkitt’s Lymphoma–an Alternative Hypothesis to a Vectored Virus,” J. Natn. Cancer Inst. 42, 19-28 1969; Whittle, Brown, Marsh, Greenwood, Seidelin, Tighe, Wedderburn, “T-cell Control of Epstein-Barr Virus-Infected B Cells is Lost During P. Falciparum Malaria,” Nature, vol. 312, 1984, 449-450.
• 33 One of these viruses, called the Duplan virus, was created by cancer researchers in 1962 by irradiating mouse leukemia viruses. According to an article published in 1989, this virus induces “a severe immunodeficiency disease with striking similarities to human AIDS.” D. C. Aziz, Z. Hanna, and P. Jolicoeur, “Severe Immunodeficiency Disease Induced by a Defective Murine Leukaemia Virus,” Nature, vol. 338, 6 April 1988, 505-508. Other researchers who tested the nearly forty-year-old virus reported, “This crude virus stock induced a severe immunodeficiency syndrome which has been designated murine acquired immunodeficiency syndrome.” M. Huang and P. Jolicoeur, “Characterization of the gag/Fusion Protein Encoded by the Defective Duplan Retrovirus Inducing Murine Acquired Immunodeficiency Syndrome,” Journal of Virology, December 1990, 5764-5772.
• 34 For a description of an experiment of this type in mice, see M. A. Chirigos, K. Perk, W. Turner, B. Burka, and M. Gomez, “Increased Oncogenicity of the Murine Sarcoma Virus (Moloney) by Co-infection with Murine Leukemia Viruses,” Cancer Research, vol. 28, June 1968, 1055-1063.
• 35 Using methods similar to those used in experiments which were conducted with mice using combinations of leukemia and other cancer viruses, experiments were also conducted with cats from the early 1970s in which attenuated or inactivated feline leukemia viruses were used to induce immunosuppression in R. G. Olsen, E. A. Hoover, J. P. Schaller, L. E. Mathes, and L. H. Wolff, “Abrogation of Resistance to Feline Oncornavirus Disease by Immunization with Killed Feline Leukemia Virus,” Cancer Research, vol. 37, July 1977, 2082-2085.

Since immunosuppressive viruses were able to increase cancer growth dramatically in mice and cats, researchers suspected that immunosuppressive viruses were also able to increase cancer growth in humans. [36] In order to gain a better understanding of the role of immunosuppression in human cancer, researchers began to conduct international studies of humans with immunodeficiency syndromes so they could watch cancer grow from its initial stages and correlate the type of cancer growth with viruses detected and the type of immune system dysfunction observed. [37] In parallel with cancer studies of naturally occurring immunodeficiency diseases in humans, in the 1970s cancer researchers began growing immunodeficiency viruses they had created for animal studies in human cell cultures. They also combined the monkey virus they had used to induce human sarcoma tumors with these immunosuppressive viruses.

In the 1980s an epidemic of sarcoma cancer due to an animal immunosuppressive virus began to explode in human populations and alert scientists to the impending AIDS epidemic. [38] As it turns out, this cancer epidemic due to AIDS is proving to be highly combination with cancer virus injections. Following the induction of immunosuppression with the modified feline leukemia virus, experimental cats were found to be much more susceptible to cat cancer viruses.

• 36 Immunosuppressive drugs used in kidney transplants resulted in increased cancer rates in humans. This fact, combined with the fact that naturally occurring immunodeficiency diseases also resulted in higher rates of cancer in humans, caused researchers to postulate that the immunodeficiency model in animalswould provide clues to human cancer growth and prevention.
• 37 By watching cancer grow in subjects predisposed to cancer, researchers could learn more about the initial stages of cancer growth (and the factors that caused it) than conducting epidemiological studies in subjects who had already contracted cancer. By watching only those patients known to be predisposed to cancer growth due to naturally occurring immunodeficiencies, the observation time required could be drastically shortened in crucial experiments designed to monitor tumor growth from its very beginning stages. These advantages (for naturally occurring forms of immunodeficiencies) were summarized by Joseph Fraumeni in a National Cancer Institute Monograph as follows: “Future attempts at identifying etiologic agents in human leukemia and lymphoma may involve the longitudinal study of individuals over a period of time that covers the critical phase of tumor induction. Such a project would be extremely difficult to carry out, perhaps impossible, if all persons had an identical risk of developing these otherwise uncommon cancers. Epidemiologic and experimental advantages would result from the use of patients at exceptionally high risk of leukemia and lymphoma, such as those affected with certain constitutional diseases.” [emphasis added] Fraumeni also noted, “There are significant advantages to the use of constitutional disorders and other ‘high-risk’ conditions in laboratory and epidemiologic research on these neoplasms.” One of these advantages was that researchers could probe the immune responses of such patients and then correlate the exact form of their deficiencies with cancer growth. J. P. Fraumeni Jr., “Constitutional Disorders of Man Predisposing to Leukemia and Lymphoma,” National Cancer Institute Monograph 32, August 1969, 228.
• 38 Lawrence Altman wrote in the New York Times, “It was the sudden appearance of the Kaposi’s sarcoma cancer in large numbers of gay men in New York City that led doctors to recognize what is now called AIDS. Until then, Kaposi’s sarcoma had been rare, and few experts suspected that it was related to a virus.” useful to researchers seeking to develop human cancer vaccines—the group that invented and tested immunosuppressive viruses for this very reason. Lawrence K. Altman, “Surviving With AIDS Is One Problem, Cancer Is Yet Another,” New York Times, May 6, 1997.

The Benefits of AIDS

The AIDS virus has allowed cancer researchers to make major breakthroughs—providing long-awaited proof that viruses cause sarcoma in humans [39] and that such cancers can be controlled by the immune system (the so-called immunodeficiency theory of cancer susceptibility). Headlines in the New York Times have announced that long-sought human cancer viruses have finally been isolated from AIDS patients suffering from the most prominent form of AIDS-related cancer called Kaposi’s sarcoma.40 Although it is not known for sure that the virus is totally responsible for the growth of Kaposi’s sarcoma in AIDS victims, this fortuitous development is extremely encouraging to those studying the viral causes of human cancers. Lawrence Altman, writing in the New York Times, recently predicted, “Ultimately, the new findings about the Kaposi’s sarcoma virus could help unravel many unknowns about how viruses cause cancers.” This line of research, which at long last correlated a herpes virus with the growth of Kaposi’s sarcoma in human subjects, [41] encouraged another group of researchers to look for other forms of cancer that might be caused by this same virus. These researchers have recently announced another major breakthrough in viral cancer research—finding a link between this same virus and a common form of blood cancer known as multiple myeloma, the second most prevalent form of blood cancer in the U.S. [42]

• 39 Recall that researchers had been systematically searching for such human cancer viruses for over forty years. Up until the advent of the AIDS epidemic, this search had been in vain. Schmeck wrote in the New York Times in 1975: “ . . . more than 100 different viruses have been proved capable of causing some kind of cancers in some animal species under some circumstances. Many viruses have been suggested as possible causative factors of some cancers in man, but no such case has been proved to date.” Schmeck.
• 40 The source of Kaposi’s sarcoma, the leading form of cancer that develops in immunosuppressed AIDS patients, has recently been traced to a type of herpes virus. Lawrence K. Altman, “Virus Linked To a Cancer Is Identified: Malignancy Is Found In Gay AIDS Patients,” New York Times, March 1, 1996.
• 41 Cancer researchers had long theorized that human cancers could be caused by herpes viruses. One government report summarized in 1967: “The virus or group of viruses most persistently detected and isolated from human leukemia and lymphoma materials is a Herpes-type agent…. This virus appears to be an important candidate for consideration as an etiologic agent of human cancer…” In the 1970s researchers wrote numerous papers speculating on the manner in which such viruses might cause human cancer. AIDS is providing the perfect research vehicle for proving these theories. F. Rauscher and R. Reisinger, Special Virus-Leukemia Program, Progress Report #4, p. 3.
• 42 Lawrence K. Altman, “A Virus Associated With AIDS Is Linked To Appearance of a Common Blood Cancer,” New York Times, June 20, 1997.

