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.

Spread of AIDS and HIV

Excerpt from book “AIDS – Origin, Spread and Healing“.

4.1     Centers for Disease Control informed in advance

Pneumocystis carinii-pneumonia in Los Angeles – Neoplasma of skin, Kaposi’s sarcoma in New York – Centers for Disease Control name “risk groups” – The “risk groups” in chronological order – The AIDS theory is complete. Contradictory information spread


To date, no epidemic of such major importance has been discovered at such an early stage as the mass disease AIDS. It was already referred to as a catastrophe at a time when it had not reached mass proportions. Within an unparalleled shortness of time as far as medical science is concerned, there not only appeared descriptions on the spread of this hitherto officially unknown disease, but the responsible agents which had not appeared before in human beings were also named.

4.1.1     Pneumocystis carinii-pneumonia in Los Angeles

On the 5th June 1981, a report was published in the Centers for Disease Control’s Morbidity and Mortality Weekly Report (MMWR) journal under the heading of “Pneumocystis pneumonia – Los Angeles”[160]. This report was the first publicised starting shot for the mass AIDS diseases that were to follow. The responsible author was a scientist of the University of California in Los Angeles, Michael S. Gottlieb. The paper began with the memorable sentence: “In the period October 1980 – May 1981, 5 young men, all active homosexuals, were treated for biopsy-confirmed Pneumocystis carinii-pneumonia at 3 different hospitals in Los Angeles, California”.

Besides suffering from Pneumocystis carinii-pneumonia (PCP), the five also suffered from two further infections which had been triggered by the Candida albicans fungus and the Cytomegalo Virus (CMV). The first four were victims of atypical mycobacteria of the Mycobacterium avium complex[161]. These agents were far more rare and much more remarkable than Pneumocystis carinii, Candida and CMV. But these were not at all mentioned until 1982. The significance which is attributed to the Pneumocystis carinii-pneumonia disease should be explained. However, this was not done in the paper. The patients’ age was between 29 and 36 years. This age group is referred to as ‘adult’, both in everyday speech and in specialist medical literature. Hitherto nearly exclusively children had fallen ill with PCP. The adjective “young” for the five men is misleading. What was also striking was the description of details of their sexual activities (“all practising homosexuals”). It later transpired that none of the patients knew of one another or had any mutual acquaintances or had any contact with someone suffering from a similar disease. The patients had no comparable history of sexually transmitted diseases. It was reported that two of these patients had “frequent homosexual contact with different partners”. What actually led the authors to research into and describe the sexual inclinations of these five patients? Up to this point in time, there were no reports stating that Pneumocystis carinii-pneumonia or immunodeficiency were sexually transmitted. The Centers for Disease Control explanation to the Gottlieb article stated that the cause of impaired cellular resistance function could be due to a “common exposure that predisposes individuals to opportunistic infections”. In cases of “previously healthy homosexual males with dyspnea and pneumonia”, physicians should in future, consider Pneumocystis carinii-pneumonia as being the cause. Such a proposal could, at that time, only be made by fortune-tellers or persons with secret imformation.

4.1.2     Neoplasma of skin, Kaposi’s sarcoma in New York

One month later, in July 1981, there appeared another Centers for Disease Control report in the MMWR entitled “Kaposi’s sarcoma and pneumocystis pneumonia among homosexual men – New York City and California”[162]. This introduced 26 cases of Kaposi’s sarcoma (KS), the second important symptomatic disease of AIDS. Of the 26 patients, 20 came from New York. The first actual scientific contribution on “Kaposi’s sarcoma in homosexual men” was published on the 19th September 1981 in Lancet[163]. It deals with the case histories of eight men. The authors were trying to justify why Kaposi’s sarcoma which, no doubt was rare but not unknown, was specifically treated as a new disease for these particular patients.

