Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After inoculation with JHM strain into DBT cell monolayers, a persistently infected DBT cell culture was established without producing typical cytopathic changes after about 15th passages. By immunofluorescence virus specific antigen was demonstrated in 10 to 15% DBT cells. This persistently infected culture (JHM-CC) was resistant to superinfection with parental JHM, but such resistance was not shown against vesicular stomatitis virus. JHM-CC virus produced small plaques on DBT cell monolayers. Temperature sensitive (TS) mutant, defective interfering (DI) particle or interferon was not detected in the JHM-CC. To intracerebral inoculation with JHM-CC virus, cortisone treated ICR mice survived without showing clinical signs, however, demyelinating lesions were produced in the brain and spinal cord of them.
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PMID:Persistent infection with mouse hepatitis virus, JHM strain in DBT cell culture. 627 88

From DBT cells persistently infected with mouse hepatitis virus JHM strain (JHM-CC), a cell line producing neither infectious virus nor intracellular viral antigen was obtained after two passages in the presence of antiserum. In addition, 11 cell clones were manipulated from JHM-CC and found to be also free from the virus. These newly obtained cell line and 4 of 11 cell clones were shown to be resistant to JHM and the virus recovered from JHM-CC (JHM-CCV), while the other 7 cell clones were susceptible to both JHM and JHM-CCV as well as vesicular stomatitis virus. The susceptibility of all the cell clones and the newly obtained cell line to JHM and JHM-CCV became higher with passages. The observations were discussed in relation to the viral persistency in JHM-CC.
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PMID:Heterologous response of antiserum-treated cell clones from a persistently infected DBT cell line to mouse hepatitis virus. 630 51

After six to eight serial undiluted passages of mouse hepatitis virus (JHM strain) in DBT cell culture, a decrease in the yield of infectious virus occurred, and with further passages fluctuating yields of infectious virus were observed. The serially passaged virus interfered with the multiplication of the standard JHM virus, but not with vesicular stomatitis virus. After sucrose equilibrium centrifugation of high passage virus, a single peak contained both infectious virus and interfering activity. This virus population resembled the original JHM virus in its structural proteins, but it contained an increased proportion of a protein with a molecular weight of 65 X 10(3). Genomic RNA from standard JHM virus contained a single species of RNA with a molecular weight of 5.4 X 10(6). After five undiluted passages, however, the virion population contained two RNA species with molecular weights of 5.4 X 10(6) and 5.2 X 10(6). RNase T1 resistant oligonucleotide finger-printing of these RNAs showed that the lower molecular weight RNA had lost several oligonucleotide spots that were present in the genomic RNA of the standard JHM virus. After several serial diluted passages of passage 10 virus, a single virus population was obtained which again had only standard virus RNA with a molecular weight of 5.4 X 10(6) and lacked interfering activity. These results indicated that defective interfering particles were generated by serial undiluted passages of JHM virus.
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PMID:Defective interfering particles of mouse hepatitis virus. 632 37

For a eukaryotic virus to successfully infect and propagate in cultured cells several events must occur: the virion must identify and bind to its cellular receptor, become internalized, uncoat, synthesize viral proteins, replicate its genome, assemble progeny virions, and exit the host cell. While these events are taking place, intrinsic host defenses activate in order to defeat the virus, e.g., activation of the interferon system, induction of apoptosis, and attempted elicitation of immune responses via chemokine and cytokine production. As a first step in developing an imaging methodology to facilitate direct observation of such complex host/virus dynamics, we have designed an immunofluorescence-based system that extends the traditional plaque assay, permitting simultaneous quantification of the rate of viral spread, as indicated by the presence of a labeled viral protein, and cell death in vitro, as indicated by cell loss. We propose that our propagation and cell death profiles serve as phenotypic read-outs, complementing genetic analysis of viral strains. As our virus/host system we used vesicular stomatitis virus (VSV) propagating in hamster kidney epithelial (BHK-21) and murine astrocytoma (DBT) cell lines. Viral propagation and death profiles were strikingly different in these two cell lines, displaying both very different initial titer and cell age effects. The rate of viral spread and cell death tracked reliably in both cell lines. In BHK-21 cells, the rate of viral propagation, as well as maximal spread, was relatively insensitive to initial titer and was roughly linear over several days. In contrast, viral plaque expansion in DBT cells was contained early in the infections with high titers, while low titer infections spread in a manner similar to the BHK-21 cells. The effect of cell age on infection spread was negligible in BHK-21 cells but not in DBTs. Neither of these effects was clearly observed by plaque assay.
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PMID:Quantifying viral propagation in vitro: toward a method for characterization of complex phenotypes. 1173 54