Western blot (immunoblot) assay of small, round-structured virus associated with an acute gastroenteritis outbreak in Tokyo.
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Small, round-structured virus (SRSV) was detected in a stool specimen of a patient during an acute gastroenteritis outbreak in Tokyo and was tentatively named SRSV-9. SRSV-9 was purified by sucrose velocity gradient centrifugation after CsCl density gradient centrifugation. The buoyant density of SRSV-9 appeared to be 1.36 g/ml in CsCl. A Western blot (immunoblot) assay using the biotin-avidin system revealed that SRSV-9 was antigenically related to the Hawaii agent but distinct from the Norwalk agent and contained a single major structural protein with a molecular size of 63.0 +/- 0.6 kilodaltons. The prevalence of SRSV-9 infection in Tokyo was surveyed by the Western blot antibody assay by using a crude virus preparation as the antigen. Seroconversion was observed in 56.5% of the patients involved in the outbreaks from which SRSV was detected by electron microscopy. (+info)
Preliminary studies on the biology of Borna disease virus.
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Borna disease virus (BDV) is an unclassified agent that causes neurological disease in a wide range of animal species and possibly in humans. The infectious nature of BDV has been long established but, despite extensive progress on the pathogenesis of the infection, the aetiological agent is still uncharacterized. Recent studies have shown that BDV replicates productively in cultures of foetal rabbit glial cells (FRG) which produce a virus-specific protein that is easily detected immunocytochemically. This provides a marker for BDV infectivity. This cell culture system was used to investigate the replication cycle of BDV. The agent required at least 1 h to bind to and penetrate the cells and the antigen was detected 24 h later. Cycloheximide and actinomycin D inhibited production of the antigen in inoculated cells, indicating that both protein synthesis and a DNA-dependent function were required for the production of viral antigen. Cocultivation of BDV-infected FRG cells with Vero cells resulted in a persistent productive infection in the latter. Use of these cells showed that the infectious agent matured exclusively in the cytoplasm and within the plasma membrane of the cell. Antigen-laden nuclei did not have infectivity. These studies showed that BDV has the physical and replicative properties typical of conventional viruses but its mechanism of replication and site of morphogenesis may be unique. (+info)
Friend and Moloney murine leukemia viruses specifically recombine with different endogenous retroviral sequences to generate mink cell focus-forming viruses.
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A group of mink cell focus-forming (MCF) viruses was derived by inoculation of NFS/N mice with Moloney murine leukemia virus (Mo-MuLV 1387) and was compared to a similarly derived group of MCF viruses from mice inoculated with Friend MuLV (Fr-MuLV 57). Antigenic analyses using monoclonal antibodies specific for MCF virus and xenotropic MuLV envelope proteins and genomic structural analyses by RNase T1-resistant oligonucleotide finger-printing indicated that the Moloney and Friend MCF viruses arose by recombination of the respective ecotropic MuLVs with different endogenous retrovirus sequences of NFS mice. (+info)
Experimental infection of sheep and goats with transmissible mink encephalopathy virus.
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In a study to learn more about the pathogenicity of transmissible mink encephalopathy virus for the natural hosts of scrapie, 20 Cheviot sheep and 19 dairy goats were inoculated intracerebrally with the Idaho strain of the virus. Five sheep and nine goats became affected with a progressive neurological disease. The incubation period in the sheep varied from 45 to 80 months (mean, 65 months) and in the goats from 31 to 40 months (mean, 35 months). Except for degeneration of the cerebral cortex (neocortex), the disease was indistinguishable clinically and neurohistologically from scrapie. During two more passages of the virus in goats, the incubation period was shortened to 12 to 15 months, the morbidity rate rose to 100% (6/6 dairy goats and 3/3 African pygmy goats), and the cortical lesion became constant and more pronounced. By the intracerebral inoculation of pastel mink, transmissible mink encephalopathy virus was detected in the brains of several affected sheep and goats but not in extraneural sites (lymphoid tissues and intestine), except for a trace amount in the proximal colon of one goat. Even after two passages in goats, the virus remained nonpathogenic for the laboratory mouse. Despite the essential likeness of the experimental disease and scrapie, the common identity of their causal viruses remains to be determined. Even so, the results of this study are still compatible with the view that transmissible mink encephalopathy virus almost certainly is scrapie virus whose biological properties became altered by chance passage in mink, a carnivore and an aberrant host. (+info)
Temporal distribution of transmissible mink encephalopathy virus in mink inoculated subcutaneously.