The first argument put forward was, that opposed to previous cases, younger men are now affected. That is quite incorrect: In his description of the clinical picture of six persons, leading to classification of the disease for the first time in 1872 and hence its introduction to medical science, the Austrian physician Moriz Kaposi actually made reference to a 45 year old, a 40 year old and an eight year old patient[164]. The eight New York patients were between 27 and 45 years of age. Furthermore, the Lancet authors believe that the skin symptoms no longer predominantly affect the lower limbs but rather the body as a whole. However, this would not correctly reproduce the observations made by Kaposi. Kaposi named: the feet, hands, chin, cheek, upper lip (patient 1); soles of the feet, hands, arms, eye lids, nose, intestine (patient 2); left sole of the foot or lower leg (patients 3, 4 and 5; Kaposi did not have anything specific to say about the 6th patient). The Lancet thus quoted, for diagnosis purposes: head (patient 1); head, trunk, arms (patient 2); head, trunk, arms (patient 3); trunk, arms, legs (patient 4); chest, arms (patient 5); trunk, arms, legs (patient 6); trunk, arms, legs (patient 7) and also the head and back (patient 8). These minor changes in the Lancet article compared with Kaposi’s observations do not justify the reporting of an allegedly new disease in a scientific journal. Also the observation, that “the disease” (even at that time designated as such in the singular, in only eight patients) was adopting a more aggressive course is wrong. Instead of eight to 13 years, the patients’ duration of survival is generally a period of less than twenty months. Hence even this is not new: Of Kaposi’s six patients, one went home after two months to die, one died after six weeks and one after one year. Kaposi estimated: “the disease ultimately leads to death, within a short period of two to three years.” Of the eight Lancet patients, four were dead after 30 months; four survived of whom two were cured at the time of publication. One of the two, a “34 year old Italian” was included in a study by Friedman-Kien[165] in 1990 as an example of a mild form of Kaposi’s sarco­ma without HIV-infection and without any impairment to the relationship between the helper cells and suppressor cells. Neither the number nor the age of the patients, nor the affected parts of the body or the aggressiveness of the diseases, would give an impartial physician cause to talk about a new disease. Let us stick with the homosexuality of the “young” men. Since Kaposi’s sarcoma occurs in men in 95% of cases and since the eight diseases were diagnosed by eight physicians in three special clinics, it is quite striking, that the patients’ sexual orientation was worth mentioning. Noticeable also is the manner in which the “black” patient was described: “The only black patient in our study was born in America and had never been to Africa”. He is characterised by the term “the only” which suggests an under representation, although one of eight US citizens (12%) has dark skin-colouring. The country of birth was only given for the patient with the dark skin colour, and not for the other seven. And exclusively with respect to this patient it is mentioned that he “had never been to Africa”.

The “Task Force on Kaposi’s Sarcoma and Opportunistic Infections”, a specialists group was founded very early by the Centers for Disease Control. The group was first mentioned under this name in August 1981 in the third MMWR paper[166] on cases of Pneumocystis carinii-pneumonia and/or Kaposi’s sarcoma.

4.1.3     Centers for Disease Control name “risk groups”

The “risk groups” in chronological order

AIDS has not become a mass infection in many states. For pale-skinned persons, in NATO-states, AIDS remained an illness affecting almost exclusively homosexual men, iv.d.u. persons, haemophilia patients and recipients of blood-transfusions. Persons with dark skin-colouring are however at risk of being affected by AIDS (see below). The Centers for Disease Control justified this obvious spread with the existence of “risk groups”. By August 1981 it was obvious, that not only homosexual men became afflicted by Kaposi’s sarcoma and opportunistic infections (OI). The “Follow-up on Kaposi’s Sarcoma and Pneumocystis pneumonia” names 95 homosexual and six heterosexual men as well as one woman, who suffered from Kaposi’s sarcoma/OI without any obvious cause at that point of time[167]. It was already mentioned in the first report, that one of the five Pneumocystis carinii-pneumonia patients was taking drugs intravenously[168]. Drugs were made an issue in the official survey first in June 1982[169]. But the question of a possible consumption of drugs was mentioned and answered at this time only for those 152 patients suffering from Pneumocystis carinii-pneumonia and not for others. The description of patients refers “races” for the first time: “Whites”, “Blacks” and “Hispanics”. The “Hispanics” designation was supposed to relate to inhabitants from one of the Latin American states. What is also remarkable is the allocation according to skin colour: Of the Pneumocystis carinii-pneumonia homosexual male patients, 68% were “white”, of the heterosexual men only 31% were “white”, and of the women 12.5% were “white”. (The same ratio applies, even when the numbers of diseases are far higher; see chapter 4.2).

