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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The single-stranded RNA genome of vesicular stomatitis virus (VSV, Indiana serotype, San Juan strain) yields approx. 75 RNase T1-resistant oligonucleotides ranging in size from 10 to 50 bases. Each of the five structural genes, isolated as duplex RNA molecules hybridized to complementary mRNA, contains two or more of these large oligonucleotides. One of the oligonucleotides is identified as part of the non-coding region near the 3' end of the genome. Comparison of these results with others indicate that the RNA sequence of VSV is apparently stable in the laboratory but not in the wild. RNase T1-resistant oligonucleotides are also shown for all five VSV mRN species. Whether the mRNA for these digestions are are isolated from duplex RNA molecules or as single-stranded RNA species, the oligonucleotide patterns for each mRNA are virtually identical, indicating that each mRNA is transcribed from contiguous sequences on the genome. Comparison with published oligonucleotide patterns obtained from other isolates of VSV or from VSV deletion mutants indicate that identity and changes in their genome structure can be correlated with specific structural genes.
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PMID:RNA synthesis of vesicular stomatitis virus. VIII. Oligonucleotides of the structural genes and mRNA. 22 8

Analyses of prototype vesicular stomatitis (VSV, Indiana serotype) mRNA-32P-labeled viral RNA duplexes have established the assignments of 65 of the 72 large oligonucleotides that are recovered by two-dimensional electrophoresis of RNase T1 digests of the viral RNA. Fifty of the oligonucleotides are recovered in the L RNA duplex, four each in the N, M, and NS duplexes, and three in the G RNA duplex. Studies of three small defective-particle RNA species indicate that they have only L gene oligonucleotides in addition to three of the seven unassigned oligonucleotides. Some L gene ordering of oligonucleotides can be postulated from the defective-particle RNA sequence analyses. Analyses of naturally occurring alternate isolates of VSV Indiana have established that by comparison to the prototype virus strain, the alternate isolates minimally have genome sequence differences in L, G, N, NS and/or unassigned regions of the genome. Changes in the genome have also been induced by vitro high-level mutagenesis of the prototype virus.
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PMID:Assignment of the large oligonucleotides of vesicular stomatitis virus to the N, NS, M, G, and L genes and oligonucleotide gene ordering within the L gene. 22 10

RNA genomes from standard vesicular stomatitis virus and two defective interfering (DI) particles dI 0.33 (DI-T) and DI 0.52, were purified and digested with RNase T1. The resulting oligonucleotides were labeled at the 5' end with [32P]ATP and separated by two-dimensional electrophoresis in polyacrylamide gels. All of the major oligonucleotides containing 20 or more nucleotides were sequenced. Those oligonucleotides that were thought to be in common by their migration on polyacrylamide gels actually did have identical sequences. Those oligonucleotides thought to be unique to the DI RNAs either differed by only one nucleotide from oligonucleotides of the standard RNA or contained new sequences which were complementary to known sequences at the 5' end. These data indicate that RNAs from DI particles are not simple deletions but contain point mutations and additional complementary sequences.
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PMID:Comparison of ribonucleotide sequences from the genome of vesicular stomatitis virus and two of its defective interfering particles. 626 Sep 89

The nucleotide sequence of the region which covalently links the complementary strands of the "snapback" RNA of vesicular stomatitis virus, DI011, is (Formula: see text). Both strands of the defective interfering (DI) particle RNA were complementary for their full length and were covalently linked by a single phosphate group. Because the strands were exactly the same length and complementary, template strand and daughter strand nucleocapsids generated during replication of DI 011 were undistinguishable on the basis of sequence, a property not shared by other types of DI particle RNAs. Treatment of the RNA with RNase T1 in high-ionic-strength solutions cleaved the RNA only between positions 1 and 1'. These results and the availability of the guanosine residue in position 1' to kethoxal, a reagent that specifically derivatizes guanosines of single-stranded RNA, suggest that steric constraints keep a small portion of the "turnaround" region in an open configuration. The sequence of the turnaround region was not related in any obvious way to the sequences at the 3' and 5' termini and limited the number of possible models for the origin of this type of DI particle RNA. Two models for the genesis of DI 011 RNA are discussed. We favor one in which the progenitor DI 011 RNA was generated by replication across a nascent replication fork.
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PMID:Structure and origin of a snapback defective interfering particle RNA of vesicular stomatitis virus. 626 Oct 12

