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.

The Plague for Non-Jewish Persons

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


“This peculiar resistance of the Jews to the noxious effects of contagious disease had already been noted in medieval times, especially during the great epidemics in Europe of the Plague, known then as the ‘Black Death’…”[1]. Aegidius Tschudi (1505-1551), an acclaimed historical writer from Switzerland, said that no Jewish persons in any country fell victim to the plague of 1346-50[2].

Pneumonia (Pneumocystis carinii pneumonia – author’s note), typhus, malaria, cholera, plague, smallpox … occur more rarely in Jews and in general take a milder course than in the rest of the population. Even during the terrible epidemics of medieval times, it was almost universally observed that the Jews were affected far less often than the Christians”[3].

 

At the time of the Jewish persecutions in medieval Europe and the plague and other epidemics that followed[4], Jewish communities in Germany usually had their own source of drinking water supplied by groundwater. These were and are known as “mikvot”, and are said to be places where women bathe and purify themselves after menstruation[5].

Before the “plague” of 1347 – 1350, only four „mikvot” were seen between the North Sea and the Alps outside Germany, i.e. in Belgium, the Netherlands, and the Burgundy region of eastern France. These „mikvot” were located in Besancon, Chalon sur Saone, Joinville, and Macon. However, in German-speaking “Aschkenaz”, the “land of displacement”, there were 27, in Andernach, Colmar, Dortmund, Erfurt, Frankfurt am Main, Friedberg, Grünberg (Hesse), Hagenau, Cologne, Kaiserslautern, Limburg, Lüneburg, Münster, Mainz, Nordhausen, Nuremberg, Oberehnheim, Offenburg, Sondershausen,[6] Strasbourg, Speyer, Schwäbisch-Gemünd, Trier, Tübingen, Worms, Würzburg, and Zurich. After the plague epidemic, when Jewish people had returned to the community after the pogroms, another 31 „mikvot” were seen in Ahrweiler, Aschaffenburg, Augsburg, Bonn, Düren, Emmendingen,[7] Deutz, Gaukönigshofen, Georgensgemünd, Göttingen, Hildesheim, Heidelberg, Heilbronn, Kalletal,[8] Kreuznach, Lich, Münzenberg. This list is not complete. “All areas (Jewish central settlements – author’s note) that usually had a cemetery also had synagogues, mikvot (seldom seen, albeit of central importance) […][9]. This means that another 28 deep wells must have been converted and added to the list. They probably existed almost every where there was a Jewish community.

According to Jewish tradition, especially after the first Crusade (1096), there was a period of four days at the change of every season when blood was added to the drinking water (rivers, wells, and springs) at sundown[10]. David Agudarham, rabbi in Seville, issued a corresponding warning in 1340. Drinking the water would cause death within a few days, but the water could be made potable by heating it with burning charcoal and immersing a red-hot horseshoe in it[11].

The most important contemporary Jewish witness of the persecutions, Israel Ben Joel Süsslin, wrote that the plague was God’s punishment for the persecution of the Jews[12]. He argued that the Christian persecutors were punished by supernatural means after the pogroms.

The „mikvot” were often referred to colloquially as “cold springs” or “cold wells”. They were uncontaminated water sources that enabled their users to survive or resettle in Silesia, Poland, which were not affected by the epidemics. Non-Jewish persons, on the other hand, were killed off by germs that attacked them in an unnatural manner. This is how 40% of Europe’s Non-Jewish population, 25 million people, came to die of “plague”, for example between 1347 and 1350.

 

A huge number of mass infections

The “Black Death” killed off an exceptionally large number of people in Europe. However, “there were 32 plague years between 1326 and 1400, 41 between 1400 and 1500, and 30 between 1500 and 1600! … The last major outbreak of plague occurred in India in 1898, where it took the lives of six million people living in Bombay”[13].

