
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 a 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 a breakdown of social relationships that are important for the preservation of 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 the 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 the 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 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.
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