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

Interferon-alpha (IFN-alpha) and -gamma differed in their action against influenza virus and vesicular stomatitis virus (VSV) on pig cells. Recombinant IFN-alpha severely impaired the cytopathic effect of VSV on PK-15 cells, whereas recombinant porcine IFN-gamma did not. IFN-alpha impaired also the replication of VSV and of influenza virus in primary pig kidney cells in contrast to IFN-gamma, which failed to induce an efficient antiviral state against both viruses. Otherwise, the IFN system seemed to work properly in pig cells since both IFN-alpha and IFN-gamma induced an efficient antiviral state to mengovirus. The establishment of the antiviral state to VSV and influenza virus correlated with the induction of two cytoplasmic proteins related to the murine Mx protein involved in the selective resistance of mice to influenza virus infection. The results are discussed in the context of the susceptibility of pigs to influenza virus strains that are in circulation in birds and in humans.
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PMID:Virus-specific effects of recombinant porcine interferon-gamma and the induction of Mx proteins in pig cells. 133 54

The antiviral, antiproliferative, and natural killer (NK) cell activation by recombinant human interferon-consensus (IFN-Con1) has been compared with that of two other type I IFNs: IFN-alpha 2a (Roferon) and IFN-alpha 2b (Intron A). The specific activity (antiviral units/mg) of IFN-Con1 was 10-fold higher than that of the other two IFNs in the vesicular stomatitis virus (VSV)-HeLa antiviral assay. The antiproliferative activity on a molar basis of IFN-Con1 on Daudi cells and Eskol (a human leukemic hairy cell-like cell line) was significantly greater than that of IFN-alpha 2a and IFN-alpha 2b. IFN-Con1 also enhanced or induced NK cell killing of target cells to a greater extent than that of IFN-alpha 2a and IFN-alpha 2b. However, on antiviral unit basis, the activities were similar. These results would suggest that IFN-Con1 may be more effective at lower protein concentrations in clinical applications than other available IFNs.
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PMID:A comparison of interferon-Con1 with natural recombinant interferons-alpha: antiviral, antiproliferative, and natural killer-inducing activities. 157 83

IFN-alpha, -beta, and -gamma protect murine fibroblasts from lysis by vesicular stomatitis virus. In this report we show that culture supernatants derived from a Th cell clone of the TH2-type completely block the protective effects of the IFN. The active component in inhibiting IFN is identified to be IL-4. rIL-4 has similar effects as the T cell supernatant.
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PMID:Murine IL-4 antagonizes the protective effects of IFN on virus-mediated lysis of murine L929 fibroblast cells. 168 93

Vasoactive Intestinal Peptide (VIP) is able at the concentration 10 to 100 nM to induce in HT-29 cells 2'5' oligoadenylate (2'5' A) synthetase activity. The kinetics of this induction show that the maximal effect is attained after 24 hrs. VIP induces 2'5' A synthetase parallel to inhibition of vesicular stomatitis virus growth. The levels of these two induced activities after VIP treatment are comparable to those induced by the poly (I).poly (C), an inducer of IFN beta/alpha in mammalian cells. Moreover the anti-IFN beta/alpha antibodies abolish the VIP-induced 2'5' A synthetase whereas anti-IFN gamma antibodies are ineffective. The fact that VIP establishes an antiviral state in HT-29 cells potentiates new pharmaceutical applications for this neuropeptide.
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PMID:[Vasoactive intestinal peptide induces 2',5'-oligoadenylate synthetase and antiviral state in cells of HT-29 colonic cancer]. 169 May 91

Both fixed and street rabies virus when cultivated in McCoy cells caused cytopathic changes 24 to 72 h after infection, depending on the multiplicity of infection. The cytopathic effect (CPE) was easily recognizable and resembles that induced by other members of the Rhabdovirus group, such as vesicular stomatitis virus, in several cell cultures. Higher titers of the Pasteur strain (PV) of fixed rabies virus were found in supernatants of McCoy cells when compared to those in VERO cells. The virus titer increased with the number of passages attaining a high titer after three passages. Rabies antigens were detected by direct immunofluorescence labeling in most McCoy cells of the infected culture, and specific antibodies neutralized the virus growth and CPE. There was also inhibition by treatment of the cells with human interferon (HuIFN) -alpha or -gamma, but not by murine interferon (MuIFN) -alpha, -beta or -gamma. Rabies-infected McCoy cell cultures may provide a useful assay system, based on the induction of CPE, the high virus production and the sensitivity to IFN.
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PMID:Cytopathic effect induced by rabies virus in McCoy cells. 169 Dec 1

The role of N2-methyl-9-hydroxy-ellipticine (NMHE) and N2,N6-dimethyl-9-hydroxy-ellipticine (DMHE) in modulating the antiviral activity of poly (A-U) was examined using a human foreskin fibroblast-vesicular stomatitis virus (HSF-VSV) bioassay in which the concentration of poly (A-U) was fixed at 0.05 mM or 0.2 mM while the NMHE or DMHE concentration was varied to produce variable NMHE (or DMHE)/ribonucleotide ratios ranging from 1:16 to 2:1. Poly (A-U), NMHE and DMHE tested individually were not efficacious antiviral agents. When the poly (A-U) was combined with the NMHE or DMHE, the antiviral activity of the poly (A-U) was potentiated 16- to 20-fold a NMHE (or DMHE)/ribonucleotide ratios in the region of 1/4. Poly (A-U), NMHE and DMHE induce beta-IFN. The interferon-inducing activity of the NMHE (or DMHE)/poly (A-U) combination was equal to the sum of the interferon-inducing activity of the poly (A-U) alone and the NMHE (or DMHE) alone. The direct viral inactivation study demonstrated that NMHE, DMHE, poly (A-U) and the NMHE (or DMHE)/poly (A-U) combinations did not inactivate VSV at concentrations near the 50% viral inhibitory dose. Photomicrographs of HSF cells incubated with NMHE alone or with a NMHE/poly (A-U) combination suggest that poly (A-U) affects the subcellular distribution of the NMHE by steering the NMHE to the nucleolus. These observations suggest that modulation of a nuclear process may be responsible for the enhanced antiviral activity.
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PMID:In vitro antiviral activity of poly (A-U) and ellipticines. 169 7

