AIDS – Origin, Spread and Healing

97% of the persons, who have HIV in their bodies, were purposely infected with this virus, which can lead to AIDS.

The majority of people affected by AIDS/HIV are dark-skinned people in some states in Africa, in the USA and Caribbean, as well as homosexual men and persons using crack or heroin in some industrialised states.

HIV was since 1957 supplied to them in vaccines, drugs, and blood-transfusions, by HIV-containing microbes in food and water, by insects and by spraying.

Only roughly 3% of infected persons were exposed to HIV unintentionally – either by sexual intercourse or as new-born infants by their mothers.

HIV impairs in particular the body’s ability to combat unknown disease causing agents.

HIV was developed out of the Virus of Infectious Anaemia of Horses.

Research work was predominantly carried out in Germany and Japan until 1945 and since then mainly in the USA and France.

The agents of the main AIDS diseases are specific, exceptionally rare and, to a certain extent, new microbes. They are intentionally transmitted in the air and food.

The agents causing the AIDS diseases were mainly researched by scientists in military service and mainly tested in Uganda and Zaire.

HIV-infections and outbroken AIDS diseases can be cured.


Human Immunodeficiency viruses in monkeys and apish immunodeficiency viruses in human beings

Excerpt from book AIDS – Origin, Spread and Healing

In the case of a female rhesus monkey, which was kept in Southborough since she was captured as a young animal in 1972, and whose cage was located next to the infected ones, a tumour developed behind one eye, in 1980. A mashed mass comprising this tumour was injected into two rhesus monkeys – MM 434-79 and MM 251-79 – in 1980. These recipients were not immunologically tested prior to the injection[1]. They therefore already could have been infected with immunodeficiency agents. The male monkey MM 251-79 became the culture medium for viruses (SIVmac-251) by which persons in Senegal (among others) were intentionally infected. This conclusion can be drawn from literature which is publicly available. The timing of the issue of publications points to an intentional misrepresentation of the spread:

August 1983: surgical transplantation of “naturally occurring” lymphoma to rhesus monkeys, including MM 251-79 in the NEPRC. MM 251-79 was slaughtered in 1982[2]. (Lymphoma did not affect one single rhesus monkey in the wild; a.).

September 1983: MM 251-79 has AIDS. Other rhesus monkeys like MM 251-79 treated with lymphoma-tissue from MM 251-79 and a further monkey – a total of 4 – catch AIDS-characteristic diseases like cryptosporidiosis, Pneumocystis carinii-pneumonia, M.a.c., TB and generalised tuberculosis[3].

June 1985: Evidence of a retrovirus in tissue of the rhesus monkey MM 251-79, which resembles the human immunodeficiency virus HTLV-III[4].

To date, this virus has been found only among a few of the thousands of rhesus monkeys in research centres, and never in a natural habitat[5].

Yet another exotic agent: the human retrovirus HTLV-I emerged in research monkeys

June 1985: serological identification and characterisation of this “new” virus in MM 251-79. Of the four rhesus monkeys with the immunodeficiency virus in Southborough, three have antibodies indicating an additional infection by a further human retrovirus – HTLV-I[6].

Preinformed researchers

June 1985: description that also in 28 out of 67 “African green healthy long-tailed monkeys caught in the wild” in research centres in Boston (USA), Cape Town (South Africa) and Frankfurt (Germany), there were antibodies against a retrovirus that was related to the human HTLV-III.

The animals were completely healthy and there was nothing to justify any investigation into AIDS agents. The reason for an examination according to the scientists: “We sought evidence for an HTLV-III-related virus in Old World primates from Africa associated with human AIDS“. HTLV-III was said to have already been present in Uganda as early as 1972[7].

The monkeys “caught in the wild” were long-tailed monkeys from Kenya and Ethiopia which had been kept for years (for example, since 1968) and to a certain extent were already the second generation in captivity in the research centers[8].

Antibodies specifically against those viruses, which originate from the Boston monkey MM 251-79

November 1985: HTLV-III related retroviruses (STLV-IIIagm) were indicated in seven out of the 27 African green long-tailed monkeys in the USA, South Africa and Germany having antibodies. They are allegedly distinguishable from the viruses in the rhesus monkeys[9].

Using the new PCR method[10] for evidence, it was possible in 1988, to determine the origin of these viruses in Boston, Cape Town and Frankfurt. The isolated viruses were exclusively SIVmac-251, the specific virus of the monkey MM 251-79 in Boston[11]. The antibodies prove that the blood samples were not contaminated by exceedingly rare viruses in each case, but that viruses were actually in the animals themselves.