How fortunate! As a direct result of the rare cancers that form in HIV victims, cancer researchers are gaining insight into the manner in which cancer viruses and viruses which cause immune system impairment interact to cause cancer. And they are able to do this thanks to the same type of viruses which government researchers had isolated, purified and made more virulent and infectious for this very purpose. [43] Lawrence Altman, who has been chronicling the AIDS epidemic through the New York Times, recognized the benefits of AIDS to cancer researcher at the very beginning of the epidemic. Altman predicted that the rare cancer caused by AIDS would provide insight into the causes of other types of cancer: The sudden appearance of the cancer, called Kaposi’s sarcoma, has prompted a medical investigation that experts say could have as much scientific as public health importance because of what it may teach about determining the causes of more common types of cancer. [44]

This prediction came true. Another researcher more recently summarized how AIDS-related cancers are providing valuable insight into the cause of cancer in general: “The etiology and mechanism of the specific cancers that are increased with HIV infection are proving highly informative for our general understanding of cancer etiology.” [45] As a result of this convenient new insight into the mechanisms of cancer growth, researchers are now predicting that the AIDS epidemic and the associated cancer epidemic will assist in the development of cancer prevention strategies. One author suggested, “The AIDS-malignancies have provided insights into the pathogenesis of neoplastic disease in general and into strategies for further therapeutic intervention.” [46] Other authors in the European Journal of Cancer summarized the benefits of AIDS to cancer vaccine research in the following manner: As disastrous as the spread of HIV is, the insights that the AIDS epidemic provides into the causes of cancer may ultimately lead to new and successful approaches to cancer prevention. [47]

Indeed, the AIDS epidemic appears to be perfectly suited to providing a research vehicle to the viral cancer research effort, which invented immunosuppressive viruses to determine the links between cancer, viruses, and immunodeficiency so that cancer vaccines could be created. One author wrote of the utility of AIDS-related cancers or neoplasms to cancer prevention efforts: The occurrence of these neoplasms offers an opportunity to study the role of viruses and immunodeficiency in development of these tumors. Also, the pathogenic mechanisms leading to specific malignancies can be elucidated. This information ought to guide development of strategies for prevention of virally determined cancers.[48]

• 43 Herpes-type viruses were isolated from human cancers and mass-produced to determine their ability to cause cancer as far back as 1967: “The production of herpes-type virus from a culture of the African Burkitt lymphoma has been increased at Chas. Pfizer and Co., Inc. by a substantial increase in the virus content of the culture.” Suspected cancer-causing viruses were isolated from humans and injected into various species to assess their cancer-causing potential: “Materials from human patients have already been inoculated into 600 newborn monkeys and chimpanzees of various species, and into large numbers of dogs, cats, mice, hamsters, etc.” Special Virus-Leukemia Program, Progress Report #4, pp. 12, 20.
• 44 Lawrence K. Altman, “Rare Cancer Seen in 41 Homosexuals,” New York Times, July 3, 1981.
• 45 C. Rabkin, “Epidemiology of AIDS-Related Malignancies,” Current Opinion in Oncology, vol. 6, 1994, 492-496.
• 46 A. M. Levine, “AIDS-Related Malignancies: the Emerging Epidemic,” Journal of the National Cancer Institute, vol. 85, no. 17, September 1, 1993, 1392.
• 47 V. Beral, et al.
• 48 D. T. Purtilo, “Opportunistic Cancers in Patients With Immunodeficiency Syndromes,” Arch. Pathol. Lab. Med, vol. 111, December 1987, 1129.

Altman provided a fitting summary of the situation: . . . scientists saw in the tragedy of the AIDS epidemic an extraordinary opportunity to study the interplay of viruses, an impaired immune system and the development of cancer. In a way, AIDS research was an extension of the war on cancer that the Government declared in 1971.[49]

It should be clear that the HIV epidemic is providing cancer researchers with extensive knowledge of human cancer viruses and the immune system reactions to them. This knowledge will certainly assist in the development of human cancer vaccines, but HIV itself may even be used in such vaccines if recent animal research is applicable to human cancer prevention. Recent cancer experiments with HIV in animals have shown that the virus can be used not only to cause cancer but to inhibit its growth in the form of cancer vaccines! By using components of HIV in experimental vaccines against tumors (which were induced by modified forms of HIV), researchers have reportedly dissected the role of CD4 and CD8 T-cells in tumor prevention through immunosurveillance. One group of scientists reported, “This model has allowed us to begin to dissect some of the mechanisms mediating and regulating tumor immunosurveillance.” The researchers who conducted this experiment optimistically noted that this line of experimentation with HIV “may provide a successful concerted approach to cancer immunotherapy.” [50] Whether HIV will be used directly as a cancer vaccine in humans in a similar manner remains to be seen. However, HIV may have much more far-reaching medical uses than cancer vaccines—as stunning as that achievement might be. Specifically, the use of HIV in the brave new world of genetic therapy in humans looks promising.

• 49 Lawrence K. Altman, “The Doctor’s World: AIDS Research Yields Clues Linking Viruses and Cancer,” New York Times, April 14, 1998.
• 50 S. Matsui, J. Ahlers, A. Vortmeyer, M. Terabe, T. Tsukui, D. Carbone, L. Liotta, and J. Berzofsky, “A Model for CD8+ CTL Tumor Immunosurveillance and Regulation of Tumor Escape by CD4 T Cells Through an Effect on Quality of CTL,” Journal of Immunology, vol. 163, no.1, 1 July 1999, 184-193.

Indeed, HIV has the potential to be a very useful experimental and therapeutic virus with broad biomedical applications. [51] Amazingly enough, researchers have begun using the HIV virus itself as a viral “vector” for the controversial line of medicine known as gene therapy—at least in the laboratory. By deleting certain genes in the deadly AIDS virus, researchers have been able to exploit its unique infectious properties while eliminating its harmful capacity. Andrew Pollack wrote in the New York Times: In a bold but potentially frightening effort to turn one of the world’s most virulent killers into a cure, scientists and biotechnology companies are trying to tame the AIDS virus and harness it to treat disease. The scientists say they have stripped the human immunodeficiency virus of its ability to cause disease, while leaving intact its ability to infect human cells. Such a crippled virus, they say, could be used to deliver genes in to human cells for gene therapy. [emphasis added]

As a result of laboratory tests, the subfamily of viruses to which HIV belongs is thought to be one of those most suited for the emerging technology of genetic therapy. This type of virus, the lentivirus, seems to have infectious properties which render it superior to other viruses for the insertion of genes in human DNA. This includes the DNA of nondividing cells, which pose a barrier to other types of viral vectors. Pollack noted: H.I.V., on the other hand, is both cunning at evading the body’s immune defenses and can carry large genes. Most important, it is one of a small class of viruses, known as lentiviruses, that can incorporate genes into the chromosomes even of nondividing cells. [52]

This convenient infectious property, together with its carrying capacity, makes HIV one of the more promising ones for use in human clinical gene therapy trials.

It should be clear that the cancer epidemic due to AIDS is proving fantastically beneficial to cancer researchers, but the question needs to be asked: Are these stunning developments merely due to coincidence? Altman had noted, “In a way, AIDS research was an extension of the war on cancer that the Government declared in 1971.” Is there more to Altman’s comment than meets the eye?

• 51 Cancer researchers are not the only ones who are benefiting from the medical knowledge gained in the fight against AIDS. The entire medical research community stands to reap tremendously useful knowledge from the AIDS catastrophe. Several knowledgeable authors summarized in the medical literature: “Furthermore, an unforeseen dividend for HIV research is the unraveling of the rich, intricate pathways of gene regulation utilized by the virus, which may well illuminate novel, fundamental cellular processes. The understanding of basic biology that we gain from the studies of HIV may be one major legacy of this epidemic to medical science.” [emphasis added] Y. N. Vaishnav and F. Wong-Staal, “The Biochemistry of AIDS,” Annu. Rev. Biochem,1991, vol. 60, 580.
• 52 Andrew Pollack, “Scientists Enlist H.I.V. To Fight Other Ills,” New York Times, January 19, 1999.

Could researchers have caused the AIDS/cancer epidemic using the tools they had developed in the government’s war on cancer? Did they continue in their human experiments with cancer-causing monkey viruses and escalate to the use of “active” immunosuppression with the monkey immunosuppressive viruses they developed for animal cancer experiments? In the human experiments with SV40 tumor transplants, researchers mimicked active immunosuppressive experiments that were conducted by Chester Southam in animals. In Southam’s animal experiments, he gave mice treatments that disabled their immune systems in an attempt to increase tumor growth due to cancer virus injections. [53] In the SV40 experiments with humans, patients undergoing immunosuppressive treatments for cancer were injected with the cancer-causing monkey virus SV40 to determine both whether such viruses were capable of causing human cancer and whether immunosuppression aided such cancer growth. [54] The SV40 researchers even got to use one of the same immunosuppressive treatments (an immunosuppressive chemical known as Cytoxan) in their human transplant studies [55] that Southam used in cancer transplant studies in mice. [56], [57]