 

Black Death caused by several pathogens

The physical symptoms indicated bubonic plague, pneumonic plague, and other diseases. The lack of solidarity and inconsiderate behavior indicated that mind-altering influences were at work. St. Vitus’ dance in Sicily, around Aachen, in the Rhineland and Cologne could have been caused by neurotoxic substances, e.g. mycotoxins or herpes viruses.

The following suggests mycotoxins as a source of plague:

If you put a loaf of newly baked bread on a stick over night, and if by morning it is moldy, green and yellow on the inside, and tasteless; if you throw it to the dogs and chickens and they die after eating it, or if the chickens drink the morning dew that has gathered it and perish, you can be sure that the plague is right before your door[14].

The “plague” was well known to be highly contagious. The Mongolian besiegers of Kaffa, the alleged source of the mass deaths in Europe, catapulted plague-infested corpses into the city, much to the horror of the Genoese inside. Both sides were familiar with plague as a biological weapon.

Many very appropriate measures were adopted:

  • Ships were quarantined for 40 days; ships suspected to be harboring plague were shot at with burning arrows.
  • Sufferers were isolated, and houses with infected inhabitants could not be entered until 40 days had passed. It was forbidden to attend church services or public gatherings and to take in travelers or goods from regions where plague was suspected.
  • Beggars, cripples, gypsies, Jews, and strangers were obliged to collect the corpses and bury them outside the cemetery; an island off Venice was even used for this purpose.

Nevertheless, “the plague spread at a furious pace”. Horses and carts managed to travel around 40 miles a day, the plague 50 miles a day. In October 1347, after the infection in Kaffa, thousands of people died in Messina and then in many places in Sicily[15].

On November 1, people began dying in Marseille, 300 miles to the north with no stop in between. The death toll there rose to 57,000. At the same time, the plague began decimating the population of Genoa, located just as far north, the first city in Italy to be affected[16].

The east side of Italy also succumbed, beginning in February 1348 with deaths in Venice, Lucca, and Pisa far to the north.

 

How could Pasteurella pestis kill off 25 million people in towns and villages scattered over thousands of miles within just 2½ years?


[1] Fishberg M. Jews A Study in Race and Environment. New York 1911:276

[2] Tschudi A. Chronicon Helveticum. Vol. 1:277. Ed. Iselin JR. Basel 1734

[3] Hoppe H. Krankheiten und Sterblichkeit bei Juden und Nichtjuden. Berlin 1903:18

[4] Niewöhner F. Erst kam der Pogrom, dann die Pest. Frankfurter Allgemeine Zeitung. Jan 5, 2004:31.

[5] Talmudic law specifies cleansing in running water or basins that can hold at least 10 cubic feet. However, the “mikvot” in Germany are usually complexes 50 feet under surface containing about 2½ cubic feet of standing groundwater. The “mikveh” in Friedberg, Hesse, is located 80 feet underground and is the deepest Gothic construction in Germany. Groundwater barely flows and has a temperature of 17 Fahrenheit. Its high iron content makes it sterile.

[6] Frankfurter Allgemeine Zeitung, Apr 12, 2007

[7] Frankfurter Allgemeine Zeitung Sept 22, 2005

[8] Frankfurter Allgemeine Zeitung Aug 29, 2006: 33

[9] Barzen R. Regionalorganisation jüdischer Gemeinden im Reich in der ersten Hälfte des 14. Jahrhunderts. In: Haverkamp A. (ed.) Geschichte der Juden im Mittelalter von der Nordsee bis zu den Südalpen. Teil 1. Hanover 2002:302

[10] Toaff A. Blood Passover. Last Revision. August 1, 2016: 215 – 216

[11] Stuczynski CD. “A Marrano Religion”? The Religious Behaviour of the New Christians of Braganca Convicted by the Coimbra Inquisition in the Sixteenth Centruy (1541 – 1605), Ramat Gan, Bar-Ilan University, 2005, pp 32-35. Cited in Toaff:216 || Abudarhamba-Shalem, by A.J. Wertheimer, Jerusalem, 1963, p. 311 – 312 in Toaff: 215-216, 221

