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Tuesday, January 3, 2017


Mad Cow Disease, a transmissible fatal brain disease found in cattle

Mad Cow Disease, a transmissible fatal brain disease found in cattle

Mad Cow Disease is caused by artificial spreading of retroviral particles

Mass-diseases of Bovine Spongiform Encephalopathy (Mad Cow Disease) is caused by artificial spreading of retroviral particles bred in Campylobacter microbes. 

Bovine Spongiform Encephalopathy (BSE) was not introduced by food prepared out of sheep. Since several decades meat and bone meal from sheep and cattle have been fed to cattle and sheep without causing BSE.

Since its official recognition in 1986, Britain BSE has not in a single study, been induced in cattle, by feeding commercially made from sheep or any other commercially available material, "no evidence of an association with any single compound of proprietary feedstuffs."

None of the companies selling the material has been made responsible for causing the mass-slaughter of 180,000 cows.

There are no comparable numbers of diseases in the north of France and in Denmark, even though the same feedstuff from the United Kingdom is sold there. About 220 of cases of BSE occurred in cattle in Switzerland.

In Portugal, 940 inborne cattle plus 300, had been imported from Britain, France, and Ireland without connection to feedstuff giving rise to Mad Cow Disease from the United Kingdom.

The appearance of BSE diseases was a simultaneous emergence in a large number of flocks in defined regions of the United Kingdom. Absolutely, percentage wise rarely affected were cattle herds of farmers in the counties Buckinghamshire and East-Sussex, Durham, Yorkshire South, Derbyshire, Merseyside, and Essex, in Northern Ireland, Scotland, and in the Isle of Man.

The diseases were allegedly provoked by "commercially induced changes in the rendering of abattoir, butchers and knackers waste, resulting collectively from a fall in the value of tallow, a rise in the cost of energy and a need to replace the old plant with safer systems."

No single details of the pretended changes are given. The accused changes were not introduced in 1981 but in the late sixties.

According to scientific articles, the agent causing BSE can only be inactivated by heating up to 180 or even 270º Celsius and hardly by chemical means. In Scotland, few cattle were affected by BSE, because allegedly the old plants were not replaced.

In reality, the agent is inactivated by the old and the new methods. The World Health Organization (WHO) for example, considers gelatine, produced from infectious bones, to be safe for medical capsules. The product only allows a processing temperature of 140º Celsius. 

The theory of S.B. Prusiner of the undetected prions transmitted in food and in genetic material is stated without any proof and contradicting basic laws of nature, for example, of the Physico-chemical binding capacities in proteins. It can not be followed.

The British government could have reintroduced the former - the Scotish - extraction methods in the whole United Kingdom.

Allegedly the mass diseases started in 1981 because cattle were exposed to a meal made from the Scrapie-infected brain from sheep. To fulfill that condition, there must have been a many fold stronger increase in Scrapie of sheep before the BSE wave. There are no statistics which would underline that. The available numbers of Scrapie and the respective numbers of BSE are:

Scrapie BSE

1980- 104,  1981-112,  1982- 139,  1983-155,  1984-169,  1985-149 15, 1986-156 63,
1987-179 662, 1988-215 2184, 1989-246 7137, 1990-348 14181, 1991-989 25032
1992-666 36681, 1993-93 34370, 1994-73 23944, 1995-75 14282.

And if there was an increase of Spongiform Encephalopathy among sheep, it is unexplained, what has caused that increase? But there was also, at the same time, the mass infection in cattle and sheep.

In 1996, eight years after the ban of feeding, the accused material to ruminants, 300 cases of BSE/week are occurring in the United Kingdom. The majority of them are descendants born after 1992 to cows that were born after the implementation of the feed ban.

Contrary to the impression which the British government tries to create, today the diseases are transmitted to a large extent from cows to calves. In Portugal, 1994, the great-granddaughter of a cow imported from Great Britain was affected by BSE. But even the British government concedes that at a nonsignificant part of BSE is transmitted by this route.

By this claim about the significant part of transmission in food produced before the feed ban in 1988, the British government expresses that thousands of British farmers bought at the time of the feed ban in advance food for many years and intentionally infect their cattle; and that the cattle ate that horrible smelling material today.

On August 1, 1996, the British Ministry of Agriculture, Fisheries, and Food quoted the forming of the Spongiform Encephalopathy Advisory Committee (SEAC), SEAC statement on maternal transmission of BSE ... Of the 273 animals born to dams with BSE, 42 have developed histological confirmed BSE.  