• 53 Southam reported, “It seemed reasonable to test this possibility by studying quantitatively the transplantability of syngeneic tumours under conditions which suppress or enhance immunological responses.” J. Reiner and C. M. Southam, “Effect of Immunosuppression on First-Generation Isotransplantation of Chemically Induced Tumours in Mice,” Nature, vol. 210, 23 April 1966, 429-430.
• 54 Although a New York Times reporter [Altman] recently noted, “[I]t would be unethical to inject humans with a virus to prove that it can cause cancer,” as documented in this work, scientists have conducted numerous experiments using just such a procedure. Lawrence K. Altman, “A Virus Associated With AIDS.”
• 55 Some of the human patients used in the monkey virus experiment were undergoing immunosuppressive treatments with Cytoxan for their cancer: “Seventy-five percent of the patients had been given cytotoxic drugs, including cyclophosphamide (Cytoxan), 5-fluorodeoxyuridine, and 5-fluorouracil in full therapeutic doses.” Researchers were able to study the injected cancer cell growth as a function of how long it had been since the immunosuppressive treatments had been halted: “[Cancer] Cells were inoculated into patients 1 to 31 days after drug administration was terminated, except for 2 patients who received their last dose of Cytoxan on the day of implantation.” F. Jensen, et al.
• 56 Southam explained, “Such an investigation has been undertaken in this laboratory and the results obtained with cyclophosphamide (‘Cytoxan’) are sufficiently interesting and reliable to merit this preliminary report. Cyclophosphamide (‘Cytoxan’) was chosen for this study because its immunosuppressive effect had previously been demonstrated in a variety of experimental systems and because its pharmacological characteristics seem well suited to the objective.” This chemical had the advantage that it “acts very rapidly after systemic administration to initiate cytotoxic changes, including destruction of those cells responsible for immunological reactions.” Conveniently, “if administration of the drug is stopped 24 h or more before a transplant is injected, it results in a host in which immunosuppression will continue for a considerable time, but in which there is no persistence of a cytotoxic drug which might inhibit the tumor transplant.” J. Reiner and C. M. Southam, “Effect of Immunosuppression on First-Generation Isotransplantation of Chemically Induced Tumours in Mice,” Nature, vol. 210, 23 April 1966, 429-430.
• 57 Experiments similar to these were also conducted in monkeys in which immunosuppression and infection with the SV40 virus were studied to determine the cancer-causing potential of SV40. G. A. Cole and K. V. Shah, “Experimental Simian Virus 40 Infection of Normal and Immunosuppressed Spider Monkeys,” Acta virol, vol. 18, 1974, 65-69.

Since cancer researchers routinely used experimental cancer-induction procedures in humans that they developed in animals, it is natural to ask whether, in addition to immunosuppressive chemicals, researchers have also used monkey immunosuppressive viruses in conjunction with SV40 or other cancer virus transplants in humans. Curiously, monkey immunosuppressive viruses were not only available to researchers prior to AIDS but were mixed with the SV40 virus and propagated in human cell cultures! While the public is completely ignorant of this fact, simian immunosuppressive viruses(SIVs) such as the Mason Pfizer Monkey Virus (MPMV)—one of three types of SIV58—were available to researchers as early as 1970 when the virus was grown in cell cultures.59 Well before AIDS, MPMV was shown to induce immunodeficiency states in monkeys in the early 1970s [60][61] as well as the 1980s. [62] In one of these early experiments, MPMV was mixed with SV40—the monkey cancer virus (which had already been injected in humans to cause cancer)—and the Rous

• 58 MPMV is one of “three independent virus isolates” of “simian acquired immunodeficiency syndrome (SAIDS) in macaque monkeys.” One group of researchers reported, “When inoculated into young monkeys, MPMV produced a spectrum of nononcogenic disease associated with an immunodeficiency condition.” R. M. Thayer, M. D. Power, M. L. Bryant, M. B. Gardner, P. J. Barr, and P. A. Luciw, “Sequence relationships of type D retroviruses which cause simian acquired immunodeficiency syndrome,” Virology, 1987 April 157(2), 317-329.
• 59 This immunosuppressive virus was isolated from a mammary tumor of a rhesus monkey in 1970. H. C. Chopra and M. M. Mason, “A New Virus in a Spontaneous Mammary Tumor of a Rhesus Monkey,” Cancer Research, vol. 30, no. 8, August 1970, 2081-2086.
• 60 The virus not only had immunosuppressive properties, it was reported to act like a slow virus—just like HIV. D. L. Fine, J. Landon, R. Pienta, M. Kubicek, M. Valerio, W. Loeb, and H. Chopra, “Responses of Infant Rhesus Monkeys to Inoculation With Mason-Pfizer Monkey Virus Materials,” Journal of the National Cancer Institute, vol. 54 no. 3, March 1975, 651-658.
• 61 In 1986 one group of researchers described how immunodeficiency states were induced in monkeys in the early 1970s using MPMV. Since the virus did not immediately induce cancer and since AIDS hadn’t started in human populations, the effects of the virus (immunosuppression and fatal infection by opportunistic diseases) at that time did not attract widespread notice. The researchers reported in one paper, “However the results were disappointing at that time because tumors were not induced by inoculation of MPMV into newborn rhesus monkeys and other nonhuman primates. Instead, many of the inoculated neonatal animals developed persistent lymphadenopathy, thymic atrophy, and weight loss and eventually died of undue susceptibility to facultative organisms. Because of the absence of transmissible tumor and the lack of occurrence at that time of human AIDS, this nononcogenic but immunosuppressive result attracted little scientific attention.” M. L. Bryant, M. B. Gardner, P. A. Marx, D. H. Maul, N. W. Lerche, K. G. Osborn, L. J. Lowenstine, A. Bodgen, L. O. Arthur, and E. Hunter, “Immunodeficiency in rhesus monkeys associated with the original Mason-Pfizer monkey virus,” J. Natl. Cancer Inst., 77(4), October 1986, 957-965.
• 62 Cryogenically preserved samples of this virus, isolated in the 1970s, were shown to induce a disease (simian acquired immune deficiency syndrome, SAIDS) very much like that due to simian immunodeficiency viruses (SIVs). The researchers who published the experiment in 1986 stated, “MPMV produces an acquired immunodeficiency similar to that caused by the recently described simian acquired immune deficiency syndrome type D retroviruses.” Ibid.

sarcoma virus in human cell cultures.63 Researchers also mixed the immunosuppressive virus with simian sarcoma virus.64 Is it not curious that cancer researchers were mixing immunosuppressive monkey viruses with sarcomas and coaxing them to grow in human cells in the late 1970s—just before HIV broke out in human populations and caused an epidemic of immunosuppression and sarcoma? Could this epidemic have been an extension of the human tumor transplant experiments with SV40, using the technology perfected over decades of research with animal immunodeficiency viruses? If researchers were going to use animal immunosuppressive viruses to conduct such experiments in man, how might they have been conducted? It would make sense for researchers to use vehicles that would allow them not only to inject subjects with viruses but to conduct follow-up studies to see how the immunosuppressive and cancer viruses resulted in immune system destruction [65] and cancer growth. Vaccine programs meet these criteria and are the perfect vehicles for implementing such experiments.

• 63 H. Ogura, T. Tanaka, M. Ocho, T. Kuwata, and T. Oda, “Detection of Mason-Pfizer monkey virus infection by syncytia formation of human cells doubly transformed by Rous sarcoma virus and simian virus 40,” Arch Virol, 57(2), 1978, 195-198.
• 64 H. Ogura, “Interactions Among Retroviruses Mason-Pfizer Monkey, Baboon Endogenous, Simian Sarcoma Virus-Associated and Murine Leukemia Detected by Virus-Mediated Cell Fusion Inhibition Assay,” Microbiol. Immunol., vol. 24, no. 8, 1980, 761-763.
• 65 Such research would not be unprecedented. A long-running program exploiting unsuspecting black men naturally infected with syphilis was supervised by the government for decades. This program, known as the Tuskegee study, was conducted “to see how the syphilis germ destroys the body. In the late stages, the germ can cause paralysis, gradual blindness and dementia.” Sanjay Bhatt, “The anthrax vaccine: Government’s shot in the dark,” Palm Beach Post, December 30, 2001. In this case, natural cases of syphilis were deliberately left untreated so victims of the disease could be monitored for medical research purposes. A government report summarized the experiment: “By the mid-1940s it was becoming clear that the death rate for the infected men in the study was twice as high as for those in the control group. The study was reviewed by PHS officials and medical societies and reported by a number of journals from the early 1930s to 1970. In the 1960s a growing number of criticisms began to appear, although the study was not stopped until 1973. Thus, men with a confirmed disease were not told of their diagnosis and were deceived into participating in the study under the guise of its being therapeutic for unspecified maladies. In addition to exposing the subjects to the additional harms of participation in the study, the false belief that treatment was being administered prevented subjects from otherwise seeking medical care for their disease. Over this forty-year history, at least 28 participants died and approximately 100 more suffered blindness and insanity from untreated syphilis before the study was stopped.” Advisory Committee on Human Radiation Experiments - Final Report, Chapter 3, Section: “The Development of Human Subject Research Policy at DHEW,” http://tis.eh.doe.gov/ohre/roadmap/achre/chap3_2.html (12/31/01)