A monkey from Boston, USA as sex tourist among 20 prostitutes in Dakar, Senegal?

December 1985: Antibodies were found in the blood of 20 (out of 289 = 7%) healthy prostitutes in Dakar and five healthy patients (out of 122) from a surgical hospital ward there, and when these were examined in the test tube, they reacted to the viruses which were found to be in the African green long-tailed monkeys[12].

Here again we must ask for the reason for carrying out this research: Why weren’t sick dogs and cats examined in New York and San Francisco – why healthy people in Senegal? There was not one single case of AIDS over there.

April 1986: A virus was cultivated from the blood of the infected healthy prostitutes. This could not be distinguished from the virus which the USA scientists had cultivated in the blood samples of the seven African green long-tailed monkeys[13]. This information gave rise to the impression that HIV originated from monkeys in Africa and was acquired by human beings in Africa, before spreading to NATO-states.

The new PCR evidence method also revealed the culprits in this case. Here too, Kanki, Essex and colleagues had cultivated in the blood samples from Senegal[14] precisely the specific virus from the one rhesus monkey MM 251-79 in Boston. The antibodies prove that it was not the blood samples that were contaminated by the exceptional rare viruses, but that viruses originating from Boston had actually been present in the persons in Dakar. The prostitutes had undergone previous regular treatment for sexually transmitted diseases.

This retrovirus STLV-III (= SIVmac-251) strikes and replicates itself in cultures of human lymphocytes[15] – it is, therefore, a human (“H”) Immunodeficiency Virus. The prostitutes were still healthy four years later. The proportion of HIV-2 (= HTLV-IV)-infected prostitutes increased annually by 0.5%- to a bare 10% respectively remained unchanged in eight years.[16] Infection with the virus occurred irrespective of the time these women worked as prostitutes[17].

Kanki and colleagues maintain that antibodies against the immunodeficiency virus of the African green long-tailed monkeys were found in one human blood sample from Dakar, which had been taken already between 1975 and 1976[18]. But the source quoted, which should have described the origin of the sample, did not indicate the domicile of the donor[19].

It is most unusual to omit this very important information in an epidemiological study.

February 1987: From among roughly 30 prostitutes and 36 prisoners in three towns in the Ivory Coast, antibodies were discovered in 1986 against those retroviruses found in the Senegalese prostitutes[20](= SIVmac-251; a.).

A third human retrovirus

July 1986: Report that a new human retrovirus was found from two AIDS patients from West Africa, which was recognised by antibodies, fighting against the immunodeficiency virus in rhesus monkeys from the NERPRC. In other words, the two viruses were very closely related[21].

However, only one of the two showed the symptoms corresponding to the actual AIDS-definition. In 1983, the patient had begun to suffer from the onset of diarrhoea, weight loss and enlarged lymph nodules. Because of this, he had come from his home country Guinea-Bissau to a hospital in Lisbon for treatment. The second patient (“ROD”) was suffering from fever and diarrhoea accompanied by weight loss in January 1982. He therefore was sent from his homeland – the Cape Verde Islands – in June 1983 to the Claude Bernard AIDS-specific hospital in Paris. At that time, he had no more clinical symptoms and had almost regained his original weight. The infection of the brain with toxoplasmosis, as claimed by the author Clavel, can only be supposed. Such could only have been diagnosed after death. The recovery of the person who returned to the Cape Verde Islands, contradicts this diagnosis. The virus from “ROD” resembles closely the SIVmac-251 virus, but was actually different.

The virus-envelopes but not the cores, had identical antigen properties[22]. This HIV-2 virus was most frequently spread in parts of the population of the Federal Republic of Germany. It was found in 4% of “Africans” living there. In “Africans” in West Africa it was found in 0.6%, and in Central Africa in 0.1%[23]. In Germany it was found in blood samples of the year 1984[24]. Necessary cofactors leading to the efficacy of the virus, seem to be missing there. The infected persons were healthy and had no immunodeficiency.

HIV-2 ROD which was obtained from the blood of the healthy patient “ROD” became prototype of the HIV-2 viruses.

Theory of sexual intercourse between human beings and monkeys in West Africa

May 1986: Retroviruses which were identical with the STLV-IIImac (= SIVmac) of the captured rhesus monkeys, were indicated in leprous, but otherwise healthy, cebus monkeys in the Primate Research Center New Orleans, USA and also in those rhesus monkeys which had been transplanted with the lepra-tissue from these cebus monkeys and which subsequently suffered from AIDS[25].