This is a 15.4% transmission rate from cows with BSE to calves. The SEAC quoted by the British government converts this fact: The average transmission from cow to calf over the 60 months duration of infection in an animal prior to developing the clinical disease will be 1%. 

Mass diseases affecting brain and immunosystem like BSE in other animals and in other areas

Cows in Great Britain

Other mass-diseases of cattle in the United Kingdom must be seen connected with the occurrence of BSE.  Of 24,000 cows slaughtered in 1994 in the United Kingdom because of symptoms suspicious of BSE, 25% did not have pathological findings of the brain indicative of BSE. 

These 6,000 were affected by neurological symptoms and immunodeficiency. Especially in March/April diseases reminding of BSE but without visible lesions in the brain are observed. They correspond, for example, Downer Cows in the USA. 

Since about 1977 there was an increase of lameness of dairy cows connected with lactation, especially occurring in March and April, in the same regions of the British island where later increased BSE incidences appeared.

Cows in USA, Canada

In the USA annually about 100,000 cattle are slaughtered because of a brain-damaging neurological disease named Downer Cow Syndrome. 

This disease affects milk fever cows. It occurs in heavy milking cows... related to the calving period and if after futile treatment with calcium hypocalcemia is excluded as causing disorder the hind legs... extended... posteriorly... hyperaesthesia... and.... non-alert... of this Downer Cows should be compared with the BSE-symptoms. 

Contrary to claims of the USA-government at a considerable part these syndromes are the result of causes comparable to those of BSE.

In 1985, mink in Wisconsin were affected by an outbreak of Spongiform Encephalopathy caused by consumption of Downer Cows. 

Two bull calves, which were infected intracerebrally with the brain of the disease developed Spongiform Encephalopathy. 

The clinical signs of Downer Cow Syndrome were presented by cattle inoculated intracerebrally in 1979, with Scrapie-agents in Mission, Texas. 

When slaughtered 43, 44, or 73 days later, their brain did not (yet?; a.) show the histological findings of Spongiform Encephalopathy. 

But inoculated into mice it produced central nervous system signs in them. And a tissue from the cattle was found to be positive for prion protein, indicative of Spongiform Encephalopathy.

In 1993, the Canadian government ordered the slaughter of 270 cows on one ranch in Alberta, and 30 others on nine farms in Ontario. The pretended reason was, that BSE was diagnosed in one cow in Alberta. This cow was alleged of British origin.

Cows in Germany

In 1988, 9,000 calves had immediately to be slaughtered in Germany under emergency circumstances. The government claimed that they had been treated with too many hormones. The calves had even to be incinerated. 

Hormones are easily removed by the body in a few weeks. So the hormones were the pretext for other findings.

Sheep in Scotland, Germany, Australia, and the USA

The slaughtering of sheep in North England and Scotland, from 1986 to 1988, was already mentioned. 

From summer 1986 to July 1988, herds of sheep in Scotland and in the north of Britain had to be slaughtered on command of the British government, and they became forbidden for human consumption in the United Kingdom: 

Their stomach was said, to contain grass contaminated by radiation from Chernobyl. This given reason is invalid because it is possible to measure radiation and to select animals accordingly. 

By radiation, contaminated grass in the stomach does not make a sheep unfit for human consumption. Possibly, the sheep were affected by the same causes of Spongiform Encephalopathy like the cattle at the same time.

1,200 sheep were slaughtered in July 1990 in Germany because of Scrapie, 240 in the year 1991.

Sheep in Australia were dying allegedly because of eating a new plant. 

Between 1984 and 1988 in the USA, the number of Scrapie outbreaks in herds of sheep has increased by ten times compared to 1979.

Elk and deer in zoos in the USA, ready for export since 1967. In Fort Collins, Colorado, in the Wild Animal Disease Center of the USA-army cofinanced by the British Burroughs Welcome Company.  

Then in Sybille Wildlife Research Unit, Wyoming a deer died. Since 1979, especially in1984, some elks died there as well as connected to wildlife research facilities in Kremmling, Colorado and also a zoo in Canada. 

They died by a new Spongiform Encephalopathy named Chronic Wasting Disease of Deer and Elk (CWD).

90% of the deer in Fort Collins died or were killed, mainly 3-4 years old. Most affected were female elk. The origin of this disease has not been published. But in experimental feeding trials, they were fed with cow's milk starting at 1-5 days of age. 

