MP3 (One 30-minute segment)
NB: This stream contains FTRs 681 and 682 in sequence. Each is a 30-minute segment.
Introduction: Continuing a decades-long exploration of evidence that AIDS was deliberately created, this broadcast highlights some of the quasi-eugenic aspects of the disease, as well as the “monkey-virus” connection to the AIDS investigation.
The program begins with a look at an excerpt from testimony before a House appropriations subcommittee that was drawing up the defense budget for the following year. (The hearings were in 1969.) The testimony discusses the possibility of using genetic engineering to produce a disease that would be “refractory” to the immune system. This is virtually the clinical definition of AIDS. It is worth noting that the project was funded, and just such a disease—AIDS—appeared in just the time frame posited.
Next, the program sets forth an important new development with regard to CCR5 delta-32–a gene that affords immunity to infection by HIV. That gene is found almost exclusively in people of Northern European extraction. It is the “Aryan gene.” After reviewing information about CCR5 delta-32 from FTR #606, the program notes the application of CCR5 delta-32 to AIDS therapy.
In June of 2009, it emerged that CCR5 delta-32 was used in transplant therapy administered by a German doctor to an HIV-positive leukemia patient. It appears that the patient was cured of HIV! The German doctor deliberately selected a CCR5 delta-32 positive donor for the stem cells used for the transplant. Dr. Gupta, quoted in the following article, wonders why more publicity wasn’t afforded this event. Why indeed?
Whereas some “Aryans” possess a gene that renders them immune from HIV infection, the opposite is the case for black folks. The program reviews (from FTR #642) information about a hereditary susceptibility to HIV infection among people of African extraction. A gene that affords people of African extraction a measure of protection against malaria infection renders them particularly vulnerable to HIV.
Turning to the subject of SIV (Simian Immunodeficiency Virus), the broadcast notes its discovery following an outbreak in primate laboratories in the United States. Spreading to primate species with no exposure to, or antibodies to, the virus, SIV created an outbreak of disease among monkeys in the laboratory.
Noting a recent report attempting to link AIDS in humans with SIV in chimpanzees, the program reviews information discussed with Ed Haslam about the premise for this “discovery.” Dr. Beatrice Hahn had previously reported the discovery of HIV present in chimpanzees. Ed notes that the chimps she had been testing had been deliberately infected with the virus in an Air Force laboratory in New Mexico, at which chimps were kept in “natural” conditions. These “natural” conditions for chimpanzee colonies entail the alpha male of the colony having sex with all of the females, thereby spreading any sexually transmitted viruses!
Turning to a primary area of theoretical inquiry, the program notes that the Nazis began researching toxic agents on apes and then moved on to humans—inmates in concentration camps. AIDS results from a monkey virus that eventually jumped to humans as well. Does the progression in the Nazi death camps of testing on apes to testing on humans have any relationship with the progression of a simian virus to infection of humans? Might the creation of AIDS have stemmed from Nazi research? Is it an accident that the hereditary immunity from HIV infection is only present in the white race, and [according to some sources] Northern Europeans in particular? Is it an accident that people of African extraction are particularly susceptible to HIV infection?
Turning to a primary element of analysis, the program reviews the career of an interesting and [possibly] very significant individual. Franz Liesau Zacharias was a German intelligence agent stationed in Spain. Among the duties he performed for the Nazis was obtaining animals, including apes, for experimental purposes. Note that the animals were to be used in experiments used for developing diseases for testing on concentration inmates.
Among the diseases that Liesau Zacharias’ animals were used for testing was “the plague”! Did the Nazis note that some people appeared to be immune to infection with plague? Were tissue and/or sera samples taken and preserved for further study? Was this in any way connected to the eventual evolution of the CCR5-delta 32 gene as a hereditary protection against infection by HIV? Is it possible that Liesau Zacharias was actually targeted for recruitment by the U.S. for Project Paperclip? Did Liesau Zacharias experience an outbreak of immunodeficiency among his primates awaiting shipment to Germany? Might such an outbreak have been due to SIV? Did Liesau Zacharias take tissue and sera samples from infected primates? Might such a development have been related to his importance to the Allies?