[12] Cluse C. Zur Chronologie der Verfolgungen zur Zeit des Schwarzen Todes. In: Haverkamp A. (ed.) Geschichte der Juden im Mittelalter von der Nordsee bis zu den Südalpen. Teil 1, Hanover 2002:225

[13] Kleio.org Alltagsgeschichte des Mittelalters X.6.1. Die Geschichte der Pest. Retrieved Apr 19, 2017

[14] Nohl J. Der schwarze Tod: Eine Chronik der Pest 1348 bis 1720. Severus Verlag, 2013

[15] Many catacombs were dug in Sicily allegedly to house Christian martyrs.

[16] Herds of horses were kept for non-agricultural purposes in the Camargue in the nearby Rhone delta.

Export from English zoos to African countries and the Persian Gulf area

Obviously English zoo’s functioned as breeding places for animals containing agents of Spongiform Encephalopathy to transmit them into parts of Africa and into Oman and Saudi Arabia. “London zoo officials have written to other British zoos suggesting that ‘careful consideration’ should be given before animals at risk are exported to foreign zoos or for reintroduction programmes. London zoo’s circular says that any ungulate fed properietary meal between 1980 and 1989 may be affected.”[44]

There is growing interest in the reintroduction of captive-bred animals to the wild for conservation programmes and these reintroductions provide a route for the accidental transmission of infectious diseases into free-living populations…[45].

In April 1989 an Arabian oryx cow died in Londons Regent’s Park because of BSE. Three month later, in July 1989, her nine month old calf, was shipped to Saudi Arabia. He died there on Aug 18, 1989.[46] In Phoenix, Arizona, USA 216 Arabian oryx are awaiting to be shipped to Saudi Arabia.

In Oman the import of the BSE agents from Great Britain was kept hidden for four years. In Jan./Feb. 1989 two cows there showed clinical symptoms indicative of BSE. They had been exported from one affected herd in Great Britain in 1985. Their BSE-illnesses were the first cases to be diagnosed outside Great Britain.[47] From January 1988 to March 1989 fully vaccinated children in Oman were attacked by an outbreak of paralytic poliomyelitis[48], indicative of immunosuppression. Soldiers from the USA, being active there at that time, became victims of “Gulf War Syndrome”, a disease indicative of retrovirus-particles connected with BSE. (See chapter 5)

In Serengeti Park in Tanzania in 1994 during 14 days over an 1,000 km distance 1,000 out of 3,000 lions died showing neurological symptoms[49] reminding of Spongiform Encephalopathy. The lions are affected by the retrovirus Feline Immunodeficiency virus[50] (see chapter 3.9). 95% of the young cheetahs there did not survive in 1994.[51] 80% of the lions in Kruger National Park, South Africa, bordering to Mozambique, are infected by Feline Immunodeficiency Virus.[52]

Jackals and foxes since 1978, wild dogs since 1991, uncounted hyaenas, foxes and leopards died in East Africa, showing neurological symptoms like the lions.

In 1994 50% of the buffalos and 25% of gnus in Serengeti died, the surviving are in a bad health condition.

Imported and domestic cows are dying in Uganda[53].

Dromedars in the north of Somalia are showing Bovine Spongiform Encephalopathy-symptoms.[54]

Measles-viruses are in most of the cases named in articles in scientific papers to be responsible for those neurological and immunosuppressing diseases of seals, wales, dolphins, of elk, of buffalos, gnus, of lions, leopards, cheetahs, jaguars, jackals, hyaenas, and foxes. But they were never proven to be the causes for these mass-diseases. And they are unlikely to have mutated at so many places in the USA, England, Germany, Tanzania, Kenya and on coasts in North-America and Europe to cross the species barrier to such an extent and at so many places. For millions of years they had not affected f.e. cats. So we have to count for an immunosppressive agent enabling the infection of measles viruses.