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At least 19 recordsLinked to original sources
PubMed1977

Latent form of Scrapie virus: a new factor in slow-virus disease.

Scrapie is an unusual slow-virus disease of sheep which is very much like kuru and Creutzfeldt-Jakob disease, both fatal, slow neuological diseases of man. In mice, scrapie usually has an incubation period of about 6 months. Intraperitoneal inoculation of virus particles into newborn mice caused no disease, and there was no detectable virus replication for 1 year, but high titers of scrapie were present in the spleen and brain at 18 months. Virus replication occurred in mice injected from 4 days after birth by all inoculation routes, wheter or not they were injected with scrapie virus on day 0. The results suggest that scrapie virus replicates peripherally only in thymocytes, which are not present in mice until a few days after birth. The latent state suggests that the comparable human diseases could appear in later life as a result of perinatal infection. In some respects these diseases resemble premature senility.

Aging↗
PubMed1977

Classic slow virus diseases.

Two human disease, kuru and Creutzfeldt-Jakob disease, and two animal diseases, scrapie and mink encephalopathy, comprise the group designated the subacute spongiform encephalopathies. Studies on these four classic conditions have generated a new philosophy, new concepts, and new technology that provide a basis for the study of chronic diseases and latent infections of man and animals. These aspects are discussed more broadly and in variable detail in the references listed on the following page.

Animals↗
PubMedDate not supplied

[Discovery of viroids and possible relationship with human and veterinary medicine].

The researches of DIENER and co-workers and those of the SEMANCIK'S group, have recently established that some plant diseases, such as potato spindle tuber, citrus exocortis disease and chrysanthemum stunt, are caused by a new class of pathogens, named viroids. These are the smallest known agents (they are smaller than viruses) having a molecular weight of ca 10(5) daltons, and composed of a highly structured RNA, rich in guanine-cytosine base pairs without a capsid. Little is known about the origin, replication model and pathogenic mechanism of viroids and until now only speculations are possible on these subjects. Some properties of the unknown agents of slow virus diseases (scrapie, Kuru, Creutzfeldt-Jakob disease and mink transmissible encephalopathy), suggest that these alterations in the central nervous system are caused by a sort of animal viroid.

Animals↗
PubMed1977

An epidemiological study on paramyxovirus antibody titers in multiple sclerosis, systemic lupus erythematosus, and rheumatoid arthritis.

The present epidemiological study concerned and evaluation of the level of measles antibodies (hemagglutination inhibition (HI) assay) and para-influenza-1 (Sendai) antibodies (complement fixation (CF) test) in serum of 107 control individuals (38 women), 176 multiple sclerosis (MS) patients (93 women), 717 relatives to MS patients (361 women), 9 patients with systemic lupus erythematosus (SLE) (all women), 46 relatives to SLE patients (28 women), 57 patients with rheumatoid arthritis (RA) (37 women), and 143 relatives to RA patients (85 women). In MS and their relatives the HI titer value was significantly raised and the CF titer only insignificantly increased. In SLE the HI titers were insignificantly raised but the CF values significantly decreased. In RA HI values were insignificatly raised, but the CF values were significantly decreased among females lacking rheumatoid factor in serum. In the individuals under study, HI values did not correlate with CF values. In MS two groups of patients could be treated, i.e. one group with raised HI values and one with normal distribution of titers. The data obtained are discussed in light of the theory, that all three disease entities may be "Slow Virus Diseases".

Adolescent↗
PubMed1978

The illusion of simplicity: the medical model revisited.

Traditional medical models have been found to be linear, restrictive, and oversimplified. Only a truly biological model, encompassing evolutionary as well as molecular and cellular biology, can account for the complex origins, forms, and effects of disease, which are illustrated by a discussion of hepatitis B and slow virus disease. An updated biological model of disease takes into account predisposition to disease, the timing and route of infection, multiple disease forms, variable adaptive response, and the role of social and cultural factors and views disease as a failure of adaptation in one or more systems. Its application to psychiatry is shown in a discussion of stress, bereavement, and separation.

Adaptation, Physiological↗
PubMed1978

["Slow virus" infections and degenerative diseases of the central nervous system].

Slow virus infections of the central nervous system are produced by both conventional and unconventional viruses. Diseases of the central nervous system which are produced by unconventional viruses are discussed. They are kuru and the Creutzfeldt-Jacob disease. Mention is also made of the fact that these disease may be transmitted to animals which allows an infectious genesis to be assumed. The author also discusses the clinical symptomatology, the results of anatomical and pathological examinations, and the mechanism of transmission of the disease from one human being to another. Slow virus infection as a cause of other neurological diseases is also dealt with by the author in her present paper.

Animals↗
PubMed1979

Slow viruses and chronic disease of the central nervous system.

Although recognized since the 1930s, slow infections have only recently received considerable attention. There are three types, group A (related to the type C RNA viruses), group B (bizarre agents such as scrapie and kuru) and group C (viruses such as measles which normally produce acute infections but which are behaving here in an unusual fashion). These viruses are only united in that they produce disease with excessively long incubation periods. Many slow infections result in neurological diseases and these will be discussed, together with some possible explanations of their action.

Animals↗
PubMed1975

Zwoegerziekte virus, the causative agent for progressive interstitial pneumonia (maedi) and meningo-leucoencephalitis (visna) in sheep.

The final results of experimental infections with virus recovered from the lungs of sheep suffering from progressive interstitial pneumonia (=zwoegerziekte=maedi) are reported. The virus could be reisolated from blood samples of all experimentally infected sheep. Every animal produced antibodies against the virus. The neutralising, complement-fixing and precipitating antibodies remained present in the blood for six years. Fourteen out of 21 intrapulmonarily infected sheep developed clinical and/or histopathological lung lesions and in three a meningo-leucoencephalitis was detected in addition. One of these three developed the clinical and pathological signs of 'visna' 14 months after inoculation. Signs of visna were seen in eight of 10 sheep that had been inoculated intracerebrally. Furthermore, nine of these sheep suffered from progressive interstitial pneumonia. Hence the name maedi-visna virus is proposed for the agent which causes both disease entities. Three sheep that yielded virus after infection and in which antibodies were detected, did not develop histopathological lesions.

Animals↗