The program concludes with review of Ed Haslsm’s musing concerning SIV and the contamination of the polio vaccine with simian viruses. Ed theorizes that AIDS may have stemmed from the irradiation of viruses under the janus-faced cancer research/biological warfare project discussed in Dr. Mary’s Monkey: Did that irradiation produce a mutated SIV which could infect humans and which resulted in the AIDS epidemic?
Program Highlights Include: Discussion of the possibility that some of the successor companies to I.G. Farben might market the CCR5 delta-32 stem cell therapy for AIDS; review of those companies’ links to the Bormann capital network and the Underground Reich. Listeners are emphatically encouraged to read a consummately important article that details the National Cancer Institute’s Viral Cancer Research Program, which was at the epicenter of U.S. AIDS research, including the “discovery” of HIV. That program is inextricably linked to the milieu of biological warfare research. As discussed in FTR #606, the Third Reich’s biological warfare program was disguised as a cancer research program.
1. The program begins with a look at an excerpt from testimony before a House appropriations subcommittee that was drawing up the defense budget for the following year. (The hearings were in 1969.) The testimony discusses the possibility of using genetic engineering to produce a disease that would be “refractory” to the immune system. This is virtually the clinical definition of AIDS. It is worth noting that the project was funded, and just such a disease—AIDS—appeared in just the time frame posited. It is also worth noting that, in the 2002 edition of A Higher Form of Killing, this passage is omitted!!
“. . . As long ago as 1962, forty scientists were employed at the U.S. Army biological warfare laboratories on full-time genetics research. ‘Many others,’ it was said, ‘appreciate the implications of genetics for their own work.’ The implications were made more specific that genetic engineering could solve one of the major disadvantages of biological warfare, that it is limited to diseases which occur naturally somewhere in the world. ‘Within the next 5 to 10 years, it would probably be possible to make a new infective micro-organism which could differ in certain important respects from any known disease-causing organisms. Most important of these is that it might be refractory to the immunological and therapeutic processes upon which we depend to maintain our relative freedom from infectious disease.’ [Italics are Mr. Emory’s.] The possibility that such a ‘super germ’ may have been successfully produced in a laboratory somewhere in the world in the years since that assessment was made is one which should not be too readily cast aside. . .”
2. Next, the program sets forth an important new development with regard to CCR5 delta-32–a gene that affords immunity to infection by HIV. That gene is found almost exclusively in people of Northern European extraction. It is the “Aryan gene.” After reviewing information about CCR5 delta-32 from FTR #606, the program notes the application of CCR5 delta-32 to AIDS therapy.
In June of 2009, it emerged that CCR5 delta-32 was used in transplant therapy administered by a German doctor to an HIV-positive leukemia patient. It appears that the patient was cured of HIV! The German doctor deliberately selected a CCR5 delta-32 positive donor for the stem cells used for the transplant. Dr. Gupta, quoted in the following article, wonders why more publicity wasn’t afforded this event. Why indeed? Might wider publicity have called undue attention to this curious feature of the AIDS epidemic–that “Aryans” have an immunity to this disease?
Another point of interest will be to see if some of the successor firms to the old I.G. Farben cartel wind up marketing this AIDS therapy, predicated on the use of stem cells from CCR5 delta-32 donors. As discussed in Martin Bormann: Nazi in Exile, the I.G. and its successor companies are inextricably linked with the Underground Reich. (The I.G.–Underground Reich axis is discussed in–among other programs–FTR #‘s 305, 576.
A Foley [Alabama] physician said what appears to be the first case of HIV/AIDS cure in the world is getting little mention in the media.
Dr. Awadhesh K. Gupta, medical director at Foley Walk-In Med Care, said he first heard of the medical breakthrough in April when he attended the Annual Conference of the American College of Physicians in Internal Medicine in Philadelphia.
It’s a conference Gupta tries to attend every year.
“This is the most prestigious organization of physicians in Internal Medicine and is responsible for certifying post graduate training in Internal Medicine. It is also one of the oldest,” he said.