Prior to AIDS, the world’s medical elite was well aware of the usefulness of immunosuppressive viruses to cancer research: World Health Organization (WHO) representatives had made statements expressing their desire that the organization get involved in research with immunosuppressive viruses capable of selectively targeting T-cells. [66] (Researchers associated with WHO were optimistic that the immunosuppressive research conducted in animals could be usefully extended to human beings.[67]) Members of WHO had also recommended that experimental agents be placed in vaccines as a vehicle for measuring the human immune response on a global scale68(as a means of separating genetic from environmental determinants of immune system function). A report by a WHO study group had also recommended an international study of naturally immunosuppressed humans with immunological deficiency syndromes for cancer research purposes (this was prior to the emergence of the international Acquired Immunodeficiency Syndrome epidemic)![69] Did WHO achieve all of these goals simultaneously by placing immunosuppressive agents in some of its vaccines, thereby creating a highly useful international epidemic of acquired immunodeficiency syndromes and cancer resulting from selective T-cell depletion? The possibility that increased cancer rates due to infectious agents present in vaccines would be useful for cancer vaccine research was evident in the 1967 report of the Special Virus-Leukemia Program. Projects were initiated to correlate cancer deaths of children and veterans with vaccines they may have received (as compared to “matched control groups”). One project recommended that a massive database be constructed and maintained by obtaining “death certificates for all U.S. children under 15 years of age who have died of cancer, 1960-1964” so that cancer deaths could correlated with names “of children believed to be at unusual risk of cancer; e.g., those given certain vaccines in the past.” Were similar databases created for vaccine recipients who were deliberately predisposed to cancer through vaccines? [70]

• 66 The following chilling recommendation for future research was made in a World Health Organization publication from 1972: “An attempt should be made to ascertain whether viruses can in fact exert selective effects on immune function . . . or by affecting T cell function as opposed to B cell function. The possibility should also be looked into that the immune response to the virus may itself be impaired if the infecting virus damages more or less selectively the cells responding to the viral antigens.” [emphasis added] This is exactly what HIV does. A. Allison, W. Beveridge, W. Cockburn, J. East, H. Goodman, H. Koprowski, P. Lambert, J. Van Loghem, P. Miescher, C. Mimms, A. Notkins, and G. Torrigiani, “Virus-Associated Immunopathology: Animal Models and Implications For Human Disease,” Bulletin of the World Health Organization, vol. 47, no. 2, 1972, 259.
• 67 “Recent studies on virus-induced immunopathological reactions in domestic and experimental animals have led to the development of concepts and technical methods that may be useful in investigating certain viral diseases in man, including hepatitis.” [emphasis added] Ibid., 258.
• 68 “In relation to the immune response, a number of useful experimental approaches can be visualized. One would be a study of the relationship of HL-A type to the immune response, both humoral and cellular, to well-defined bacterial and viral antigens during preventive vaccination.” [emphasis added] Federation Proceedings, vol. 31, no. 3, May-June 1972, 1102.
• 69 The pre-AIDS WHO report recommended that an “international co-operative study of patients with immunological deficiency syndromes should be carried out.” It also suggested that “[o]bservations on patients with immunological deficiency diseases should be as complete as possible, and it is desirable that they should enable valid comparisons to be made between patients studied in different institutions.” [emphasis added] A. C. Allison, B. A. Askonas, B. Benacerraf, R. Ceppellini, R. A. Good, E. S. Lennox, H. O. McDevitt, R. S. Nezlin, and M. Seligmann, “Genetics of the Immune Response,” World Health Organization Technical Report Series, no. 402, 34, 52.
• 70 Special Virus-Leukemia Program, Progress Report #4, Program Staff, National Cancer Institute, Etiology Area, May 1967, pp. 29, 31.

Unfortunately, there is evidence to support the radical hypothesis that humanitarian vaccine programs were used to conduct inhumane cancer experiments. Promiscuous homosexuals were selectively targeted with an experimental vaccine against hepatitis B beginning in the late 1970s.[71] And the AIDS epidemic in promiscuous homosexuals began almost immediately after the first of these vaccine experiments.[72] It has been documented that recipients of this experimental hepatitis vaccine have been disproportionately afflicted with AIDS [73] and that immunosuppressed homosexuals are being targeted with numerous follow-up studies to monitor how cancer develops in immunosuppressed victims versus healthy populations.[74] Interestingly enough, the suspect experimental hepatitis B vaccine given to homosexuals just prior to the AIDS epidemic appears to have been a subset of a proposed global cancer vaccine experiment administered by the World Health Organization.[75] It was thought that hepatitis B was the cause of a form of cancer called hepatocellular carcinoma and that by immunizing people against hepatitis, immunity to this form of cancer might be obtained.[76] Hepatitis B vaccination trials were conducted as a means of developing vaccines for use in these international hepatitis/cancer vaccine trials. [77] (Hepatitis was also mentioned in WHO publications discussing the experimental merits of extending animal immunosuppressive techniques to human research.)

• 71 W. Szmuness, C. E. Stevens, E. J. Harley, E. A. Zang, W. R. Oleszko, D. C. William, R. Sadovsky, J. M. Morrison, and A. Kellner, “Hepatitis B Vaccine: Demonstration of Efficacy in a Controlled Clinical Trial in a High-Risk Population in the United States,” The New England Journal of Medicine, vol. 303, no. 15, 9 October 1980, 834.
• 72 G. J. P. Van Griensven, N. A. Hessol, B. A. Koblin, R. H. Byers, P. M. O’Malley, N. Albrecht-van Lent, S. P. Buchbinder, P. E. Taylor, C. E. Stevens, and R. A. Coutinho, “Epidemiology of Human Immunodeficiency Virus Type 1 Infection among Homosexual Men Participating in Hepatitis B Vaccine Trials in Amsterdam, New York City, and San Francisco, 1978-1990,” American Journal of Epidemiology, vol. 137, no. 8, 913.
• 73 Studies show that forty percent of the recipients of some of these vaccine trials developed AIDS. (Half of the volunteers participating in these trials were given a placebo.) Ibid.; C. E. Stevens, P. E. Taylor, E. A. Zang, J. M. Morrison, E. J. Harley, S. Rodriguez de Cordoba, C. Bacino, R. C. Y. Ting, A. J. Bodner, M. G. Sarngadharan, R. C. Gallo, and P. Rubinstein, “Human T-Cell Lymphotropic Virus Type III Infection ina Cohort of Homosexual Men in New York City,” JAMA, April 25, 1986, vol. 255, no. 16, 2167-2172.
• 74 D. W. Lyter, J. Bryant, R. Thackeray, C. R. Rinaldo, L. A. Kingsley, “Incidence of Human Immunodeficiency Virus-Related and Nonrelated Malignancies in a Large Cohort of Homosexual Men,” J. Clin. Oncol., October 1995, vol. 13, no. 10, 2540-2546; C. R. Rinaldo, L. A. Kingsley, D. W. Lyter, B. S. Rabin, R. W. Atchison, A. J. Bodner, S. H. Weiss, and W. C. Saxinger, “Association of HTLV-III with Epstein Barr Virus Infection and Abnormalities of T Lymphocytes in Homosexual Men,” Journal of Infectious Diseases, vol. 154, no. 4, October 1986, 556-561.
• 75 The hepatitis vaccine developed in these trials has been referred to by some observers as the first human cancer vaccine.
• 76 Researchers affiliated with the WHO noted in one publication, “The Meeting considered that there were good grounds to suppose that vaccination of children with hepatitis B vaccine at birth, or shortly thereafter, would confer long-term protection against the development of hepatocellular carcinoma.” “Prevention of Liver Cancer,” World Health Organization Technical Report Series 691 (Geneva: World Health Organization, 1983), 27.
• 77 These cancer vaccine trials have been declared a success. One paper reported, “Universal childhood vaccination against hepatitis B in Taiwan appears to have reduced the incidence of hepatocellular carcinoma.” Mei-Hwei Chang, Chien-Jen Chen, Mei- Shu Lai, Hsu-Mei Hsu, Tzee-Chung Wu, Man-Shan Kong, Der-Cherng Liang, Wen-Yi Shau, and Ding-Shinn Chen, “Universal hepatitis B vaccination in Taiwan and the incidence of hepatocellular carcinoma in children.” The New England Journal of Medicine, 26 June 1997, vol. 336, no. 26, 1855.

Given the admitted experimental nature of this cancer vaccine effort employing hepatitis vaccines, and, given the useful immunosuppression subsequently associated with one branch of it, it seems logical to ask: Was this direct attempt at cancer vaccination using the hepatitis B vaccine augmented through the addition of immunosuppressive viruses, as was done in experimental animal populations? [78] In other words, was there a covert cancer vaccine experiment within the overt cancer vaccine experiment associated with the hepatitis B program? Could this explain why immunosuppression in homosexual populations is proving so beneficial to cancer research? Such a procedure would represent the replication in human populations of a published experiment conducted in cats in which kittens were injected with a “vaccine” containing a mixture of immunosuppressive viruses and cancer agents. Four-week-old specific-pathogen-free cats were immunized with a combined vaccine composed of killed feline leukemia virus and killed feline oncornavirus-associated cell membrane antigen-containing tumor cells.