In vivo transcription and polyadenylation at the junction of the L cistron and the 5'-terminal extracistronic region of vesicular stomatitis virus RNA was investigated. Annealing of 5'32P-labeled RNA representing the 5'-terminal noncoding 77 nucleotides of vesicular stomatitis virus genomic RNA to L gene mRNA resulted in specific duplex formation. Two specific RNase T1- and RNase A resistant duplexes, 66 and 77 nucleotides long, bound to oligodeoxythymidylic acid cellulose. The specific sizes of the duplexes and their selection by oligodeoxythymidylic acid cellulose chromatography demonstrated that they were covalently linked to the polyadenylic acid tail of L gene mRNA. These data strongly suggest that the viral polymerase polyadenylates L gene mRNA in vivo by using the stretch of seven uridine residues at the end of the L cistron and that the polymerase can resume transcribing the 5'-terminal extracistronic region, resulting in a covalent linkage of the transcript to the polyadenylic acid tail of L gene mRNA.
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PMID:In vivo transcription of the 5'-terminal extracistronic region of vesicular stomatitis virus RNA. 626 2

Detergent-disrupted vesicular stomatitis virus carried out in vitro transcription at a reduced rate in the presence of deoxyguanosine triphosphate. The transcripts annealed completely to excess vesicular stomatitis virus genomic RNA and consistent of the short leader RNA and even polyadenylated messenger RNA. Incubation with RNase T1 showed that the transcripts were resistant to cleavage. Nearest-neighbor analysis demonstrated that approximately two-thirds of the guanosine residues had been replaced by deoxyguanosine. The hybrid "deoxyguanosine-RNAs" carried cap structures which contained deoxyguanosine instead of guanosine. Competition experiments using both guanosine- and deoxyguanosine triphosphates indicated that GpppA and dGpppA cap structures were synthesized in approximately equal amounts at a ratio of 20 microM guanosine triphosphate to 50 microM deoxyguanosine triphosphate. Deoxyguanosine triphosphate was accepted by the polymerases of various strains and serotypes of vesicular stomatitis virus, demonstrating that its incorporation was a common characteristic. Deoxycytidine triphosphate could also substitute for cytidine triphosphate but to a lesser degree. Deoxyadenine, deoxyuridine-, and thymidine triphosphates were not or were very poorly accepted even at concentrations of 2 MM.
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PMID:In vitro transcription of vesicular stomatitis virus. Incorporation of deoxyguanosine and deoxycytidine, and formation of deoxyguanosine caps. 627 19

We examined the kinetics of synthesis in vitro of the 5' ends of the vesicular stomatitis virus mRNAs by analysis of specific RNase T1 oligonucleotides located near the 5' ends of the mRNAs. Our results indicate that, like synthesis of full-length mRNAs, the 5' ends of the mRNAs are synthesized sequentially, following the gene order N, NS, and M. Additional experiments with UV-irradiated virus demonstrated that synthesis of the mRNA regions containing these oligonucleotides is dependent on synthesis of the mRNA from the preceding gene. These results are inconsistent with a model of vesicular stomatitis virus transcription involving simultaneous initiation and presynthesis of leader RNAs 30 to 70 nucleotides long for each mRNA. We also characterized two small RNA species whose synthesis is highly resistant to UV irradiation. Partial sequence analysis indicates that these RNAs are a 5'-capped fragment of the N mRNA and a 5' fragment of the leader RNA.
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PMID:Sequential synthesis of 5'-proximal vesicular stomatitis virus mRNA sequences. 629 97

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