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Information was sought on the temporal distribution of transmissible mink encephalopathy virus in royal pastel mink inoculated subcutaneously with 10(3.0) 50% intracerebral lethal doses of the Idaho strain. As determined by intracerebral assay in mink, extremely little replication of the virus occurred during the preclinical stage of infection. It seemed largely limited to lymph nodes draining the site of inoculation. Virus first appeared in the central nervous system (CNS) at 20 weeks, when all mink were still clinically normal. Early spongiform degeneration, limited to the posterior sigmoid gyrus of the frontal cortex, was first found at 28 weeks, or a few weeks before onset of clinical disease in most of the mink. Once virus reached the CNS, where greater concentrations occurred than elsewhere, it appeared in many extraneural sites (spleen, liver, kidney, intestine, mesenteric lymph node, and submandibular salivary gland). These seemingly anomalous findings, especially the limited extraneural replication of virus as a prelude to infection of the CNS, suggest that mink are not natural hosts of the virus. The results of this study support the generally held view that transmissible mink encephalopathy arises from chance or inadvertent infection of ranch mink with an exogenous virus, most likely feed-borne wild scrapie virus. (+info)
Temporal replication of the Pullman strain of Aleutian disease virus in royal pastel mink.
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Information was sought on the temporal replication of Aleutian disease virus in 27 royal pastel mink. Groups of three were examined 8 to 126 days after they were inoculated subcutaneously with 10(3) 50% lethal doses of the Pullman strain. Much individual variation was noted in the onset of infection, occurrence of viremia, and extent of virus replication in the tissues. Thus, virus was detected in lymph nodes regional to the site of inoculation in only some mink during the first 14 days after inoculation. During this period, virus was often present as well in the mesenteric lymph node and spleen. First detected on day 10, viremia was present in all mink examined on day 28 but occurred irregularly thereafter, even when virus was widespread in the tissues. Except in five mink succumbing to the disease, the tissue distribution of virus after day 28 tended to be more limited, and the titers were generally lower than they had been earlier. Even though present in the lymph nodes and spleen, virus was often absent from the kidney, liver, and intestine after day 28. Specific antibody was detected on day 28 and was present in all mink thereafter, ostensibly without any adverse effect on virus replication. In most mink, the infection was considered subclinical, for it was usually not accompanied by a rise in serum gamma globulin or by morphologic evidence of the disease. The virologic findings in this study have a bearing on the relationship of subclinical infections to both horizontal and vertical transmission of the virus. (+info)
Characterization of the Snow Mountain agent of viral gastroenteritis.
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Snow Mountain agent (SMA) is a 27- to 32-nm virus which is the etiologic agent of outbreaks of acute gastroenteritis in Colorado and Vermont. SMA is morphologically similar to but antigenically distinct from the Norwalk and Hawaii agents of viral gastroenteritis but, like those agents, has not been cultivated in vitro. We purified and characterized SMA directly from human stool specimens containing the virus. The density of the SMA virion was 1.29 g/cm3 and 1.21 to 1.22 g/cm3 on potassium tartrate-glycerol gradients and 1.33 to 1.34 g/cm3 on cesium chloride gradients. SMA had an S value of 170 to 183S on a sucrose velocity gradient. The purified virion was iodinated, immunoprecipitated with acute and convalescent sera from volunteers challenged with SMA, and analyzed on polyacrylamide gels. The virion contains one major structural protein of 62,000 molecular weight, which is similar in size to the 59,000-molecular-weight protein found in the Norwalk virion. The biophysical properties and single structural protein of SMA most closely resemble those of the calicivirus group. (+info)
Enzyme-linked immunosorbent assays for Snow Mountain and Norwalk agents of viral gastroenteritis.
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Enzyme-linked immunosorbent assays (ELISAs) for antigen detection and blocking ELISAs for serum antibody rises were developed for the Snow Mountain and Norwalk agents of viral gastroenteritis. The ELISAs were as sensitive as the existing radioimmunoassays and were specific for the Snow Mountain or Norwalk agent. The blocking ELISAs detected the same number of significant rises in antibodies to these agents as did the existing blocking radioimmunoassays. (+info)