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Monday, February 26, 2018


HIV-Aids virus: Diseases are deliberately and easily spread in many ways, for example, through food, water, vaccines, air-spray, and blood transfusion

HIV-Aids virus: Diseases are deliberately and easily spread in many ways, for example, through food, water, vaccines, air-spray, and blood transfusion

In 1969, at the age of twenty-three, Johan van Dongen was appointed as a laboratory animal keeper at the Department of General Surgery, in the basements of the Dijkzigt Hospital in Rotterdam, part of the Erasmus University, in Holland.

Because of his experience with dead animals as a butcher/poulterer, he acquired much knowledge about the anatomy of animals. 

During a period of six years, Johan studied the professions of Laboratory Animal Keeper, Animal Technology at the University of Leiden, The Netherlands, and graduated in 1973. 

From May 1972 till 1976, Johan studied at HBO/LOI Leiden, as Experimental Microsurgery at the Erasmus University Rotterdam, the Netherlands and graduated as an “Around Experimental Microsurgeon” in May 1976.

In 1972, during a weekly laboratory meeting, Johan van Dongen asked his professor Dr. Westbroek, about Cytomegalovirus infection amongst kidney patients in the hospital.

And he replied “Cytomegalovirus CMV? Johan, that dangerous virus could be a cross between flu and a herpes virus, built into a bacterium and then it looks like protozoa.”

The words of his mentor Professor Dr. D.L. Westbroek, at the Erasmus University Rotterdam, the Netherlands, never left Johan's mind because, during his forty-two years of investigation into the origin of Ebola and AIDS-causing viruses, he came to the same conclusion.

Immediately after the statement of  Westbroek made it forced Johan to dive into the university's library at once, exactly on his birthday May 15, 1972, at the age of 26 and discovered that those microorganisms were tested predominantly on black people in concentration camps and Africa.

In a monomaniac circumstance, Johan investigated the role of the medical, pharmacological and military presence of foreign countries in Africa and what they were doing in their bio-warfare plants in the African Jungle and why several outbreaks of horrific diseases took place. 

Johan was shocked about his discoveries after he found 16 scientific papers the same day in world's famous medical journals (references below).

During his appointment at the Erasmus University, Rotterdam, Johan van Dongen was involved with pre- and postoperative treatment with cyclosporine in 1971, the management of small bowel allograft rejection and graft-versus-host disease. 

This investigation was meant to find a solution for the atomic bombs era and the fall out in Sub Saharan countries.

Together with his colleague Dr. Wil Kort, Johan van Dongen performed hundreds of small bowel transplantations in rats in order to investigate graft versus host reactions with the same results as described by Daniel Kuritzkes.

Daniel Kuritzkes

Daniel Kuritzkes, a researcher working with two 'Boston patients' who may have been cured of HIV, speaks at an AIDS conference in Kuala Lumpur, Malaysia. Still, researchers and doctors are excited about the news, especially because the Boston patients’ treatment differ from the Berlin HIV number zero patient’s regimen in one key way. 

Timothy Ray Brown was given stem cells that were predisposed to resist HIV infection, because the donor happened to have a mutated version of a key protein — CCR5 — that is needed for HIV to infect cells. So Brown’s transplant was akin to gene therapy with HIV-resistant cells. 


According to Krech CMV is the single most important cause of infectious diseases after organ transplantation. It affects 75% of the organ recipients during one year after transplantation. 

In a prospective study, it was found that 80% of seronegative recipients converted to seropositivity after they received a kidney from a seropositive donor.

Summarizing 16 studies of kidney transplantations, scientists calculated that 52% of pretransplant seronegative recipients became primarily infected after transplantation and converted to seropositivity. 

Since not all donors of kidneys were seropositive, one can surmise that practically all seropositive donors had latent CMV infections that were reactivated in the recipient. 

Similar figures were obtained after cardiac, liver and marrow transplantations. This is evidence that probably all organs in seropositive subjects have latent CMV infection.

The most important statement of Krech was, after Johan van Dongen contacted him in September 1972, after the discovery of CMV in kidney patients, that 100% of all black blood donors were infected with CMV most probably caused by contaminated vaccines.

Krech U, Jung M, Sonnabend W. A study of complement-fixing, immunofluorescent, and neutralizing antibodies in human cytomegalovirus infections. Z Immunitatsforsch Exp Klin Immunol. 1971 Jun;141(5):411–429.

An overview of the former university lecturer's professional career

The Dutch scientist/micro-surgeon and former lecturer at the University of Maastricht, Johan Van Dongen, and Belgian journalist and writer, Joel Savage

The Dutch scientist/micro-surgeon and former lecturer at the University of Maastricht, Johan Van Dongen, and Belgian journalist and writer, Joel Savage

Johan van Dongen's experience with Cyclosporin, a medicine that causes lymph node cancer

However, when a new immunosuppressive agent was introduced in our laboratory in renal, heart and small bowel transplantation, such as cyclosporine or tacrolimus, CMV disease was not enhanced. 

In fact, all types of transplantations cited above were performed at our university where similar prednisone-cyclosporine immunosuppressant regimes without anti-lymphocyte serum ALS were used.