Transforming growth factor-beta (TGF-beta) at concentration of 10 ng/ml inhibited the development of the interferon-alpha- (IFN-alpha) or IFN-gamma-induced antiviral state in quiescent human embryonic fibroblasts. The action of the cytokines was dose-related; TGF-beta had no direct effect on the replication of either vesicular stomatitis virus (VSV) or encephalomyocarditis virus (EMCV) used as the challenge viruses in the IFN assays. We suggest that despite the fact that TGF-beta acts mainly as a "negative" growth factor, its interactions with IFNs in the antiviral assays resemble known effects of the typical "positive" peptide growth factors.
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PMID:Transforming growth factor-beta inhibits the antiviral action of interferons in human embryonic fibroblasts. 171 87

The early events that occur after treatment of the highly interferon alpha (IFN-alpha)-sensitive human lymphoblastoid Daudi cell line with human leukocyte IFN-alpha have been examined. IFN-alpha treatment of Daudi cells results in a rapid and transient increase in the cellular content of diacylglycerol, which occurs in the absence of inositol phospholipid turnover, or an increase in intracellular calcium concentration. Furthermore, IFN-alpha treatment results in a selective, time-dependent activation of the Ca(2+)-independent epsilon isoform of protein kinase C (PKC), while the alpha isoform is unaffected by IFN-alpha treatment. In contrast, IFN-alpha treatment of an IFN-resistant subclone of Daudi cells had no effect on the diacylglycerol content of cells and on the activation of PKC-epsilon. The selective PKC inhibitor staurosporine blocked the transcriptional activation of IFN-alpha-stimulated genes, the cytoplasmic accumulation of mRNAs for these genes, and the induction of antiviral activity by IFN-alpha against vesicular stomatitis virus in IFN-sensitive cells. These observations suggest that transmembrane signaling of IFN-alpha involves diacylglycerol production and activation of PKC-epsilon in Daudi cells.
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PMID:Transmembrane signaling by interferon alpha involves diacylglycerol production and activation of the epsilon isoform of protein kinase C in Daudi cells. 183 72

CTL-mediated selection for loss of expression of Mta by H-2-heterozygous SV40-transformed mouse fibroblasts (line 24SV) produced an unusual phenotypic class of maternally transmitted Ag negative mutants defective in both MHC expression and in anti-viral activity. Severely reduced surface expression of class I MHC Ag from multiple loci of both haplotypes correlated with low levels of MHC H chain and beta 2-microglobulin mRNA. Inasmuch as IFN can up-regulate class I expression and some fibroblasts elaborate autocrine IFN-beta, we examined whether IFN could restore wild-type expression of class I MHC Ag. However, IFN could not restore wild-type expression. Moreover, the fold-increases in class I Ag and mRNA expression were significantly reduced in mutant cells compared to wild-type cells. These results suggested that the mutants might have generalized defects in IFN response. Inasmuch as the induction of an anti-viral state is a hallmark of IFN responses, we exposed cells to IFN-alpha, -beta, or -gamma and challenged with virus. 24SV cells, exposed to any of the three IFNs, were completely protected from destruction by vesicular stomatitis, mengovirus or respiratory syncytial viruses. In contrast, MHC and anti-viral defective mutants could not be protected from virus-induced lysis by any IFN. Somatic cell hybridization analyses indicated that both basal MHC and IFN-inducible phenotypes were recessive to wild-type, and that a trans-acting regulatory factor required for basal MHC expression is defectively expressed in the mutants. Such a factor may integrate the organismal response to virus infection, encompassing both immune and nonimmune anti-viral responses.
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PMID:Mutational analysis of regulation of MHC and anti-viral genes. 184 75

Interferon-alpha (IFN-alpha) production was investigated in whole-blood cultures of 66 bladder cancer patients and 65 control subjects. IFN synthesis was induced with Sendai virus, and IFN activity was assayed in FL cells challenged with vesicular stomatitis virus (VSV). The mean levels of the IFN-alpha produced were 5,724 +/- 2,288 IU/ml in the control subjects and 4,800 +/- 2,353 IU/ml in the bladder cancer patients. IFN-alpha production was significantly suppressed in the bladder cancer patients compared with that in the control subjects (P less than 0.05). The impairment in IFN-alpha production correlated with the tumor grade, and it was shown that the tendency toward decreased IFN-alpha production was closely associated with the advancement of the tumor stage. Our results suggested that the decreased IFN-alpha production may contribute to the disordered immunoregulation in bladder cancer patients.
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PMID:Impaired interferon-alpha production in whole-blood cultures from bladder cancer patients. 185 48


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