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21. |
Autoimmune Diseases in Humans, e.g. Autoimmune Rheumatic Diseases |
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Intervirology,
Volume 35,
Issue 1-4,
1993,
Page 176-185
J.R. Kalden,
M. Herrmann,
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摘要:
In spite of increasing evidence that viruses and especially retroviruses could act as etiologic factors in autoimmune and especially autoimmune rheumatic diseases, clearcut evidence for an involvement of these agents is still missing. Findings, which, for example, indirectly support the hypothesis that retroviruses might play a part, are the demonstration of antibodies to the gp24 in SLE and Sjögren’s patients as well as the description of retroviral atnigens in the inflammed synovium of rheumatoid arthritis patients. Furthermore, evidence comes from animal models that viruses, such as the Visna or Caprine arthritis encephalitis virus, induced chronic inflammatory diseases in sheep and goats. More recently, a mouse model for rheumatoid arthritis and Sjögren’s syndrome was reported in mice transgenic for HTLV-ltax. It is hoped that, especially from the experimental animal models, the possible role of retroviruses as etiological factors in autoimmune rheumatic diseases can be clar
ISSN:0300-5526
DOI:10.1159/000150308
出版商:S. Karger AG
年代:1993
数据来源: Karger
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22. |
Viroids: The Smallest and Simplest Agents of Infectious Disease. How Do They Make Plants Sick? |
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Intervirology,
Volume 35,
Issue 1-4,
1993,
Page 186-195
T.O. Diener,
R.A. Owens,
R.W. Hammond,
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摘要:
Viroids are autonomously replicating pathogens of higher plants that consist solely of unencapsidated, single-stranded, circular RNAs of 246-375 nucleotides. Despite their extreme simplicity, viroids cause syndromes in plants that are about as varied as those caused by plant viruses. Because viroids are not translated, their effects on plants must be a consequence of direct interaction of the viroid with host constituents. Although the molecular mechanisms of viroid pathogenesis are still unknown, analysis of molecular chimeras between viroids of different pathogenicity levels has revealed that the severity of symptoms is the result of complex interactions among three of the five viroid domains. In vitro experiments with purified mammalian protein kinase P68 have shown that the enzyme is strongly activated (phosphorylated) by viroid strains that incite moderate to severe symptoms, but far less by a mild strain. Activation of a plant homolog of P68 may be the triggering event in viroid pathogenesis.
ISSN:0300-5526
DOI:10.1159/000150309
出版商:S. Karger AG
年代:1993
数据来源: Karger
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23. |
Foamy Viruses |
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Intervirology,
Volume 35,
Issue 1-4,
1993,
Page 196-207
D. Neumann-Haefelin,
U. Fleps,
R. Renne,
M. Schweizer,
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摘要:
Foamy viruses share complex genome organization with lentiviruses and certain oncoviruses. The open reading frame 3’ of env encodes a transcriptional transactivator. Distinct responsive sequences were identified in the long terminal repeats (LTRs) of simian (SFV-1 and SFV-3) and human foamy viruses (HFV). Transactivation of heterologous LTRs was described including those of simian and human immunodeficiency viruses. Foamy viruses persist for the whole lifetime in infected hosts (primates, cats, hamsters, cattle, and probably other mammals). The virus may be orally shed and transmitted, while being latent in various internal organs. Selective viral gene expression in the brains of mice transgenic for HFV has suggested a particular relationship to neural tissue. In latently SFV-3-infected cultured cells, methylation of proviral DNA is apparently involved in the control of latency. Demethylation as well as transfection with the transactivator were shown to be instrumental in viral reactivation. Natural infections with foamy viruses are common, elicit strong immune responses, and seem to be asymptomatic in nonhuman primates. Detection of such infections, however, may not be a triviality in man. While accidental transmission of foamy viruses to man is well documented, reported seroprevalence in human populations and the association of HFV with specific pathology (e.g. thyroiditis de Quervain, amyotrophic lateral sclerosis, and Graves’ disease) are controversial and remain to be pro
ISSN:0300-5526
DOI:10.1159/000150310
出版商:S. Karger AG
年代:1993
数据来源: Karger
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24. |
Bovine Spongiform Encephalopathy: An Appraisal of the Current Epidemic in the United Kingdom |
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Intervirology,
Volume 35,
Issue 1-4,
1993,
Page 208-218
Richard H. Kimberlin,
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摘要:
Bovine spongiform encephalopathy (BSE) is a food-borne infection of cattle caused by the use of contaminated meat and bone meal in concentrated feeds. The UK epidemic was initiated by a sudden exposure to infection in 1981-1982, which was associated with a dramatic reduction in the use of organic solvents in the manufacture of meat and bone meal. This change almost certainly removed two partial disinfection steps and allowed enough contamination with a scrapie-like agent to infect cattle. Although it is assumed that the epidemic originated with scrapie infection crossing the species barrier, cattle-to-cattle recycling of infection, via feed, amplified the epidemic very considerably. There would have been a strong tendency for recycling to select a single cattle-adapted strain of agent, and this strain of BSE could well be different from scrapie. There is evidence to support both predictions. Because the median incubation period of BSE is 4-6 years, clinical cases did not appear until 1985-1986, by which time the recycling of infection in cattle was probably well established. However, the average food-borne exposure to infection has remained low resulting in a mainly sporadic occurrence of BSE. Signs of an imminent decline in the epidemic were unmistakable early in 1993, which is over 4 years after the feeding of ruminant-derived protein was banned to prevent new infections of cattle.
ISSN:0300-5526
DOI:10.1159/000150311
出版商:S. Karger AG
年代:1993
数据来源: Karger
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25. |
Author Index, Vol. 35, 1993 |
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Intervirology,
Volume 35,
Issue 1-4,
1993,
Page 219-219
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PDF (59KB)
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ISSN:0300-5526
DOI:10.1159/000150312
出版商:S. Karger AG
年代:1993
数据来源: Karger
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26. |
Subject Index, Vol. 35, 1993 |
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Intervirology,
Volume 35,
Issue 1-4,
1993,
Page 220-220
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PDF (111KB)
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ISSN:0300-5526
DOI:10.1159/000150313
出版商:S. Karger AG
年代:1993
数据来源: Karger
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