The authors further explained that the immunosuppressive leukemia virus present in the vaccine increased susceptibility to the oncornavirus cancer agents: “Thus, it appears that the protective immunity to feline oncornavirus disease was hindered rather than enhanced by inclusion of inactivated, purified FeLV as a vaccine component.”[79] The Source of the International AIDS EpidemicIn addition to the AIDS outbreak in American homosexuals, there is evidence supporting the theory that the international HIV epidemic is also the result of a premeditated international “cancer vaccine” experiment implemented using existing vaccine programs associated with the World Health Organization.

While gay recipients of the hepatitis B/cancer vaccination program have been disproportionately stricken by the AIDS virus, according to a front page article in The Times of London, it is a segment of the recipients of the international smallpox vaccination administered by the WHO which have been disproportionately afflicted with AIDS in the developing world. Pearce Wright summarized in the Times: The World Health Organization, which masterminded the 13 year campaign, is studying new scientific evidence suggesting that immunization with the smallpox vaccine Vaccinia awakened the unsuspected, dormant human immuno defence virus infection (HIV).[80]

• 78 This process might allow long-term immunocompetence (through vaccine development) to be attained through short-term immunocompromise induced in a group of unfortunate human test subjects.
• 79 R. G. Olsen, et al.
• 80 Pearce Wright, “Smallpox vaccine ‘triggered Aids virus,’” The Times of London, Monday, May 11, 1987.

The Times elaborated, “The smallpox vaccine theory would account for the position of each of the seven Central African states which top the league table of most affected countries; why Brazil became the most afflicted Latin American country; and how Haiti became the route for the spread of Aids to the U.S.” ConclusionAIDS is providing a fantastic laboratory model on a large-scale—essentially duplicating research efforts conducted earlier on a smaller-scale to prove the immunodeficiency and virus model of cancer growth. For example, AIDS is providing answers that studies of immunosuppressed transplant patients and children with naturally occurring immune deficiency syndromes sought with respect to the viral nature of cancer and the breakdown of the immunological surveillance mechanism.[81] Indeed, the AIDS epidemic is providing a near ideal research vehicle for proving theories about cancer causation that were popular shortly before the epidemic broke out. In 1972 the Proceedings of the National Academy of Sciences published numerous articles speculating not only on the relationship between immunodeficiency [82] and viruses [83] in cancer formation, but specifically on the relationship between herpes viruses and cancers. [84] AIDS has made international headlines apparently showing that immunodeficiencies can be a major contributor to cancer due to viruses and that one of the main forms of cancer due to such immunodeficiencies—Kaposi’s sarcoma—is due to a herpes virus.

Thus, in addition to providing evidence that the “breakdown of the immunological surveillance mechanism” can lead to cancer, AIDS is helping to identify the specific viruses involved in the resultant conversion to cancer. Consequently, the damage inflicted by HIV on the immunological surveillance mechanism will be useful in the development of cancer vaccines and, as is evident in animal experiments, the deadly AIDS virus itself may even be used in experimental human cancer vaccines.

• 81 One author summarized the situation in 1969: “Although further analyses are obviously required, the results suggest that children with immune deficiency syndromes or adults treated with immunosuppressives have a greatly increased risk of developing tumours, especially of the lymphoreticular system. Presumably this represents breakdown of the immunological surveillance mechanism, allowing proliferation of tumour cells that would otherwise be restrained by an immune response. Whether one or more viruses are involved cannot be stated on existing evidence.” A. C. Allison, “Immune Responses to Virus-Induced Tumours,”Proc. Roy. Soc. Med, vol. 62, September 1969, 956-958.
• 82 R. A. Good, “Relations Between Immunity and Malignancy.”
• 83 H. Temin, “The RNA Tumor Viruses—Background and Foreground, Proc. Nat. Acad. Sci. USA, vol. 69, no. 4, April 1972, 1016-1020.
• 84 G. Klein, “Herpes viruses and Oncogenesis,” Proc. Nat. Acad. Sci. USA, vol. 69, no. 4, April 1972, 1056-1064.

In summary, it seems improbable that, by sheer chance, an unprecedented epidemic infection due to a type of virus invented by cancer researchers began benefiting cancer researchers almost immediately after they grew it in human cell cultures.

Given the immense benefits of the disease in combination with the history of human experimentation with cancer-causing viruses by the cancer research establishment, it seems more likely that AIDS is the result of human experimentation and not accident. This type of human experimentation would be directly in line with the type of cancer research perfected over decades of animal experiments with immunosuppressive viruses. It would also represent the culmination of a long series of experiments in humans in which immunosuppression was exploited as a mechanism to induce cancer by various means (including monkey sarcoma viruses) in the search for cancer vaccines. While this conclusion may seem extreme, the open medical literature contains many surprises that run contrary to what a blind faith in the medical research establishment would foster. One can only wonder what surprises the classified records of the CIA (which had an entire wing of a hospital to experiment in as part of its MKULTRA program [85]) and the National Cancer Institute hold. It is hoped that this brief study will provide insight into what areas should be further investigated. A more detailed study, titled AIDS: THE “PERFECT” DISEASE, which examines not only the cancer research benefits of AIDS described above, but also the benefits to the national security establishment, is available at http://www.authorhouse.com/BookStore/.

In this study, disturbing links between the national cancer research establishment and the biowarfare establishment are revealed as is the manner in which AIDS is helping to fulfill long-standing national security goals related to international population control in addition to fulfilling the goals of the cancer vaccine research establishment. Additionally, the sordid history of previously secret national and international testing programs of the U.S. government is reviewed. The proposed cancer experiment to explain the AIDS epidemic is placed within the context of this backdrop of unethical human experimentation under humanitarian pretexts. These unconscionable testing programs serve as a warning to those who would doubt that an experiment of the size and scope of that proposed to explain the AIDS epidemic could and would be carried out by the U.S. government under the auspices of cancer research.

• 85 “In another MKULTRA project, CIA secretly provided funding for the construction of a wing of Georgetown University Hospital in the 1950s so that it would have a locale to carry out clinicaltesting of its biological and chemical programs.” Advisory Committee on Human Radiation Experiments,Appendix E: http://www.gwu.edu/~nsarchiv/radiation/dir/mstreet/interim/intret.txt (12/31/01)

Can you give someone cancer?

In December 2011, following his diagnosis of cancer, Venezuelan president Hugo Chavez speculated that American agents had induced the disease in him and possibly other South American leaders by injecting them with cancer cells. Despite the State Department’s rejecting Chavez’s claims, there nonetheless was no shortage of CIA conspiracy theorists who accepted the charge. The media too grabbed onto the story, not only because of the outlandish nature of the accusation but also because of the underlying question it raised: Can you give someone cancer? (Miami New Times, March 7, 2013; Slate, December 30, 2011).

While direct communication of cancer from one host to another has been documented, and transplanting cancer cells to another person in an effort to cause cancer is possible, it is extremely rare. It has been shown in organ transplant recipients, mother-to-fetal transmission, and a few rare events such as one reported in 2015 in the New England Journal of Medicine where cancer cells from a tapeworm invaded a man’s body, spreading to his lymph nodes and his lungs. While ordinarily, the immune system would not allow this, in this case the man was severely immunosuppressed due to HIV/AIDS (Muehlenbachs et al. 2015). Other reported cases include transmission to a lab worker via a needle stick or a cut on the hand and one where a surgeon’s laceration developed into a sarcoma. In these cases, however, while the cancer cells grew locally at the point of entry, they failed to progress beyond the site of entry (Welsh, 2011). It is well established that in normally functioning immune systems such cells (including cancer cells from another person) would be recognized as foreign and destroyed before they have a chance to wreak havoc (Janeway 1993). The reason we know this today is because decades ago researchers attempted to do just such a thing: injecting prison inmates and chronically ill hospitalized patients with live cancer cells. These experiments, carried out with little or no informed consent, took place in New York City, at one of the leading cancer research centers in the United States, despite the safeguards of the American healthcare and research ethics systems. While the scandal garnered headlines at the time (e.g., New York Times, January 26, 1964),it has since been largely forgotten, as have the people who unknowingly placed their bodies on the line to advance scientific knowledge, and it is a story that deserves retelling.

A brief history of ethics in medical research

While the Nuremberg Code of 1947 is generally regarded as the first document to set out ethical regulations for human experimentation based on informed consent, rules to protect the welfare of people subjected to medical experimentation were in fact in place long before this including in Germany. The first detailed regulation of non- therapeutic research in Wester medicine came from the Prussian minister for religious, educational, and medical affairs in 1900, following the public outcry at the work of Albert Neisser, the discoverer of the gonococcus (Vollmann and Winau, 1996).