The similarity of the disease with one caused by a neurotropic retrovirus ... in wild mice is mentioned in the reporting articles.

A possible effect of the diseases has been described: CWD should be of concern in interstate and international trade in captive cervids.

Elk in Sweden, deer in Austria

From 1985 till 1995, mostly female elk, in the southwest of Sweden bordering Lake Vanern, died in masses following neurological and immunodeficiency symptoms caused by retroviruses. In 1994, this disease was observed also among roedeers and deer. 

Since December 1986, masses of young deer died in Austria showing neurological symptoms and necrotic lesions of the brain.

Seals, whales, dolphins, sea cows

In 1988, 18,000 seals died on European coasts showing neurological symptoms, whales died around New Foundland, Canada and around Soviet-Union-Russia, dolphins around the North-American coasts. 

Sea cows died in masses in Florida, in 1990 and 1996. The Armed Forces Institute of Pathology of the USA military forces took care of the dead animals which had shown neuromuscular signs before death. 

The incidence in 1990 was explained by cold water stress and crashes with motorboats.  The incidences in 1996 are allegedly mysterious.

Tropical animals in zoos in England, Germany, and the USA, were affected by Spongiform Encephalopathy

Since 1983, in zoos in England, 6% of all Nyala-antelopes, 11% of Eland-antelopes in one zoo together with a mouflon and an Ugandan Ankole-cow and two domestic cats, 35% of Greater Kudu-antelopes (62% of those born since 1987), an Arabian Oryx cow and her calf, a Scimitar-horned Oryx, a puma and four cheetahs and in a German zoo three ostriches died because of Spongiform Encephalopathy. They were percentage wise much stronger affected than the British cows (less than 2% in 1996).

Lions, tigers, leopards in zoos in USA and Western-Europe affected by encephalopathies and retroviruses.

50 lions, three tigers, and one puma died between 1969 and end of 1972 because of an unknown infectious encephalomeningitis in a safari park in Germany. They had been fed with the meat of horses and of cows. In zoos in the USA because of unexplained neurological symptoms in 1982, two tigers died, and in 1988 two leopards in Iowa, in 1991 two leopards and a jaguar in Illinois.

In 1989 ten lions in a Safari Park in Germany died of similar neurological symptoms. In 1992, in a zoo in San Fernando, California, 35 big cats showed strange neurological symptoms. 

Of them, seven African lions, four Asian tigers, four African leopards, one Chinese leopard, and one jaguar died. Other indigenous North American cats were unaffected. In 1992, five tigers and one lion in a zoo in Acton, California showed the same neurological symptoms: two of the tigers died. 

Even though the symptoms of all the cats in Europe and the USA were unexplained, exclusively in only one lion of all those diseased cats an electroencephalogram and an analysis of the cerebrospinal fluid was done. The electroencephalograms of Spongiform Encephalopathies show typical changes.

57% of tested African lions in European zoos were infected by the retrovirus Feline Immunodeficiency Virus (FIV), but 0% of Asiatic lions in India.  


Encephalopathy is caused by particles of retroviruses, but 73% of Asiatic lions in the Lincoln Park Zoo in Chicago had Feline Immunodeficiency Virus-antibodies. FIV infection. 

It may well be that the high prevalence is caused by a factor associated with the zoo, the author of the article suspected.

In 41 of 109 tested big cats in the zoos in Europe, antibodies against the Virus of Infectious Anaemia of Horses (EIAV) were present. (EIAV is the original virus of HIV). 

Antibodies to EIAV found in most of the FIV positive animals indicates that there may exist an additional feline lentivirus. In one region in Florida, 30% of panthers captured between 1986 - 1988 had FIV antibodies.

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

Obviously, English zoos 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 programs. London zoo's circular says that any ungulate fed proprietary meal between 1980 and 1989 may be affected.

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

In April 1989, an Arabian oryx cow died in Londons Regent's Park because of BSE. Three months later, in July 1989, her nine-month-old calf, was shipped to Saudi Arabia. He died there on Aug 18, 1989. In Phoenix, Arizona, USA, 216 Arabian oryxes 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. 

From January 1988 to March 1989, fully vaccinated children in Oman were attacked by an outbreak of paralytic poliomyelitis, 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.

In Serengeti Park in Tanzania in 1994, during 14 days, over a distance of 1,000 km, 1,000 out of 3,000 lions died showing neurological symptoms reminding of Spongiform Encephalopathy. 