According to Gupta, who has been practicing medicine in the South Baldwin area since 1997, the cure was first reported in early 2008 by a group of physicians from Germany at the annual conference on “Retroviruses and Opportunistic Infections” in Boston. The New England Journal of Medicine, one of the most prestigious medical journals in the world, finally published the report in its Feb. 12, 2009, issue, Gupta said.
So why has the news of the first case of HIV/AIDS cure received so little attention where the public is concerned?
“I can’t be sure as to why so little publicity,” Gupta said recently.
“My guess is that most scientific researchers are somewhat stunned that a clinician — not a research scientist — has been able to come up with the cure. Most of the big research money and big name American institutions are somewhat embarrassed to acknowledge that the very first case of HIV cure is not coming from their institutions.”
The cure, instead, is coming from Charity University Hospital in Berlin, Germany, and the doctor is Gero Huetter, who works in the Department of Hematology, Oncology and Transfusion Medicine at the same hospital.
Asked about the reaction of attendees at the medical conference in Philadelphia as regarded the news of an HIV/AIDS cure, Gupta said, “Unfortunately, because of the hectic schedule, I did not try to engage too many physicians. However, the doctor presenting this information seemed extremely excited about it.”
As Gupta explains the case and cure in question, a 40-year-old American working in Berlin had been HIV-positive for 10 years. The patient’s HIV infection had been under control for four years with “conventional HAART treatment regimen” (Highly Active Anti-Retroviral Therapy).
When the patient developed leukemia, however, a bone marrow transplant of stem cells was done using standard protocol, which Gupta said includes radiation therapy and chemotherapy prior to the transplant.
“Remember, once you stop HIV drugs, the HIV viral count rises very rapidly, usually within a few days to a week,” Gupta said.
According to Gupta, Huetter, the German physician treating the American, deliberately chose a stem cell donor who had a gene mutation known as “CCR-5 Delta– 32,” rather than using the best matched donor.
Gupta said Huetter remembered research first observed in 1996 — research Gupta said is well known in the scientific community. That research found that certain gay men in the San Francisco area remained uninfected with HIV in spite of engaging in risky sexual activities. As it was later discovered, those men had the CCR-5 Delta-32 gene mutation.
As it turned out, the patient’s stem cell transplant was a success, Gupta said, even though the patient had to have a second stem cell transplant (from the same donor) when his leukemia relapsed.
“This patient has been off all his HIV drugs for two years now,” Gupta said. “He continues to show no detectable signs of HIV in all the known places HIV is detected — no signs of HIV in his blood, bone marrow, lymph nodes, intestines or brain.” Also, the patient’s T-cell count remains normal.
Thus, according to Gupta, within the limits of scientists’ ability to detect HIV, it appears this patient’s HIV has been “eradicated.”. . .
3. The program reviews (from FTR #642) information about a hereditary susceptibility to HIV infection among people of African extraction. A gene that affords people of African extraction a measure of protection against malaria infection renders them particularly vulnerable to HIV.
“An international team of AIDS scientists has discovered that a gene variant common in blacks protects against certain types of malaria but increases susceptibility to HIV infection by 40 percent.
Researchers, keen to find some biological clues to explain why people of African descent are bearing a disproportionate share of the world’s AIDS cases, suspect this subtle genetic trait — found in 60 percent of American blacks and 90 percent of Africans — might partly explain the difference.
Ten percent of the world’s population lives in sub-Saharan Africa, but that region accounts for 70 percent of the men, women and children living with HIV infection. In the United States, African Americans make up 12 percent of the population but account for half of newly diagnosed HIV infections. . . .”
4. Turning to the subject of SIV (Simian Immuno-Deficiency Virus), the broadcast notes its discovery following an outbreak in primate laboratories in the United States. Spreading to primate species with no exposure to, or antibodies to, the virus, SIV created an outbreak of disease among monkeys in the laboratory.
Research on an AIDS-like disease in monkeys continues to help scientists understand problems such as how HIV causes AIDS, how the virus “hides” from the immune system and how the disease might be prevented or treated, two decades after the human and monkey diseases were identified.