In 1898, Neisser, who was attempting to develop a syphilis vaccine, published a study that outlined his results as well as his methods and study participants. Public debate in the press as well as among academicians ensued: Neisser had injected serum from patients with syphilis into patients who were admitted to hospital for other medical conditions, none of whom had suffered from syphilis at the time of the experiment. The controversy rested on two issues: the first was that most (but not all) of these patients were prostitutes, while the second was that none of them had been informed about the experiment or asked for their consent. After four of the prostitutes subsequently developed syphilis, it raised the issue of whether or not it was the injected cells that had in fact caused their illness, or as Neisser insisted, they had contracted it separately by pursuing their occupation (Toellner, 1981).

The majority of physicians aware of the case supported Neisser; the single exception was Albert Moll, a Berlin psychiatrist and highly regarded sexologist (Maehle 2012). While largely unrecognized in the medical literature, Moll is largely responsible for the formulation and elaboration of a theoretical conception of the contractual nature of the patient–doctor relationship and the development of informed consent, saying,

• “I have observed with increasing surprise that some medics, obsessed by a kind of research mania, have ignored the areas of law and morality in a most problematic manner. For them, the freedom of research goes so far that it destroys any consideration for others. The borderline between human beings and animals is blurred for them. The unfortunate sick person who has entrusted herself to their treatment is shamefully betrayed by them, her trust is betrayed, and the human being is degraded to a guinea pig….” (Maehle 2009) Moll would go on to author one of the most comprehensive books on the subject of medical ethics, Arztliche Ethik (Medical Ethics) (Katz, 1997).

Following increasing pressure from Moll as well as the press, the Neisser case came under investigation by the public prosecutor and the Royal Disciplinary Court. The court found that although Neisser was a well-known medical authority and may have been convinced that the trials were harmless, he should have sought the patients’ consent; he was fined, and was lucky not to receive a more stringent punishment, because two years later, upon further investigation into the case, government lawyers stated that conducting non-therapeutic research on a subject without consent fulfilled the criteria for causing physical injury (battery) in criminal law (Vollmann and Winau, 1996).

Additional action was taken by the Prussian Landtag (parliament), which commissioned a detailed report from the Scientific Medical Office of Health, which was composed of leading German physicians, including Rudolf Virchow. The commission stated that a physician who recognized that injected serum might cause infection had no right to inject such a serum, but that in any case both informing the subject and obtaining the subject’s consent were preconditions to experimentation. Informed consent became a mandatory precondition for any non-therapeutic research. Written documentation and clear responsibility of an institution’s medical director for all human experimentation became legal doctrine, and all hospitals, clinics and medical directors were advised that any medical interventions other than for diagnosis, healing, and immunization were excluded under all circumstances if “the human subject was a minor or not competent for other reasons” or if the subject had not given “unambiguous consent” after a “proper explanation of the possible negative consequences of the intervention (Goss, 2017). Others took the somewhat extreme position that purely scientific experimentation on human subjects was unethical even if they gave voluntary consent and that self-experimentation should always precede experiments on patients, noting that the scientific validity of the experiment did not serve to mitigate these conditions (Vollmann and Winau, 1996).

Ironically, the other main early attempt to protect a human research subject’s autonomy would occur in Hitler’s Germany. In the German Reich’s Rundschreiben (Reich’s Circular) of 1931 the Reich government issued detailed guidelines that clearly distinguished between therapeutic (“new therapy”) and nontherapeutic (“human experimentation”) research and set out strict precautions for each. The rules for new therapy were explicit: “New therapy may be applied only if consent or proxy consent has been given in a clear and undebatable manner following appropriate information. New therapy may be introduced without consent only if it is urgently required and cannot be postponed because of the need to save life or prevent severe damage to health….” When it came to non-therapeutic research there was no wiggle room; the law clearly stated that “under no circumstances [is it] permissible without consent” (Sass, 1983).

While it’s thus clear that the basic concept of informed consent was developed long before the Second World War and these guidelines remained in place throughout the reign of Adolf Hitler, they failed to stop the unethical experiments taking place in Nazi concentration camps (Caplan, 1991). It would be these experiments and the subsequent postwar trials of the physicians involved in them that would lead to the creation of the Nuremberg Code, a document among whose 10 principles the longest is on informed consent (Kumar 2013).

Informed consent

While it is widely believed that the Nuremberg Code has legal standing, in fact this document has no legal force behind it (Ghooi, 2011). In the US, legal informed consent owes its genesis to two landmark legal cases. Schloendorff vs. The Society of New York Hospital (1914) established the principle of patient consent and is considered one of the landmark legal cases in bioethics, while Salgo v. Leland Stanford etc. Bd. Trustees is responsible for adding ‘informed’ to the notion of ‘consent.’ A brief review of the Schloendorff case follows.

Mary E. Schloendorff agreed to have her physician examine her under anesthesia and to have her fibroid tumor biopsied. Prior to the procedure, Schloendorff specified that she was not consenting to the removal of the tumor; nonetheless, while she was anesthetized, the surgeon, believing the mass was malignant, removed the tumor. Schloendorff then sued the hospital. the course made its way to the New York Court of Appeals, which found that the operation to which the plaintiff did not consent constituted medical battery. Justice Benjamin Cardozo wrote that in the court’s opinion:

• “Every human being of adult years and sound mind has a right to determine what shall be done with his own body; and a surgeon who performs an operation without his patient’s consent commits an assault for which he is liable in damages. This is true except in cases of emergency where the patient is unconscious and where it is necessary to operate before consent can be obtained.”

Schloendorff, however, received no monetary gain, since she had sued the hospital and not the surgeons; the court found that a non-profit hospital could not be held liable for the actions of its employees due to the legal principle of charitable immunity. Justice Cardozo’s opinion is widely cited as the basis for the requirement to seek consent from patients before medical intervention is provided, upholding a patient’s right to autonomous decision-making (Deverette, 1995).

The second case, the Salgo decision, marks the birth of the doctrine of informed consent as it is known today; the term “informed consent” was first used in this case. In 1957, Martin Salgo, age 55, consented to undergo a diagnostic procedure to locate the source of chronic pain in his leg; it was believed he was suffering from arteriosclerosis and that his aorta was also involved. He was advised to undergo diagnostic aortography. While under anesthesia, his aorta was injected with a contrast medium, and images were taken of the abdominal aorta. The next morning Salgo awoke to find that his lower limbs were paralyzed as a result of the contrast agent used in the procedure. Salgo subsequently sued his doctor, claiming that he was not informed about paralysis being a risk or possible complication of the contrast material. The court noted that a physician violates his duty to the patient if he withholds any facts necessary to form the basis of an intelligent consent by the patient to the proposed treatment. The court also noted that when discussing risk, the physician has discretion “consistent with the full disclosure of facts necessary to an informed consent.” Salgo’s doctor’s defense argued that if patients were informed of all the possible complications, they would become frightened and would not consent to treatment. The court rejected this defense and ruled that simple consent was not sufficient for medical procedures; instead, sufficient disclosure of possible risks and complications, allowing “informed consent,” was necessary for patients to make autonomous decisions, whether regarding a surgical procedure or a medical experiment (Osman, 2001).

While lacking legal standing, the Nuremberg Code did form an outline of what are now considered a physician’s ethical duties, which were codified in a subsequent document created in 1964 in Helsinki, known as the Declaration of Helsinki, which addressed clinical research and humane treatment of study participants as well as issues such as informed consent. Like its predecessor, the Declaration of Helsinki has no legal standing or power (Shuster, 1997), but together they serve as models for regulators in most countries and inform the current US federal research regulations, which require not only the informed consent of the research subject (with proxy consent sometimes acceptable, such as for young children) but also prior peer review of research protocols by a committee (the institutional review board) (NIH Office for Protection from Research Risks 1991). With such protections in place, one might assume that US citizens were protected against unethical or life-threatening medical experimentation; unfortunately, as we will see, this was not the case.

Unclean hands

In jurisprudence, there is a doctrine known as “unclean hands”—if a defendant can prove that a plaintiff has “unclean hands,” that is, has acted unethically, then the plaintiff’s complaint will be dismissed (Upcounsel.com n.d.). During the doctors trial in Nuremberg, defense attorneys argued that this doctrine applied, stating that the German experiments were essentially equivalent to those that had been and were still being performed in US penitentiaries (Weindling, 2001). This statement had more than a kernel of truth to it. While there had been relatively little medical research into human disease in the US during the 1930s, this would change dramatically in the 1940s, when for the first time there would be US government funding for such research (Baader et al. ,2005).