The lions were affected by the retrovirus Feline Immunodeficiency virus. 95% of the young cheetahs there did not survive in 1994. 

80% of the lions in Kruger National Park, South Africa, bordering to Mozambique, are infected by Feline Immunodeficiency Virus.

Jackals and foxes since 1978, wild dogs since 1991, uncounted hyenas, 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 rest that survived were in a very bad condition.

Imported and domestic cows are dying in Uganda 

Dromedary in the north of Somalia is showing Bovine Spongiform Encephalopathy-symptoms.

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, whales, dolphins, elks, buffalos, Gnus, lions, leopards, cheetahs, jaguars, jackals, hyenas, 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, for example, cats. So we have to count for an immunosuppressive agent enabling the infection of measles viruses.

BSE-agents cause also Chronic Fatigue Syndrome or Gulf War Syndrome

In the United Kingdom, in same regions, where BSE is prevailing in 1988, about 100,000 in 1996, 150,000, persons were reported to be affected by a mysterious, new disease affecting the brain, spinal cord, and immune functions called mostly Chronic Fatigue Syndrome. 

In the USA, the HIV-regions California-Nevada, Boston, New York, Houston, and Florida, since 1984 five million persons are reported to be affected. Clusters were reported in 1985 for Tuscon, Arizona, Lake Tahoe, Nevada, more than 400 patients in1984 till 1988. Lyndonville, N.Y, rural, transmission in raw milk since 1979, for Charlotte, North Carolina, for soldiers from the USA stationed in the Persian Gulf Area. 

It was reported among persons in Natal, South Africa in 1987. (Kwazulu in Natal experiences today the worst HIV/AIDS explosion in South Africa.) 

It is also called Chronic Fatigue Immune Dysfunction Syndrome (CFIDS), or Post Viral Fatigue Syndrome (PVFS), or Myalgic Encephalomyelitis (ME), or Gulf War Syndrome. 

Fatigue, depression, poor concentration, loss of memory, impaired balance, are the reported neurological symptoms, and fever, sore throat, cough, night sweats, painful lymph nodes, weakness, the pain of muscles, the rash caused by viruses and fungi are indicating an impaired function of T-lymphocytes. 

The disease starts with a flu-like illness with respiratory or gastrointestinal symptoms. Affected persons are women about 20 to 45 years old. White persons are eight times more frequent affected than non-white. 

Bovine Spongiform Encephalopathy, Downer Cow Syndrome, Creutzfeldt-Jakob Disease, Scrapie, Chronic Fatigue Syndrome, and AIDS are caused by exogenous and endogenous parts of retroviruses

Retroviruses cause Spongiform Encephalopathies by the direct effect of retroviral particles on neurons, Spongiform Encephalopathy is evoked.  Spongiform Encephalopathy is caused in mice by a retrovirus. 

Structures, indicative of retroviral infection, existing in all cases of Spongiform Encephalopathies

Tubulofilamentous (virus-like) particles are seen under electron microscope in all cases of Spongiform Encephalopathies in the brains of all affected animals and human beings.

In human beings, they had been observed beside Creutzfeldt-Jakob Disease-Kuru only extremely seldom; namely in the brain of some persons with Systemic Lupus Erythematosus, in Encephalomyelitis disseminata, in HTLV-1-infection, in cases of leukemia. 

These diseases are at least suspicious of retroviral involvement. Since 1983, it became known that lymphocytes, macrophages and endothelial cells of every person with AIDS contained this tubule filamentous particles which have to be considered subviral structures defective viruses.

Creutzfeldt-Jakob Disease is connected with retroviral particles,
the agent of Creutzfeldt-Jakob Disease has a virus like size and density. 

The agent of Creutzfeldt-Jakob Disease is a viral oncogenic particle.

The similarities of Creutzfeldt-Jakob Disease and infections of central nervous system by retroviruses like HIV were outlined by E. and L. Manuelidis. They point out that CJD-like agents might contain truncated or mutated retroviral sequences. 

Alternatively, the CJD agent might require `helper' functions of an endogenous retrovirus. As outlined for HIV among hemophilia patients the necessary cofactor for such endogenous retroviral particles could be Parvovirus.

The same might apply to Spongiform Encephalopathies. Aleutian Mink Disease underlines that.

