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)

The cytopathic effects of vesicular stomatitis virus (VSV) that result in the rounding of BHK21 cells have been studied. The results indicate that they are mediated by a sequential alteration in the distribution of the components of the cytoskeleton, an effect that requires the expression of the viral L protein. The constituents of the cytoskeleton of BHK21 cells were analyzed by fluorescence microscopy. Actin filaments were the first component to become disorganized, so that disassembly of stress fibers were detected 1 hr after infection. The distribution of microtubules and intermediate filaments was unchanged at 2 hr after infection; however, both these cytoskeletal elements exhibited an altered distribution at 3-4 hr after infection. Actinomycin D and cycloheximide did not cause the same effects as infection with VSV, suggesting that inhibition of host-cell gene expression was not responsible. However, viral gene expression was required, since cells infected with uv-irradiated VSV showed the same distribution of cytoskeletal constituents as mock-infected controls. Cells infected at 39.5 degrees (the nonpermissive temperature) with mutants of VSV temperature sensitive in the viral NS (ts G22), N(ts G41), M(ts 0 23), and G(ts 0 45) proteins showed the same changes in the cytoskeleton as those detected with wild-type virus. In contrast, cells infected with ts G11 (L-) showed the characteristic effect of VSV on the cytoskeleton when incubated at 34 degrees (the permissive temperature), but not when incubated at 39.5 degrees. The T-1026 R1 mutant of VSV, which has a much less dramatic effect on cell morphology than wild-type virus, also caused a less marked disruption of the cytoskeleton.
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PMID:Sequential disassembly of the cytoskeleton in BHK21 cells infected with vesicular stomatitis virus. 216 5

We investigated optimal conditions for cytotoxicity to tumor cell lines by recombinant human tumor necrosis factor (rhTNF) and the effect of amino-terminal deletions on the bioactivity of the rhTNF molecule. Two of four deletion muteins (-4 and -7) of rhTNF exhibit 2- to 3-fold enhancement of cytotoxicity/cytostasis against a variety of human carcinomas, a fibrosarcoma, and a melanoma cell line with no toxicity on normal fibroblastic and epithelial cultures. Of the two other muteins the -8 displayed equivalent and/or increased cytotoxicity/cytostasis while the -10 was consistently less cytotoxic than the parent on the same cell lines. Continuous exposure to TNF for greater than or equal to 96 h led to maximal cytotoxicity to tumor lines (99.99% with L929 cells) with no evidence of recovery. Pretreatment with actinomycin D (0.003-10 micrograms/ml for 1 h) rendered 82% of rhTNF-resistant cell lines (both tumor and normal) susceptible to its cytotoxic action within 24 h. However, the highest nontoxic concentrations of Actinomycin D necessary for rendering normal cell lines susceptible to TNF action were about 10-3000-fold higher than those necessary for converting resistant tumor cell lines. Similarly, preinfection of L929 cells with vesicular stomatitis virus (multiplicity of infection, 10(-2)-10(-4) for 1 h) rendered the cells 2-10-fold more susceptible to the cytotoxic action of rhTNF in 18 h. Our data suggest that rhTNF and its muteins represent potentially useful anticancer agents; however, adequate dosing and prolonged exposure may be critical in demonstrating cytotoxicity/cytostasis. The data also show that although normal and tumor cell lines became susceptible to cytotoxicity by rhTNF and actinomycin D, combination therapy of the two agents may be possible at defined concentrations.
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PMID:Biological effects of recombinant human tumor necrosis factor and its novel muteins on tumor and normal cell lines. 379 Dec 1

The in vivo synthesis of polycistronic transcripts of vesicular stomatitis virus in human amnion U cells and mouse L cells was detected by RNA blot hybridization. Within the molecular weight range resolved by this gel electrophoresis system, all possible combinations of sequentially linked messages were observed, as identified by their patterns of hybridization and their apparent molecular weights. Actinomycin D pretreatment of mouse L cells did not affect the frequency or size of polycistronic messages, nor did these differ between L cells and U cells. Vesicular stomatitis virus polycistronic transcripts were synthesized in vivo in a roughly uniform distribution, except for the NS-M dicistronic mRNA, which was much more frequent. Most of the polycistronic RNA species were found to be poly(A)+, but at least one, the tetracistronic molecule N-NS-M-G, was clearly poly(A)-. Analysis of RNA following treatment with RNase H in the presence of oligo(dT) indicated that the in vivo-synthesized poly(A)+ polycistronic species NS-M, M-G, and N-NS-M had poly(A) tracts at their 3' molecular termini but not internally at their intercistronic junctions.
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PMID:Detection of in vivo synthesis of polycistronic mRNAs of vesicular stomatitis virus. 615 26

In cultured Drosophila melanogaster cells, vesicular stomatitis virus (VSV) established a persistent, noncytopathic infection. No inhibition of host protein synthesis occurred even though all cells were initially infected. No defective interfering particles were detected, which would explain the establishment of the carrier state. In studies of the time course of viral protein synthesis in Drosophila cells, N, NS, and M viral polypeptides were readily detected within 1 h of infection. The yield of G protein and one of its precursors; G1, was very low at any time of the virus cycle; the released viruses always contained four to five times less G than those produced by chicken embryo cells, whatever the VSV strain or serotype used for infection and whatever the Drosophila cell line used as host. Actinomycin D added to the cells before infection enhanced VSV growth up to eight times. G and G1 synthesis increased much more than that of the other viral proteins when the cells were pretreated with the drug; nevertheless, the released viruses exhibited the same deficiency in G protein as the VSV released from untreated cells. Host cell control on both G-protein maturation process and synthesis at traduction level is discussed in relation to G biological properties.
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PMID:Vesicular stomatitis virus growth in Drosophila melanogaster cells: G protein deficiency. 624 42

Prostaglandins are potentially useful antiviral agents, however their mechanism of action is unclear. Recent evidence suggests that RNA transcription of vesicular stomatitis virus (VSV) is inhibited by prostaglandins (Bader and Ankel, J. Gen. Virol. 71, 2823-2832, 1990). Prostaglandins are known to have multiple effects on cells which may or may not be related to their antiviral action. We examined the effects of prostaglandins on cells and on VSV RNA polymerase in vitro to seek the mechanism of antiviral action. Actinomycin D inhibited cellular RNA synthesis but failed to block the antiviral activity of prostaglandins on VSV. Thus induction of host cell RNA transcription is not involved in the antiviral action. Neither modulation of the cellular glutathione level by prostaglandins nor formation of prostaglandin-glutathione conjugates was required for the antiviral action. The relative inhibition of VSV RNA polymerase in vitro by prostaglandins with different structures correlated to inhibition of VSV replication in infected cells. This result indicates that the same step in VSV replication is inhibited by prostaglandins both in the in vitro RNA polymerase assay and in the infected cell.
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PMID:Antiviral effect of cyclopentenone prostaglandins on vesicular stomatitis virus replication. 753 50