July 1986: 14 of the 15 cebus monkeys captured and examined carry this SIVsmm-virus without showing any clinical symptoms. It is unknown, whether it is the same as SIVmac-251[26].

June 1989: three years after the description of the retroviruses (SIVsmm) in captured, healthy cebus monkeys in USA research centres, the head of research, PN Fultz, maintained that these viruses had also been isolated in cebus monkeys living wild in “West Africa”.

Silence about the numbers, place and time of this evidence. But:

this (alleged) occurrence outside research centres together with an (alleged) extensive spread of HIV-2 ROD (= Cabo Verde occurrence) amongst people in West Africa was said to be an indication that 30 to 40 years ago, retroviruses from a cebus monkey must have penetrated a human organism and then had transformed itself into the HIV-2 retrovirus. As an alternative, the USA scientists state, that HIV-2 ROD had passed from human beings to monkeys and had changed in the latter[27]. They don’t even discuss the possibility that HIV could have been transmitted by insects, parasites, birds, fishes, by sea-men and tourists to people and animals in “West Africa”.

How could human beings have infected monkeys with HIV? To date, there is no indication whatsoever that West African cebus monkeys living in the wild, consume intravenous drugs, transfuse untested blood pints, use contaminated blood products, or frequently use unsterilized injection syringes. These possibilities explaining infection with the human virus, obviously do not apply to animals. Since human beings do not bite monkeys, the research authors impertinently expect us to believe transmission from a human being to an animal by way of sexual intercourse between a West African person and a wild 24 inch tall monkey.

How could human beings have acquired SIV from monkeys? Since, of the 15 million or so HIV-infected persons, there is not a single case of transmission via saliva (the exception was supposed to be a dentist from the USA – see chapter 3.3.8) or through biting[28], this possibility must also be rejected for West Africa with regard to transmission from animal to human. Here too, we will have to imagine the transmission of the SIVsmm from a little monkey to a West African person as an hurly-burly circus stunt in a tree-top.

A fourth human retrovirus

The alleged precursor virus of HIV-2, HIV-2-D205 was also found in Germany in a healthy woman from Ghana[29]. This virus is a further human retrovirus.

[1]Hunt RD, Blake BJ, Chalifoux LV, et al. Transmission of naturally occurring lymphoma in macaque monkeys. Proc Natl Acad Sci USA 1983;80:5085-9.

[2]Hunt RD, Blake BJ, Chalifoux LV, et al. Transmission of naturally occurring lymphoma in macaque monkeys. Proc Natl Acad Sci USA 1983;80:5085-9.

[3]Letvin NL, Aldrich WR, King NW, et al. Experimental transmission of macaque AIDS by means of inoculation of macaque lymphoma tissue. Lancet 1983;2:599-602.

[4]Daniel MD, Letvin NL, King NW, et al. Isolation of T-cell tropic HTLV-III-like retrovirus from macaques. Science 1985;228:1201-4.

[5]Lowenstine LJ, Pedersen NC, Higgins J, et al. Seroepidemiologic survey of captive old-world primates for antibodies to human and simian retroviruses, and isolation of a lentivirus from sooty mangabeys (Cercocebus atys). Int J Cancer 1986;38:563-74.

Ohta Y, Masuda T, Tsujimoto H, et al. Isolation of simian immunodeficiency virus from African green monkeys and seroepidemiologic survey of the virus in various non-human primates. Int J Cancer 1988;41:115-22.

Kestler HW, Li Y, Naidu YM, et al. Comparison of simian immunodeficiency virus isolates. Nature 1988;331:619-22.

[6]Kanki PJ, McLane MF, King NW Jr, et al. Serologic identification and characterization of a macaque T-lymphotropic retrovirus closely related to HTLV-III. Science 1985;228:1199-201.

[7]Kanki PJ, Kurth R, Becker W, et al. Antibodies to simian T-lymphotropic retrovirus type III in African green monkeys and recognition of STLV-III viral proteins by AIDS and related sera. Lancet 1985;1:1330-2.

[8]Paul-Ehrlich-Institut. Bundesamt für Sera und Impfstoffe, Frankfurt/M., Deutschland. Personal communication to Krügel R. 1988 Mär 15.

Kessler M. Caribbean Primate Center, Sabana Seca, Puerto Rico. Personal communication to Krügel R. 1988 May 3.