“These animals have been indispensable for understanding how the virus works and in working toward vaccines,” said Murray Gardner, professor emeritus of medical pathology at the UC Davis Center for Comparative Medicine.
About 300 researchers from around the world will reflect on those past achievements and discuss new data when they gather Sept. 8–11 in Monterey, Calif., for the 20th Annual Symposium on Nonhuman Primate Models for AIDS. The California National Primate Research Center (CNPRC) at the University of California, Davis, is hosting the conference.
More than 20 years ago, scientists at the UC Davis primate center were confronted with a mysterious and deadly outbreak of infections in their monkeys. Showing signs of weakened immune systems, the monkeys were succumbing to a variety of infections that normally did not cause disease.
At about the same time, a deadly new disease known as AIDS was making the headlines. Bearing a striking resemblance to the monkey syndrome, the human disease also led to opportunistic infections, wasting and death.
Scientists would later discover that the monkey disease, called simian AIDS, was caused by the simian immunodeficiency virus (SIV), a close relative of the human immunodeficiency virus (HIV) that causes human AIDS.
The striking similarities between the human and simian disorders and the viruses that cause them enabled scientists to gain otherwise unobtainable insights into the origins and progression of human AIDS — work that continues today.
Today, scientists at the UC Davis center are using the SIV monkey model of AIDS to study ways to vaccinate against HIV transmission from adult to adult and from mother to offspring. They are also tackling the problem of eliminating latent virus — virus that is inactive and “hiding” inside cells in the body — in individuals taking medications to fight the virus. Finally, they are testing the ability of microbicides to prevent sexual transmission of SIV/HIV.
“The monkey disease is a remarkably accurate facsimile of the human disease,” said Gardner.
An authority on retroviruses and the intersection of the simian and human immunodeficiency viruses, Gardner will give the keynote address at the conference, highlighting important contributions of nonhuman primate research to knowledge of AIDS.
According to Gardner, some of the key achievements made by researchers studying immunodeficiency viruses in monkeys include: gaining an in-depth knowledge of the natural history of both the human and simian AIDS viruses, including the potential for and mechanisms of cross-species transmission; demonstrating the feasibility of an AIDS vaccine by showing that monkeys became resistant to simian AIDS when injected with weakened versions of the virus; demonstrating that SIV alone, rather than environmental or other factors, causes simian AIDS; defining the mechanisms of HIV/SIV transmission between hosts; and identifying the role of antibodies and cellular immunity, especially CD8 cells — a specific immune system component — in fighting the virus.
The symposium traces its origins to 1983, when about 30 researchers from the then seven U.S. primate research centers met at Tulane University to discuss what was then a poorly understood, spontaneously occurring immunodeficiency syndrome of macaque monkeys. The monkey disease had many strong similarities to AIDS, which was first described in 1981. HIV was first identified in 1983 and SIV in 1985. . . .
5. Noting a recent report attempting to link AIDS in humans with SIV in chimpanzees, the program reviews information discussed with Ed Haslam about the premise for this “discovery.” Detailed analysis of Ed Haslam’s debunking of the chimpanzee theory can be accessed in FTR #269. Dr. Beatrice Hahn had previously reported the discovery of HIV present in chimpanzees. Ed notes that the chimps she had been testing had been deliberately infected with the virus in an Air Force laboratory in New Mexico, at which chimps were kept in “natural” conditions. These “natural” conditions for chimpanzee colonies entails the alpha male of the colony having sex with all of the females, thereby spreading any sexually transmitted viruses!
Although the AIDS virus (HIV-1) entered the human population through chimpanzees, scientists have long believed that chimpanzees don’t develop AIDS. But a new study from an international team, including University of Minnesota professors Anne Pusey and Michael Wilson, shows that chimpanzees infected with SIV (simian immunodeficiency virus), the precursor to HIV-1, do contract and die from AIDS. The discovery is published in the July 23 issue of Nature.
The authors report that infected chimpanzees in their study group were 10–16 times more likely to die than those who were uninfected. The team also found that infected females were less likely to give birth and infants born to infected mothers were unlikely to survive. The virus, they learned, was transmitted sexually and through mother’s milk. Over the nine-year study period, 10–20 percent of the 94 chimpanzees were infected at any one time.