With the outbreak of WWII and the potential for American involvement in the conflict, there was a push for governmental involvement in and funding of academic research. In 1941, President Franklin D. Roosevelt authorized the establishment of the Office of Scientific Research and Development (OSRD). From 1941 through 1945, the OSRD’s Committee on Medical Research would be responsible for developing and funding projects involving both human and animal subjects that studied, among other things, disease transmission and vaccine development. Susan Lederer, a professor of medical history and bioethics, notes that the human subjects involved in these studies were primarily “subjects of convenience”—individuals or populations conveniently and readily available to researchers, who included children in orphanages, patients in mental institutions, military personnel, and those incarcerated in penal institutions (Lederer 1995). This was an era in medicine when no one thought it necessary to ask permission to remove tissue samples from a patient or to ask permission to use such samples in medical experiments (Javitt, 2010). One such patient was an African-American women who, following delivery of her fifth child by age 30, developed intense vaginal bleeding and sought care at the Johns Hopkins Hospital, which, although segregated, was the only hospital in her hometown of Baltimore that would treat African-American patients. Hopkins was a charity hospital, as its benefactor Johns Hopkins, founder of the university and hospital, stipulated in his will (Johns Hopkins Medicine n.d.). Although the woman would expire on October 4, 1951, from what would be diagnosed as cervical cancer, she would nevertheless become immortal.

Henrietta and her HeLa cells

On October 4, 1951, Johns Hopkins–trained physician and director of the Tissue Culture Laboratory in the Hopkins Department of Surgery George Otto Gey appeared on national television to announce that a major breakthrough had occurred in cancer research (Skloot, 2000, Hanks and Bang, 1971). Gey had spent the majority of his career attempting to develop a method to grow cells outside the body. The problem was that cells cultured for laboratory studies survived for only a few days at most; but if he were able to keep cells alive “in culture,” this would allow researchers to experiment on the cells in ways not possible in the body, thus increasing their knowledge of cell biology, especially that of cancer cells, and thus potentially leading to a cure (Gold, 1986:16).

For Gey to accomplish his goal, he would require a constant supply of cancerous tissue samples. Luckily for him, he had a readily available supply at the major medical institution where he worked; however, these sample were obtained without the patient’s or their family’s knowledge or permission (Lucey et al., 2009). One such sample would come from the 31-year-old African American women, Henrietta Lacks, who had died earlier on the day of Gay’s televised announcement.

Gey had earlier observed that Lacks’s cells were the first he had come across that could be divided multiple times without dying, and so on the day of her death, Gey had had Mary Kubicek, his lab assistant, take additional tissue samples while Lacks’s body lay in the Johns Hopkins morgue (Gold, 1986:19–22). Gey was able to start a cell line from Lacks’ sample by isolating one specific cell and repeatedly dividing it, meaning that the same cell could then be used to conduct many experiments. They became known as HeLa cells, because Gey’s standard method for labeling samples was to use the first two letters of the patient’s first and last names (Gold, 1986:18). These HeLa cells were in high demand by other researchers and were put into mass production. They were mailed to scientists around the globe, and the cell line would be used to make many important breakthroughs in biomedical research. For example, by 1954, Jonas Salk was using HeLa cells in his research to develop the polio vaccine; the cells used in the vaccine were mass-produced in the first- ever cell production factory at the Tuskegee Institute, in Tuskegee, Alabama, where African-American scientists not only helped to grow the HeLa cells but also evaluated Salk’s vaccine (Brown and Henderson 1983). In a twist of irony, “Black scientists and technicians, many of them women, used cells from a black woman to help save the lives of millions of Americans, most of them white. And they did so on the same campus—and at the very same time—that state officials were conducting the infamous Tuskegee syphilis study” (Skloot, 2010:97). What many people are unaware of, however, is that the HeLa cells were also participants in one of largest ethical breaches in cancer research (Prison Legal News, March 15, 2008).

Chester Southam, MD

Chester Southam earned his BS and MS degrees from the University of Idaho and received his MD degree from Columbia University in 1947. Following a one-year internship at New York City’s Presbyterian Hospital, he began training at Memorial Hospital for Cancer (the forerunner to Sloan-Kettering Cancer Hospital), also in New York. Over the next 4 years he would rise to become a research fellow and eventually director of the hospital’s Division of Virology/Immunology. In 1951, he joined the faculty of Cornell’s medical college, where he was eventually awarded a full professorship (New York Times, April 10, 2002).

From 1954 through 1966, Southam would concentrate his research on two main questions: whether cancer could be transmitted from person to person and whether certain virus antibodies had anti-neoplastic properties. To answer these questions, he would utilize society’s most vulnerable citizens, including patients already diagnosed with cancer and undergoing gynecological surgery at Memorial Sloan-Kettering Cancer Hospital, incarcerated inmates, and frail, chronically ill nursing home patients (The BMJ Opinion, July 3, 2017). It was research that would raise ethical and moral issues that government regulators would later compare to those raised by Nazi experimentation (Arras 2008:75).

In 1953, Southam began what appear to have been his first human experiments to test his theory about virus antibodies with anti-neoplastic properties. To do this, he and various colleagues routinely inoculated cancer patients with dangerous viruses, including West Nile, Ilheus, and Bunyamwera viruses. A review of their published work makes the following statement:

• “All patients were volunteers who had advanced neoplastic disease of an extent, type, and stage which precluded the possibility of therapeutic benefit from surgery, x-ray, or anti-neoplastic chemotherapeutic agents.”

The general physical condition of these patients varied extremely, from apparently well to terminal. There was a wide range of diagnostic types, including epidermoid carcinomas, adenocarcinomas, lymphomas and leukemia and other sarcomas. Blood for antibody studies was obtained immediately prior to each virus inoculation and usually at weekly intervals thereafter during the period of hospitalization, and as frequently as was practicable after patients had been discharged to their homes. (Southam and Moore, 1954)

Nowhere in the statement is there any indication of informed consent having been obtained from the patients; what is clear is the overreaching attempt to make it known that these patients were terminal, with the implication that they were going to die anyway. These early studies, not unlike Southam’s later ones, would at times have serious consequences for the patients involved. An earlier paper authored by Southam noted some of the negative reactions suffered by some patients: “…caused mild encephalitis in 3 patients, and in the other patients caused no symptoms. Bunyamwera virus caused a very severe encephalitis with residual mental damage in one patient” (Southam and Moore, 1951).

Sloan-Kettering and cancer immunology

Beginning in February 1954, Southam and his colleagues initiated their first human experiments in cancer immunology by injecting 14 previously diagnosed terminal cancer inpatients at the Memorial Hospital (which became Sloan-Kettering in 1948) with cancer cells. While hospital administrators stated that informed consent was given by these patients, it was highly questionable whether this consent met the standards for informed consent, both from a legal and an ethical standpoint. In explaining their consent policy, the hospital administration said this: “…these patients knew that they were receiving cancer cells, understood the reasons for the experimentation, and consented to it orally” (Langer, 1964). In a paper (Southam et al., 1957) reporting the results of this experiment the description of informed consent is somewhat vague: “…All recipients were volunteers who were aware of the general purposes of the study and the nature of the implanted materials and who were agreeable to subsequent biopsies.” This loose interpterion of informed consent would continue throughout Southam’s professional career.

While the results of the study showed that the transplanted cancer cells did grow in the cancer patients, producing small nodules that if excised did not return and if left alone would continue growing for 4–6 weeks and then spontaneously disappear, this wasn’t the whole story. Two of the patients died before the anticipated regression; while they had been diagnosed as terminal at the time of implanting the cells, the fact that they died before regression had occurred meant that one could only assume that these patients’ nodules were not excised. Nonetheless, their deaths were attributed to their existing cancer. In four patients, cancer regrowth occurred at the implantation site following removal of the nodule, and in one patient, the implanted cells were found to have metastasized to the axillary nodes. This patient had been suffering from uterine adenocarcinoma, which according to Southam could “readily be distinguished from the implanted cells,” and at autopsy her adenocarcinoma was found to be confined to the abdomen and perineum, confirming that the metastasis that had occurred was a result of the implanted cells (Katz et al., 1972:11).

With this information, Southam believed he could argue that cancer patients lacked immunity to the cancer cell implants and were in fact suffering from an immune deficiency to cancer cells; however, to prove this theory, it would be necessary to demonstrate that the effects observed with cancer patients did not also occur in healthy individuals. Of course, being able to recruit subjects willingly volunteering to be injected with cancer cells was unlikely, and as a result, in situations like this, many researchers have used themselves as their subject; when asked if he ever considered using himself, Southam replied that “I would not have hesitated,…if it would have served a useful purpose. But, he continued, “to me it seemed like false heroism, like the old question whether the General should march behind or in front of his troops. I do not regard myself as indispensable— if I were not doing this work someone else would be—and I did not regard the experiment as dangerous. But, let’s face it, there are relatively few skilled cancer researchers, and it seemed stupid to take even the little risk.” While Southam would later say that this statement regarding self-injection was misquoted (Katz et al., 1972:49), it was a moot point, as he would find a ready supply of test subjects in the state of Ohio.