One month later – in July 1982 – the Centers for Disease Control published a report depicting Haitians being a “population” particularly afflicted by the new disease[170]. Already one week later haemophilia patients were named as  a further “risk group”, after three cases of Pneumocystis carinii-pneumonia were registered from among these[171]. This is the first time, the assumption is voiced, that agents could also be possibly transmitted through blood products. On the 15th of September 1982 the categorisation of the spread of AIDS was complete. Under the title “Current Trends: Update on Acquired Immunodeficiency Syndrome (AIDS)-United States”, the Centers for Disease Control for the first time claimed that this was an epidemic with a high growth-rate. It also named the “risk groups” affected and supplied a case definition[172]. Classification into “risk groups” is hierarchical: Whosoever is listed in a higher ranking category, will not be listed in any further group, even if he is ascribed to a further group. At this point in time, the risks lay in the following hierarchical sequence: “homo- or bisexuality” (75%), “intravenous drug users” (13%), “Haitian origin” (6%) and “haemophiliacs” (0.3%). However, 5.7% of patients are not registered in this classification. In December 1982 the first report of an AIDS case due to blood-transfusion was published[173]. This was a newborn baby which was given a blood-transfusion together with red corpuscles and blood platelets. One of the donors had developed AIDS and died in August 1982[174].

At the end of 1982, the Centers for Disease Control published case-histories of four children who were suffering from serious infections and immunodeficiency. Two children had Haitian parents whose condition of health was said to be unknown to the Centers for Disease Control. The mothers of the other two, allegedly consumed drugs and were affected by immunodeficiency[175]. At the beginning of 1983, the Centers for Disease Control finally introduced two women with immunosuppression whose steady partners were AIDS patients[176]. Whilst the AIDS-definition of the Centers for Disease Control proved right for one of the women, the other woman only had swollen lymph nodes and a reversed helper cells/suppressor cells-quotient less than 1. In the “Editorial” “Note” to the report, the Centers for Disease Control emphasised that there must obviously be an infectious agent for AIDS which is transmitted by homosexual or heterosexual intercourse. Four out of the 12 other female patients, who were neither Haitian women nor iv.d.u. persons, were the regular sexual partners of men taking intravenous drugs. This served as a further justification of the thesis[177]. Besides them, reference was also made to six children of whom five were suffering from Pneumocystis carinii-pneumonia and one from Mycobacterium avium intracellulare-infection. A further 12 children known to the Centers for Disease Control were supposed to have suffered from immunodeficiency but not from life-threatening opportunistic infections. Consequently by the end of 1982, there were 22 children in the USA suffering from unexplained immunodeficiency. Ten of these had mothers who were taking drugs intravenously, and two mothers were of Haitian origin. No “risk” was mentioned for the ten others.

AIDS theory is complete. Contradictory information on spread

In March 1983, the Centers for Disease Control stated, that the following were at risk: homosexual men, iv.d.u. persons, Haitians, recipients of blood or blood products, sexual partners of AIDS-infected persons or persons coming under one of the “risk group” categories, as well as children of mothers from the “risk groups”. The distribution of AIDS cases is similar to that of hepatitis-B, which is transmitted either via sexual intercourse, through contaminated syringes or blood products[178]. This statement, however, had to be restricted by the authors themselves, since up to that time no cases of AIDS were established from among hospital staff or laboratory employees. In the case of hepatitis-B these latter represented roughly 1/3rd of patients affected. Up to that time, according to the article no other form of person to person transmission could be recognised to have taken place other than through intimate contact or blood-transfusion[179]. To these “risk groups” named until the beginning of 1983, an addition was made in 1984 to include all persons born in the Caribbean, and the largest “risk group” – all persons born in Africa, South of the Sahara.[180]