[9]Kanki PJ, Alroy J, Essex M. Isolation of T-lymphotropic retrovirus related to HTLV-III/LAV from wild-caught African green monkeys. Science 1985;230:951-4.

Kanki PJ, McLane MF, King NW Jr, et al. Serologic identification and characterization of a macaque T-lymphotropic retrovirus closely related to HTLV-III. Science 1985;228:1199-201.

[10]Mullis KB, Faloona FA. Specific synthesis of DNA in vitro via a polymerase-catalyzed chain reaction. Methods Enzymol 1987;155:335-50.

[11]Kestler HW, Li Y, Naidu YM et al. Comparison of simian immunodeficiency virus isolates. Nature 1988;331:619-22.

[12]Barin F, M’Boup S, Denis F, et al. Serological evidence for virus related to simian T-lymphotropic retrovirus III in residents of West Africa. Lancet 1985;2:1387-9.

[13]Kanki PJ, Barin F, M’Boup S, et al. New human T-lymphotropic retrovirus related to simian T-lymphotropic virus type III (STLV-IIIAGM). Science 1986;232:238-43.

[14]Kornfeld H, Riedel N, Viglianti GA, et al. Cloning of HTLV-4 and its relation to simian and human immunodeficiency viruses. Nature 1987;326:610-3.

Kestler HW, Li Y, Naidu YM, et al. Comparison of simian immunodeficiency virus isolates. Nature 1988;331:619-22.

Hahn BH, Kong LI, Lee S-W, et al. Relation of HTLV-4 to simian and human immunodeficiency-associated viruses. Nature 1987;300:184-6.

[15]Daniel MD, Letvin NL, King NW, et al. Isolation of T-cell tropic HTLV-III-like retrovirus from macaques. Science 1985;228:1201-4.

Kannagi M, Yetz JM, Letvin NL. In vitro growth characteristics of simian T-lymphotropic virus type III. Proc Natl Acad Sci USA 1985;82:7053-7.

[16]Kanki PJ, Travers KU, MBoup S, et al. Slower heterosexual spread of HIV-2 than HIV-1. Lancet 1994;343:943-6.

[17]Kanki P, M’Boup S, Romieu I, et al. Epidemiology of HIV-2 in female prostitutes in Senegal. V International Conference on AIDS. Montreal, 1989:abstract M.A.O.15.

[18]Kanki PJ, Barin F, M’Boup S, et al. New human T-lymphotropic retrovirus related to simian T-lymphotropic virus type III (STLV-IIIAGM). Science 1986;232:238-43.

[19]Maupas P, Goudeau A, Coursaget P, et al. Hepatitis B virus infection and primary hepatocellular carcinoma: Epidemiological, clinical and virological studies in Senegal from the perspective of prevention by active immunization. In: Essex M, Todaro G, ZurHausen H, eds. Viruses in naturally occurring cancers. New York: Cold Spring Harbor Laboratory, 1980;7:481-506.

[20]Denis F, Barin F, Gershy-Damet G, et al. Prevalence of human T-lymphotropic retroviruses type III (HIV) and type IV in Ivory Coast. Lancet 1987;1:408-11.

[21]Clavel F, Guetard D, Brun-Vezinet F, et al. Isolation of a new human retrovirus from West African patients with AIDS. Science 1986;233:343-6.

[22]Clavel F, Brun-Vezinet F, Guetard D, et al. LAV type II: Un second retrovirus associe au SIDA en Afrique de l’Ouest. C R Acad Sci [III] 1986;302:485-8.

Clavel F, Guetard D, Brun-Vezinet F, et al. Isolation of a new human retrovirus from West African patients with AIDS. Science 1986;233:343-6.

Clavel F. HIV-2, the West African AIDS virus. AIDS 1987;1:135-40.

Clavel F, Guyader M, Guetard D, et al. Molecular cloning and polymorphism of the human immune deficiency virus type 2. Nature 1986;324:691-5.

[23]Schmitz H, Meyer A, Büttner W, et al. Antikörper gegen HIV-2 (LAV-II) in Afrika und in der Bundesrepublik. Dtsch Med Wochenschr 1987;112:1363-6.

[24]Werner A, Staszewski S, Helm E-B, et al. HIV-2 (West Germany, 1984). Lancet 1987;1:868-9.

[25]Murphey-Corb M, Martin LN, Rangan SRS, et al. Isolation of an HTLV-III-related retrovirus from macaques with simian AIDS and its possible origin in asymptomatic mangabeys. Nature 1986;321:435-7.

