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)

Vesicular stomatitis virus and encephalomyocarditis virus do not multiply in the majority of peritoneal macrophages freshly explanted from 4- to 8-week-old male or female mice. However, when peritoneal macrophages were cultivated in vitro for 3 to 5 days, these cells became permissive for both viruses. The loss of antiviral state in "aged" macrophages paralleled a significant decrease in the intracellular levels of (2'-5')oligo-adenylate synthetase activity. Although biologically active interferon was not detected in the nutrient medium of macrophage cultures, freshly harvested peritoneal cells could confer an antiviral state on monolayer cultures of mouse cells (aged macrophages, embryonic fibroblasts, and L cells) but not on heterologous chicken embryo, rabbit kidney, or human cells infected with vesicular stomatitis virus or encephalomyocarditis virus. The conferred antiviral state required at least 7 h to develop in target cells and was totally inhibited by the presence of antibody to mouse interferon alpha/beta but not to interferon gamma in the cocultures. Heterologous guinea pig and rabbit peritoneal cells could not transfer an antiviral state to target mouse cells. Donor peritoneal cells from mice preinjected with antibody to interferon alpha/beta could not transfer an antiviral state to target mouse cells. This ensemble of results indicating that freshly harvested peritoneal cells transfer interferon (which is responsible for inducing an antiviral state in susceptible mouse target cells) adds further experimental evidence that interferon is spontaneously expressed in normal mice and plays an important role in maintaining some host cells in an antiviral state.
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PMID:Mouse peritoneal cells confer an antiviral state on mouse cell monolayers: role of interferon. 300 78

RD-114 is a cell line which is partially responsive to interferon (IFN). Although both IFN-alpha and IFN gamma inhibit production of the resident retrovirus, they do not inhibit replication of other viruses, such as vesicular stomatitis virus and encephalomyocarditis virus, in these cells. In the studies reported here, we studied the characteristics of induction of seven IFN-inducible mRNAs in RD-114 cells. We observed that mRNAs 561, 6-16, 1-8, 2A, and 6-26 have similar induction characteristics in RD-114 cells and in HeLa cells, a fully responsive line. mRNA 2'-5'-oligo-adenylate synthetase (2-5(A) synthetase), however, was induced more efficiently by IFN-alpha in HeLa cells than in RD-114 cells. The same was true for the induction of metallothionein II mRNA by IFN-gamma. However, the latter mRNA was induced equally strongly in both lines when ZnCl2 was used as the inducer, suggesting that the gene is not defective in RD-114 cells. Although IFN-alpha induced 2-5(A) synthetase mRNA poorly and IFN-gamma did not induce it at all in these cells, a mixture of IFN-alpha and IFN-gamma induced this mRNA quite effectively, to a level of induction comparable to that in HeLa cells. Only 1 U of IFN-gamma per ml was sufficient to elicit this synergism, and the data suggested that an IFN-gamma-inducible protein was needed for this process. Induction of mRNA 561 by IFN-alpha in RD-114 cells, unlike that in HeLa cells, did not need ongoing protein synthesis. Once induced, this mRNA turned over rapidly in both cell lines, and this turnover could be slowed down by inhibiting protein synthesis in either cell line. IFN-induced mRNAs, such as 561 and 1-8, were polysome associated in IFN-treated RD-114 cells, suggesting that they were actively translated. Therefore, it is unlikely that the products of these IFN-inducible genes, by themselves, mediate the inhibition of replication of those viruses which are insensitive to IFN action in RD-114 cells.
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PMID:Expression of interferon-inducible genes in RD-114 cells. 310 49

Poly(1-vinyluracil) and poly(9-vinyladenine), as well as the corresponding polynucleotides poly(uridylate) and poly(adenylate), inhibit acute murine leukemia virus infection in mouse-embryo cells, but they do not significantly inhibit the replication of Sindbis and vesicular stomatitis viruses. The polymers were most effective as inhibitors when added during an early stage of virus replication. Effects of vinyl polymers on the RNA-dependent DNA polymerase from the virions of murine leukemia virus were also observed.
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PMID:Inhibition of murine leukemia virus replication by poly(vinyluracil) and poly(vinyladenine). 412 32