Scrapie connected with retrovirus HIV

Parts of HTLV-3 (HIV) and Scrapie are identical. Other researchers were diminishing these findings. The relationship between PrP27-30 is at best distant but they admit the similarities.

Chronic Fatigue Syndrome connected with retroviral particles and effects

Sections of the genetic material of the human retrovirus HTLV-2, a close relative of the AIDS-virus, were present in Chronic Fatigue Syndrome patients and non-sexual contacts, but not in controls.

Some authors tried to create a diverging impression. For example Gow et al. selected as controls persons with diseases, which are itself suspicious of retroviral effects like Systemic Lupus Erythematosus, Rheumatoid Arthritis, Epilepsy, Migraine. 

Finding retroviral particles in the Chronic Fatigue Syndrome patients and in these controls, they claim these to be endogenous retroviral sequences, without any reason.

The existence of a virus containing sequences of both herpes virus and retrovirus in persons with CFS was proven with PCR (Polymerase Chain Reaction; a.) technique in 1991. (Emphasis by a.)

In Japan, where HTLV-1 and HTLV-2 are prevailing endemically, 30 Chronic Fatigue Syndrome patients showed a weak reaction comparable to the healthy controls. 

But in Western immunoblotting, 16 patients with Chronic Fatigue Syndrome showed clearly positive lanes in rgp21, gp21, Env gp46, and gag p26, indicative of HTLV-2 seropositivity.  They were different from the healthy controls which showed nothing. The article tries to create a different impression.

In the muscle of patients with Postviral Fatigue Syndrome, seven times more often than in controls persistence of enteroviruses proves the involvement of a retrovirus or endogenous retroviral sequences evoking immunosuppression.

In Jamaica, the existence of HTLV-1, another close relative of the AIDS-virus, was proven in persons with pains of muscles, impaired balance, weakness, resembling Myalgic Encephalomyelitis.

D. Diack reported having found by electron microscopic studies particles similar to the ultrastructure of Visna Virus (retrovirus) in lymphocytes of patients with Chronic Fatigue Syndrome. 

Research suggests that ME (Myalgic Encephalomyelitis; a.) is the result of a persistent infection, probably caused by a virus.

The abnormal results of the MRI (magnetic resonance imaging; a.) scan observed among these persons, similar in a population positive for human immunodeficiency virus.

Several types of retroviruses in respective mass diseases

Particles of different types of retroviruses are occurring in AIDS (HIVEIAV and HTLV-1 and HTLV-2), in Chronic Fatigue Syndrome (HIVEIAV and HTLV-1 and HTLV-2) in Creutzfeldt-Jakob Disease/Kuru (HIVEIAV and Scrapie-agent), and in Downer Cow Syndrome (BLV and Scrapie-agent and EIAV).

Identity of retroviral amino-acid sequences and amino acid sequences of messenger substances of animals and humans

Important biochemical effects of HIV-retrovirus are outlined in my book. It is described, here again, to show the parallels between biochemically induced hypothalamic effects of HIV and of the agents of Chronic Fatigue Syndrome, of Creutzfeldt-Jakob Disease, of Downer Cow Syndrome, and of Scrapie:

HIV attacks the body's forces of defense in two places:

One amino acid sequence of the core structure of HIV coincides in 44-50% with the amino acid sequence in one part of the hormone alpha1-thymosine-alpha1, which is produced by the human thymus gland. 

This hormone is required for the formation of the helper cells. When infected with HIV, the body incorrectly assumes, that it has sufficient alpha1-thymosine-alpha1: new thymosin is only produced to a lesser extent with the result that fewer helper cells are produced. 

Over and above that, antibodies formed by the body to fight the HIV then go into action, destroying both the HIV, which has penetrated from the outside and also the body's own alpha1-thymosine-alphal.

On the other hand, an amino acid sequence of the HIV-envelope (gp 120) equals the amino acid sequence of the Vasoactive intestinal peptide (VIP) formed in intestinal cells. 

This hormone is a messenger substance which regulates the release of important hormones, including Corticotropin Releasing-Hormone (CRH), which in relation to AIDS, is of decisive importance: CRH encourages production of cortisol.

Cortisol triggers off a vicious circle

Cortisol is a hormone produced by the human body which counteracts inflammations and allergies. Among others, it restricts helper cells activity and transfers them from the active blood circulation to the dormant area of the bone marrow.

Where the hormone balance is stable, a daily rhythm regulates the cortisol level in the blood, which in turn determines the daily rhythm of the helper cells in the blood. 