[26]Fultz PN, McClure HM, Anderson DC, et al. Isolation of a T-lymphotropic retrovirus from naturally infected sooty mangabey monkeys (Cercocebus atys). Proc Natl Acad Sci USA 1986;83:5286-90.

[27]Hirsch VM, Olmsted RA, Murphey-Corb M, et al. An African primate lentivirus (SIVsm) closely related to HIV-2. Nature 1989;339:389-92.

[28] Tsoukas C, Hadjes T, Theberge L, et al. Risk of transmission of HTLV III/LAV from human bites. II International Conference on AIDS. Paris, 1986:Poster 211.

[29]Dietrich U, Adamski M, Kreutz R, et al. A highly divergent HIV-2-related isolate. Nature 1989;342:948-50.

Kühnel H, VonBriesen H, Dietrich U, et al. Molecular cloning of two West African human immunodeficiency virus type 2 isolates that replicate well in macrophages: A Gambian isolate, from a patient with neurologic acquired immunodeficiency syndrome, and a highly divergent Ghanian isolate. Proc Natl Acad Sci USA 1989;86:2383-7.

German Weapons Against Palestinians Since 1944

Excerpt from book “The Jubilee Murders – Originators and Methods of Mass Murders“.

In 1948, the newly proclaimed state of Israel had 250,000 soldiers under arms right from the start. The weapons used by the Jewish guerrilla troops included German Me-109 fighter planes, MG-42 machine guns, K-98 Mauser assault rifles, and Rheinmetall anti-tank weapons[1]. German “Königstiger” and “Panther” tanks may well have helped decide the outcome of the war in Egypt, Syria, and Jordan. During the Ardennes offensive in December 1944, among others, the German troops left them intact and ready for action in parts of Belgium, but they then disappeared without a trace.

In 1944, Organisation Todt transferred all the assembly lines and individual parts for the production of the Me-109, including the “Daimler-Benz 605” and “Junkers Motoren 211” engines, to the Avia plant in Prague-Letňany, Czechoslovakia[2]. The production of the Fieseler Fi-156 was also relocated to Czechoslovakia. After the war ended, these plants continued supplying the Jewish Agency and started supplying the state of Israel in 1948. One of the two German aircraft carriers that remained unused until the end of the war, initially named “A” and “B”, then “Graf Zeppelin”, then, hinting at its intended use, „Zugvogel” (“migratory bird”), was taken to just off the coast of Palestine to serve as a runway and landing strip for Me-109 fighter planes during the conquest of Palestine[3].

A British patient of mine once confirmed that the German troops in North Africa left behind extensive stores of clean water, munition, and military equipment. A patient who had served Rommel and others as a driver told me that the British troops had helped the Germans by leaving them huge quantities of fuel, munition, and conserved foods.

In Israel, naturalized citizens who had once belonged to the German Wehrmacht, e.g. Shlomo Perel, Günter Ballauch, Siegfried Behrendt, Ephraim Glaser, Nachemia Wurmann, Karl Heinz Maier, and Bob Winter[4], continued Hitler’s racist war of conquest. During the Six-Day War of 1967, “hundreds” of former German „Waffen-SS” and Wehrmacht soldiers fought for money and – on being informed that they had committed war crimes – against Egyptian, Jordanian, and Syrian troops[5].

[1] Verlag für geschichtliche Dokumentation. Illustrierte Weltgeschichte von 1945 bis heute. Manfred Pawlak Verlag, Herrsching 1980.

[2] From September 1944 to the end of April 1945, those involved included Franz Roman Nüsslein and Marga Henseler, whose activities were discussed in the Foreign Office publication Das Amt in 2010. They continued supplying weapons to Israel from 1955 and 1960 respectively, also under the aegis of the company “Sportavia Pützer”, Bonn, which was founded some time later.

[3] This supply of the Israeli army with German arms also explains why 11 years after the war, they are known to have fitted themselves out with all kinds of weapons, including tanks, vehicles, and spare parts, obtained – of all places – from demilitarized Germany under Minister of Defense Franz Joseph Strauss. The “Merkava” tank used by Israel is the equivalent of the Thyssen tank “TAM” built in Argentina.

[4] Rigg B. Hitlers jüdische Soldaten. Paderborn: Verlag Ferdinand Schöningh, 2003:60, 350

[5] Son of a former Waffen-SS member