The prison volunteers

“CANCER RESEARCH VOLUNTEERS NEEDED” was the headline of a notice posted in the May 19, 1956, issue of the Ohio Penitentiary News, a weekly newspaper written and published by prisoners that was distributed throughout the US for annual subscription fee of $.50. The notice went on to explain that one of the ongoing issues in cancer research was why and how individuals without cancer (can) fight off cancer cells and prevent them from multiplying. But the explanation went further—it almost was made to sound diagnostic in nature, with the implication in the verbiage that any volunteer who had a previously undiagnosed or “hidden” cancer would be able to be diagnosed early and perhaps have a greater rate of survival. Below is such an example from the British Medical Journal.

For many years there has existed, one of many puzzling phenomena in the growth of cancer cells that still needs an answer; is still unsolved. Live cancer cells can be transferred from one individual to another. In the person who has cancer, the cancer cells will live and grow. In the person who has no cancer in his body, all of the transferred cells will die, eventually, after a short period of growth. It is this part of the problem that requires some further observation and study. Just how the normal individual who does not have cancer can kill off the transplanted ‘Foreign’ cancer cells, is the present important problem. So far, in past experiments, all attempts at growing one person’s cancer cells in another individual, who does not have cancer, have ultimately failed. This is so, definitely, as far as we know now, that if transplanted cells do not grow, when injected into another person, it follows, that the injected person does not have cancer. If the cells do grow, it would indicate that the person injected probably does have a hidden or lurking cancerous growth somewhere in his body. (BMJ, 1956)

Researchers may have worried that they would have difficulty recruiting volunteers, or they may have honestly believed that the project was so benign that selection criteria were not needed—in any case, those criteria were almost non-existent. Inmates with history of TB, syphilis, osteomyelitis, cardiac disease, or hypertension would all be eligible to participate in the study. The researchers need not have worried: while the study called for 25 volunteers, the warden received applications from 130 of the 3,800 convicts in the penitentiary. While using prisoners for medical experimentation was common practice in the US at the time, most studies offered some form of financial incentive or a reduction in sentence, whereas in this case no incentives were offered. Most participants indicated that their reason for volunteering was that someone in their family had died of cancer, while others felt that this would be a way of redeeming themselves in the eyes of society: they had been “blanks all their lives” and were glad to have the opportunity to do something useful.

Each inmate was given a release to sign that indicated that the experiment was being carried out by the Division of Medical Research, College of Medicine, The Ohio State University, and the Sloan-Kettering Institute for Cancer Research, New York City. The release text ran as follows: “This study, as it has been explained to me, is intended to determine whether or not presumedly live cancer cells can be successfully transplanted, indirectly, from one individual to another. I have been told that the cancer cells will be transplanted to my body by means of direct needle injection under my skin….” The principal investigators were listed as “Doctors Charles A. Doan, Alice E. Moore, and Chester M. Southam, or their associates.”

While Southam’s prison inmate experiments raised ethical concerns, and some of his peers in the medical community believed that the research had violated the bioethical principles of informed consent, non-maleficence, and beneficence, the research would nonetheless continue for 12 years, eventually involving over 200 inmates. Sloan- Kettering received between $300,000 and $500,000 (between $3 million and $5 million in today’s dollars) in federal funds from the National Cancer Institute and funding from the American Cancer Society (AP News, August 16, 1985). With his reputation as a cancer expert, and emboldened by the backing of prestigious institutions such as Sloan-Kettering, the American Cancer Society, and the federal government, Southam would now find a new research study for his HeLa cells, which he had injected into the Ohio State Penitentiary inmates (Skloot, 2010:168). This next project would not go as well for Southam, however.

The Jewish Hospital for Chronic Diseases

In 1963, with funding from the United States Department of Public Health and the American Cancer Society, Southam and colleague Emanuel Mandel began a study to test Southam’s hypothesis that chronically ill patients who were not suffering from cancer would be able to reject implanted cancer cells as rapidly as patients who were not suffering from any disease and faster than those who were already afflicted with cancer. Southam hoped to be able to demonstrate that the apparent absence of immunity in the cancer patients was in fact attributable to cancer, and not simply to the general debility that accompanies any severe, chronic illness.

While his theory was proven correct and was recognized as one of the leading research experiments in the cancer field, there was a problem: how he had reached that conclusion. When it was revealed, the press had a field day, with magazines such as Good Housekeeping blaring vivid and critical headlines like “How doctors use patients as guinea pigs” (October, 1965:79). Science Magazine put it thus:

• “A number of circumstances made the case particularly newsworthy. The patients in question were 22 seriously ailing and debilitated inhabitants of a relatively obscure Brooklyn institution, The Jewish Chronic Disease Hospital(JCDH).

Nazi doctors?

In August 1963, a group of three physicians at JCDH, Avir Kagan, David Leichter, and Perry Fersko, expressed their concern about the methods used in Southam’s research, and the issue was brought to the Hospital’s Medical Grievance Committee for investigation however, instead of condemning these practices, the committee found no irregularities and instead commended the research. The three physicians resigned in protest and took their concerns to William Hyman, a hospital board member and an attorney. When Hyman asked the hospital for the relevant patient records, he was refused; then, believing that the hospital board of directors would side with him, he asked for their support, but the board instead endorsed the findings of the grievance committee. This forced Hyman to go through the courts and the press, with the latter quoting Hyman’s description of Southam’s experiments as “acts which belong more properly in Dachau” (Katz, 1972) and labeling the case “the hottest public debate on medical ethics since the Nuremberg trials of Nazi physicians” (Langer, 1964).

On July 7, 1964 in another twist of irony, the Appellate Division of the State Supreme Court ruled that a member of a hospital’s board of directors did not have the right to inspect the medical records of patients, citing patient physician privacy protection (New York Times, July 7, 1964). This ruling would eventually be overturned by the New York State Court of Appeals on the grounds that “[t]he privacy of the patient could be protected, as the trial court had pointed out, by a simple order requiring that the patient’s name be concealed” (Ratnoff 1966).

Following this ruling, Hyman pressed his case with New York Attorney General Louis L. Lefkowitz, who rejected Southam’s assertion that oral consent had been given, saying that the patients “had not sufficient mental or physical ability to comprehend what was being told to them or what was being done to them,” and that those patients with such capacity had been misled.

Lefkowitz’ who was outraged, saying “every human being has an inalienable right to determine what shall be done with his own body,” and sought to revoke Southam’s license to practice medicine (Katz 1972).

Following a lengthy hearing, the New York State Board of Regents said that the “[z]eal for research must not be carried to the point where it violates the basic rights and immunities of a human person,” and found both Southam and Mandel guilty of “fraud or deceit” and unprofessional conduct, voting to suspend their licenses. However, this was later changed to a period of probation, Mand the disciplinary action had little if any effect on Southam’s professional career, as he eventually published the results of his study from the JCDH in the Annals of the New York Academy of Sciences, where no mention was made of the lack of informed consent.

In 1968, Southam was elected president of the American Association for Cancer Research. He died in 2002.

While the 1966 expose on the shortcomings of patient consent procedures penned by Harvard professor Henry Beecher (1966) in the New England Journal of Medicine cited the Southam case, it would take more than a decade until the post-Tuskegee outcry propelled the formation of the National Commission for the Protection of Human Subjects of Biomedical and Behavioral Research, the publication of the commission’s Belmont Report, and, ultimately, the proliferation of institutional review boards to monitor experimentation.

Conclusion

One might wish to believe that unethical medical experimentation on human subjects is a thing of the past and that today’s modern medicine still hides its collective head in shame for its ethical stumbles in the mid–20th century, unfortunately this is not the case. While stricter enforcement of rules and the introduction of IRBs have had a dramatic effect on unethical practice in the United States, this cannot be said of other some countries, where US-based companies and research organizations continue to exploit the absence of adequate laws to protect human subjects. While these issues are beyond the scope of this paper, it is important to understand that they do continue.

A 2008 report published by the Center for Research on Multinational Corporations revealed details of many such unethical trials, carried out in India, Nigeria, Russia, Argentina, and Nepal, among others. It revealed, for instance, the unrecorded deaths of 14 women in Uganda during a trial of the anti-HIV transmission drug Nevirapine, in a study sponsored by Boehringer Ingelheim and the US National Institutes of Health (NIH). It also revealed that eight patients in Hyderabad, in India, had died during a trial of the anti- clotting drug streptokinase—and that none of them were aware that they were part of an experiment (Somo.nl, n.d.) Even at Sloan-Kettering, almost 60 years after Southam’s research, the institute would again make headlines when, in December 2018, a report in the New York Times disclosed that the hospital’s chief medical officer, José Baselga, failed to disclose corporate ties in dozens of scientific articles he authored.

In fact, Baselga received millions of dollars in payments from companies involved in medical research, potentially compromising the work (New York Times, September 8,2018)