The cortisol level is highest at around six a.m.; by lunch time it has dropped sharply and only starts to rise again slowly from midnight onwards. 

The cortisol level in the blood of HIV-infected patients is higher than that of non-infected persons. 16 tests involving HIV patients yielded this result. 

Four study groups showed normal amounts of cortisol, whilst only one out of the 21 groups of scientists involved in this topic, up to 1990, found smaller amounts of cortisol in the blood of HIV-infected patients. 

All examinations based on the 24-hour rhythm produced higher values. There are fewer helper cells as a result of the raised cortisol level in the blood of patients affected by AIDS or who are in a possibly preliminary stage of the disease. Of decisive significance is the changing of the rhythm of cortisol production. 

The cortisol level of AIDS patients is constantly slightly raised, even during the night. Such a change in cortisol rhythm was already described in 1977 by physicians working in the Mulago hospital in Kampala, Uganda. 

What the twelve patients examined were actually suffering from, was not divulged. A sustained increase of cortisol, to a small degree, produces a particularly marked reduction in the quantity of T cells in the blood.

The Human Immunodeficiency Virus manages to upset the central regulation. The organism is taken in by the structure of HIV.

On one hand it figures to face neuro leu kin VIP, which is produced by the helper cells, and on the other hand, it figures to face its own hormone alpha1-thymosine-alpha1, while in reality, it is facing HIV-core-protein. 

Deception of the immunosystem thus sets in motion a chain-reaction: the Corticotropin-Releasing Hormone (CRH) yielded and scattered in error leads to increased release of the Adrenocorticotropic Hormone (ACTH). 

Because of the ACTH, the adrenal glands increase the production of cortisol. The cortisol then brings the organism to a state of partial immunodeficiency: agents of the AIDS diseases can now strike because the immunoreaction to unknown agents is impaired. 

(Against well-known agents several protecting mechanisms, which can not be influenced by cortisol were developed.) Neuroleukin - or rather HIV-gp120 in the case of HIV patients - leads also to a release in growth hormones, watery diarrhea, outbreaks of sweating, fever, and increased immunoglobulin synthesis.

An effect of feedback in healthy subjects is that cortisol impedes the production of the CRH signaling substance which has set this mechanism in motion. However, with AIDS, the feedback effect is canceled out once again because of production of ACTH at other places: leukocytes and lymphocytes being attacked by the virus release ACTH, which stimulates cortisol production. 

And HIV-infected monocytes stimulate even by themselves the adrenal glands to produce cortisol HIV increases the amount of cortisol and cortisol accelerates as a growth substance for HIV.

We see as HIV-effect an increase of neuro leu kin - VIP - type sequences of eight respectively five amino-acids, which evoke Growth hormone.

Growth hormone identical sequences can stimulate protein synthesis and are multiplied under the conditions of growth. (Growth hormone deficient persons in Central Africa, so-called Pygmies are unexpected rarely infected by HIV.) Comparable effects are produced by agents of Spongiform Encephalopathy-diseases.

The agent of Creutzfeldt-Jakob Disease evokes secretion of Growth Factor out of infected cells

Retroviral amino-acid sequences can stimulate lactation and can be multiplied under the conditions of lactation.

Affected cows (Downer Cows; a.) had significantly increased plasma levels of cortisol, fatty acids, high cortisol levels in the blood, significantly lower erythrocyte concentrations.

Patients with Chronic Fatigue Syndrome have enhanced release of ACTH and enhanced sensitivity to exogenous ACTH. But values for Cortisol are diminished.

DHEA is decreased in Chronic Fatigue Syndrome-like in AIDS patients. EIAV (HIV) is enhanced by the deficiency of calcium. Downer Cow Syndrome is likewise enhanced by the deficiency of calcium. This is connected with the functioning of the Reverse 

People of Jewish (and Italian) origin are preferred by attacks of agents causing AIDS diseases like Kaposi Sarcoma, Pneumocystis Carinii, as well as by agents causing Creutzfeldt-Jakob Disease. 

HIV prefers white persons before black persons, the same do the agents of Chronic Fatigue Syndrome.

15% of cases of Scrapie and of Creutzfeldt-Jakob Disease are caused by inherited agents. 12.8% of children of mothers with HIV-infection are born with HIV. 15.4% of calves of BSE-cows are born with BSE-agents according to the British SEAC. These figures signal similarities too.


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