Organ transplantations must have some unknown general or local immunosuppressive effect apart from the drugs used. Indeed, CMV pneumonia, pneumocystis pneumonia PCP, is such a problem after organ transplantations. 

During his experiments what exactly happened also with kidney, heart, and small bowel transplantation in rats had a similarity with patients in Dijkzigt Hospital Rotterdam. He told professor Westbroek about his findings.

History of an AIDS-like virus

Over hundred years ago, developments in pathologic anatomy led to the recognition of the morphological cellular characteristics of infection by CMV. It took another fifty years before the virus was successfully cultured and isolated. 

The elucidation of its epidemiology and its wide scope of infection followed when methods to measure intact virus and specific immunity became available.

The second half of the twentieth century was characterized by rapid advances in human technology and medicine as well as break down of social relationships that are important for the preservation of the family and individual health. These changes have had a profound effect on CMV infection and diseases.

There are increasing numbers of individuals who are immunodeficient in general or specific ways and who are prone to CMV infection such as is the case in HIV patients. 

The scope of CMV diseases has extended from a previously rare lethal, congenital infection to increasing numbers of patients who have undergone organ transplantation and who are immunosuppressed for the survival of their grafts leading to AIDS.

Break down of social relations contributed in the eighties to the emergence of a worldwide pandemic of AIDS, a new disease of mankind that specifically destroys cellular immunity, the type of immunity responsible for holding latent CMV infection in check. CMV diseases are an integral part of a clinical side of AIDS. Moreover, retroviruses starting to grow when CMV is added.

The understanding of the molecular and chemical events of viral reproduction has made possible the development of effective antiviral compounds. They are able to arrest viral replication and restrict some of the pathologic processes of CMV diseases. They do not have a long-lasting effect, however, unless immunological competence can be restored.

The basis of persistence of CMV infection is a latent infection. As long as CMV infection can revert to the latent state, it is incurable. Latent CMV lurks behind appearances and acts like fifth columnists which can activate into a lytic infection and subvert the host. Our understanding of latency, limited though it is, has not been dedicated technologically to its elimination.

We need new approaches to antiviral therapy targeted against latency. Along with a basic understanding of the molecular biology, a parallel technological, pharmacological approach is needed. 

One is faced with the same type of challenge in this regard as in the development of a vaccine against CMV and subsequently HIV.

According to the discoverer of the HIV virus, Luc Montagnier, CMV is equal to HIV, Equine Infectious Anaemia virus EIAV, and Mucosis Fungoides, discovered by a Dutch scientist Elisabeth van Der Loo.

And as far as the American Centers for Disease Control CDC is concerned, in your weekly reports MMWR's, it is stated CMV is discovered in the mid-fifties of the last century. To remind this so-called authoritative institute CMV is discovered long before and used as biowarfare agents by Hitler's scientists in order to make Jews and blacks susceptible.


Ribbert H (1904) Ueber protozoenartige Zellen in der Niere eines syphilitischen Neugeborenen und in der Parotis von Kindern. Zbl All Pathol 15:945–948

Jesionek A, Kiolemenoglou B (1904) Ueber einen Befund von protozoenartigen Gebilden in den Organen eines hereditar-luetischen Foetus. 

Muenchner Med Wochenschr 51:1905–1907
Lòwenstein C (1907) Ueber protozoenartige Gebilde in den 

Organen von Kindern. Zbl Allg Pathol 18:513–718
Von Glahn WC, Pappenheimer AM (1925) Intranuclear inclusions in visceral disease. Am J Pathol 1:445–465

Lipschuetz B (1921) Untersuchungen ueber die Aetiologie der Krankheiten der Herpes genitalis. Arch Dermatol Syph 136:428–482

Farber S, Wolbach S (1932) Intranuclear and cytoplasmic inclusions (protozoan-like bodies) in the salivary glands and other organs of children. Am J Pathol 8:123–135

Wyatt JP, Saxton J, Lee RS, Pinkerton H (1950) Generalized cytomegalic inclusion disease. J Pediatr 36:271–294

Fetterman GH (1952) A new laboratory aid in the diagnosis of inclusion disease of infancy. Clin Pathol 22:424–425

Minder WH (1953) Die Aetiologie der Cytomegalia infantum. Schweiz Med Wochenschr 83:1180–1182

Enders JF, Weller TH, Robbins FC (1949) Cultivation of the Lansing strain of poliomyelitis virus in cultures of various human embryonic tissues. Science 109:85–87

Weller TH, Macauley JC, Craig JM, Wirth P (1957) Isolation of intranuclear inclusion producing agents from infants with illnesses resembling cytomegalic inclusion disease. Proc Soc Exp Biol Med 94:4–12

Smith MG (1956) Propagation in tissue cultures of a cytopathogenic virus from human salivary gland virus (SVG) disease. Proc Soc Exp Biol Med 92:424–430

Rowe WP, Hartley JW, Waterman S et al (1956) Cytopathogenic agent resembling human salivary gland virus recovered from tissue cultures of human adenoids. Pro Soc Exp Biol Med 92:418–424

Weller TH (1953) Serial propagation in vitro of agents producing inclusion bodies derived from varicella and herpes zoster. Proc Soc Exp Biol Med 83:340–346

Weller TH (1970) Cytomegalovirus: the difficult years. J Infect Dis 122:532–539


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