The finding opens up new opportunities for research.
“We hope this will lead to a better understanding of the virus that will benefit both humans and chimpanzees,” said Jane Goodall, whose focus has shifted in recent years from research to conservation of chimpanzees and their habitats.
The study focused on chimpanzees at Gombe National Park, Tanzania, where Goodall and her colleagues have studied chimpanzees for nearly 50 years. Researchers used data that Pusey, a long-time associate of Goodall’s, archived at the Jane Goodall Institute’s Center for Primate Studies at the University of Minnesota, to understand how SIV is transmitted among chimpanzees, and how the virus affects chimpanzee survival and reproduction.
Virologist Beatrice Hahn at the University of Alabama led the Nature study, which involved Pusey and her colleagues. Brandon Keele and Rebecca Rudicell in Hahn’s lab used techniques they developed to detect SIV in chimpanzee fecal samples. Samples were collected by research staff at Gombe and shipped to Alabama for analysis.
Examination of tissue samples from dead chimpanzees revealed a loss of CD4+ T cells (which are vital to immunity) in SIV-infected chimpanzees. Loss of these cells renders victims susceptible to many other infections – the classic indication of AIDS. Wilson organized a team of Tanzanian and American specialists to conduct the first post-mortem exam of a chimpanzee that died from AIDS.
“From a scientific perspective, it is fascinating to learn that the virus affects chimpanzees in similar ways to humans,” Wilson said. “But it is difficult knowing that there isn’t much we can do to help those whose lives may be shortened by the virus.” Wilson is a McKnight Land-Grant Professor with a joint appointment in Anthropology and Ecology, Evolution and Behavior.
“It isn’t practical to treat the chimpanzees for SIV infections, but it appears that SIV in chimpanzees is not quite as pathogenic as HIV-1 in humans,” said Pusey, who is a Distinguished McKnight University Professor in the College of Biological Sciences Department of Ecology, Evolution and Behavior. “So far, the main study community has maintained its size despite mortality from diseases.”
Including Pusey and Wilson, six of the co-authors are associated with the University of Minnesota. Doctoral candidate Emily Wroblewski sequenced DNA from fecal samples. Research Administrator Joann Schumacher-Stankey prepared demographic and behavioral data. Elizabeth Lonsdorf (Ph.D. 2003) is now based at Lincoln Park Zoo and leads a health-monitoring project at Gombe. Anna Moser (Ph.D. 2008) is director of Research at Gombe.
6. Turning to a primary area of theoretical inquiry, the program notes that the Nazis began researching toxic agents on apes and then moved on to humans—inmates in concentration camps. AIDS results from a monkey virus that eventually jumped to humans as well. Does the progression in the Nazi death camps of testing on apes to testing on humans have any relationship with the progression of a simian virus to infection of humans? Might the creation of AIDS have stemmed from Nazi research? Is it an accident that the hereditary immunity from HIV infection is only present in the white race, and [according to some sources] Northern Europeans in particular? Is it an accident that people of African extraction are particularly susceptible to HIV infection?
“Guinea pigs and white rats, animals traditionally used for testing purposes, were deemed inadequate for measuring the effect of the nerve gases on humans. Early in the war, it was decided to substitute apes, whose biological reactions to such gases were believed to be more like those of human beings. However, apes were not readily available in Germany, and Speer’s office supplied 200,000 Swiss francs, a precious foreign currency, to buy them in Spain. They were transported to Germany with great difficulty; many died before the experiments were concluded (TWC I, p. 351, Brandt Document Book 12, Defense Exhibit 11). Eventually it was decided to experiment on concentration camp Jews. It is suspected that the testing of I.G.’s poison gases on humans was known in the highest echelons of I.G. After the war, Georg von Schnitzler swore that Ambros, Schmitz, and Ter Meer were aware of these activities. According to British intelligence, one of them was reported to have ‘justified the experiments not only on the grounds that the inmates of concentration camps would have been killed anyway by the Nazis, but also on the grounds that the experiments had a humanitarian aspect in that the lives of countless German workers were saved thereby’ (Hearings before a Subcommittee of the Committee on Military Affairs, U.S. Senate, 79th Congress, 1st Session (1945), pursuant to S. Res. 107 and 146, Elimination of German Resources for War, part X, p. 1276)”
7. Turning to a primary element of analysis, the program reviews the career of an interesting and [possibly] very significant individual. Franz Liesau Zacharias was a German intelligence agent stationed in Spain. Among the duties he performed for the Nazis was obtaining animals, including apes, for experimental purposes. Note that the animals were to be used in experiments used for developing diseases for testing on concentration inmates.