Oligonucleotides enriched in adenylate residues have been demonstrated in the genomes of two positive-strand RNA viruses, Sindbis and Columbia SK. Such oligonucleotides were not found in the genome of vesicular stomatitis virus, a negative-strand virus. The adenylate-rich oligonucleotides from Sindbis and Columbia SK viruses appeared similar when analyzed by zonal sedimentation in sucrose-sodium dodecyl sulfate.
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PMID:Correlation of messenger RNA function with adenylate-rich segments in the genomes of single-stranded RNA viruses. 433 95

Replication of vesicular stomatitis virus (VSV) is restricted in one human lymphoblastoid cell line (Raji), but not in another similar cell line (Wil-2), compared with growth in HeLa cells. This restriction is characterized by a low proportion of cells yielding infectious virus and is associated with limited production of 42S virion RNA. Primary transcription of 13S and 26S VSV-specific RNA is not restricted in Raji cells, and the 13S RNA produced contains adenylate-rich sequences. This suggests that the block in Raji cells involves some step required for the replication of virion RNA.
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PMID:Restricted replication of vesicular stomatitis virus in human lymphoblastoid cells. 435 8

Rabies virus polysomes contained two sizes of messenger RNAs, one of which had a sedimentation value of 30S and another which sedimented at 12 to 16S. RNA extracted from infected cultures contained virion-size RNA, 42S, as well as 30S and 12 to 16S RNA species. Hybridization studies indicated that the 30S and 12 to 16S RNAs had nucleotide sequences which were complementary to virion RNA. RNA. RNA isolated from virus polysomes contained adenylate-rich sequences which were heterogeneous in size and were determined to be about 100 to 250 nucleotides in length on the basis of their migration rates in polyacrylamide gels. Acid-urea agarose gel electrophoresis established that the 30S RNA material was composed of a single RNA species (mol. wt. greater than or equal to 1.65 X 10(6)), whereas the 12 to 16S material could be resolved into at least four distinct species whose mol. wt. ranged from 0.28 to 0.87 X 10(6). When labelled rabies-infected cell RNAs, which were purified by oligo(dT)-cellulose chromatography, were annealed to excess unlabelled virus RNA, digested with ribonuclease T2 and the RNA duplex molecules analysed by polyacrylamide gel electrophoresis, five duplexes could be separated. The mol. wt. of these duplexes were estimated to be 3.2, 1.4, 0.96, 0.55 and 0.39 X 10(6), when compared to the known mol. wt. of vesicular stomatitis virus (VSV) RNA duplexes. This study suggests that the replicative processes of rabies virus are very similar to VSV and that rabies virus proteins are probably translated from smaller than virion-size RNAs.
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PMID:Rabies virus-induced RNA synthesis in BHK21 cells. 742 63

Tumor necrosis factor (TNF) produces a dose-dependent inhibition of vesicular stomatitis virus (VSV), encephalomyocarditis virus (EMCV), and herpes simplex virus type 1 (HSV-1) replication in WISH cells. The antiviral activity of TNF against VSV and EMCV is greatly enhanced by combination with quercetin. Induction of 2',5'-oligo-adenylate (2-5A) synthetase by TNF is also enhanced by quercetin. Addition of polyclonal antibodies to human interferon (IFN)-beta completely blocked both enhancement of antiviral activity and 2-5A synthetase induction.
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PMID:Quercetin potentiates TNF-induced antiviral activity. 827 19

Tobacco infected with the plant rhabdovirus sonchus yellow net virus (SYNV) contains short, 139- to 144-nucleotide (nt) transcripts complementary to the 3' terminus of the negative-strand genomic RNA. These transcripts are similar to the leader RNAs associated with several animal rhabdovirus infections in that they are encoded by the same region of the genome, but the SYNV transcripts are nearly 3 times longer than the animal rhabdovirus leader RNAs. The SYNV leader RNAs differ markedly in sequence from the leader RNAs associated with strains of vesicular stomatitis virus and rabies virus, although the first 30 nt of all three transcripts are rich in adenylate residues. The nucleotide sequence determined directly from SYNV RNA and from recombinant DNA clones derived from SYNV RNA reveals a possible initiation site for transcription of the N-protein mRNA that is located 147 nt from the 3' end of genomic RNA. The sequence (UUGU) at this site is complementary to the first 4 nt of the N-protein mRNAs of animal rhabdoviruses. In SYNV, the first AUG codon in the putative N-protein mRNA is located 57 nt downstream (at positions 203-205 in the viral genome) and is followed by an open reading frame for the remainder of the 1020 nt determined in these experiments.
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PMID:Detection and sequence of plus-strand leader RNA of sonchus yellow net virus, a plant rhabdovirus. 1659 26