“One tortured French citizens in ice baths. Another was a Gestapo agent who packed bombs into crates of Spanish oranges bound for England. They were just two of 104 Nazi secret agents in Spain whom the Allies sought near the end of World War II. But Spanish dictator Francisco Franco—Adolf Hitler’s ally—refused to hand them over, according to an investigative report by El País, a Madrid newspaper. . . .Another agent was Franz Liesau Zacharias, whose job fori Hitler’s Abwehr spy agency was to obtain monkeys and other animals from Spain’s colonies in Africa. The animals used for experiments in Germany aimed at manufacturing killer diseases that were to be unleashed on concentration camp inmates, El Pais reported. . . .”
(“Report: Spain Protected Undercover Nazis from Allies” by Ciaran Giles [AP]; Associated Press; 3/31/1997.)
8. Among the diseases that Liesau Zacharias’ animals were used for testing was “the plague”! Did the Nazis note that some people appeared to be immune to infection with plague? Were tissue samples taken and preserved for further study? Was this in any way connected to the eventual evolution of the CCR5-delta 32 gene as a hereditary protection against infection by HIV? Is it possible that Liesau Zacharias was actually targeted for recruitment by the U.S. for Project Paperclip, like Erich Traub? Did Liesau Zacharias experience an outbreak of immunodeficiency among his primates awaiting shipment to Germany? Might such an outbreak have been due to SIV? Did Liesau Zacharias take tissue and sera samples from infected primates? Might such a development have been related to his importance to the Allies?
“ . . . Another ‘German on the list is Franz Liesau Zacharias, who died in Madrid in 1992 at the age of 84. A member of the German military intelligence agency, the Abwehr, he had been in charge of obtaining animals in Spanish territories in Africa for experiments in Germany, the allies said. These experiments included ‘spreading horrific diseases, such as the plague, in concentration camps,’ the newspaper said. . . . It added that man of those on the list started up businesses in Spain after the war, mainly in the Basque country. . . .”
(“Spanish Newspaper Publishes List of Nazis Protected by Franco”; Agence France Presse [English]; 3/30/1997.)
9. The program concludes with review of Ed Haslsm’s musing concerning SIV and the contamination of the polio vaccine with simian viruses. Ed theorizes that AIDS may have stemmed from the irradiation of viruses under the janus-faced cancer research/biological warfare project discussed in Dr. Mary’s Monkey: Did that irradiation produce a mutated SIV which could infect humans and which resulted in the AIDS epidemic?
” . . . SIV is the Simian Immunodeficiency Virus, one of several monkey Viruses known to have contaminated the polio vaccine. The more carcinogenic SV-40 has received most of the press. SIV, a single-strand RNA retrovirus, is considerably smaller than SV-40 (a double-strand DNA virus). The technology of the 1950’s was not able to filter SIV from the viral extracts. Further, researchers of the day did not consider retroviruses to be dangerous, so they basically ignored them. AIDS has taught us how dangerous retroviruses can be. If ‘the project’ in New Orleans was intentionally exposing SV-40 to radiation they have exposed SIV to radiation at the same time. Simply stated, HIV-1 is a mutated form of SIV. Did the mutation which changed SIV into HIV-1 occur when SV-40 was exposed to radiation? Was this the moment of conception of AIDS? Could this artificially-induced mutation explain why HIV-1 is mutating so rapidly? Why it is behaving so ‘unnaturally’? . . . .”
Discussion
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