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)

Mouse L-A9 cell interferon was induced by infection with Newcastle disease virus. Interferon production was 1.5 X 10(5) IU/10(7) cells. Interferon was partially purified by precipitation with ammonium sulphate, chromatography on CM-Sephadex and hydrophobic chromatography on octyl-agarose. The specific activity of the final preparation was 1.7 X 10(7) IU/mg protein. Treatment of L-A9 cells with 20 IU/ml interferon prior to viral infection inhibited the intracellular accumulation of reovirus-specific double-stranded RNA. Dose-response studies of the cells to interferon indicated that L-A9 cells require 10, 13 and 15 IU/ml to obtain 50% viral plaque reduction for Marituba virus, vesicular stomatitis virus and reovirus, respectively. The present results demonstrate the potential of mouse L-A9 cells as an interferon-producing system and also as a model for the study of the effect of cellular response to exogenous interferon treatment on the replication of RNA viruses.
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PMID:Interferon induction in mouse fibroblast L-A9 cells. 383 78

A mutant cell line of porcine kidney cells that resists the cytopathic effect of influenza virus has been obtained and characterized. These cells, designated ESK-R, were originally obtained by prolonged cultivation of cells surviving influenza B/Kanagawa/73 virus infection. No infectious virus was recovered from ESK-R cells, and no evidence for the presence of virus antigens in the cells was demonstrated by immunofluorescent staining. ESK-R cells also showed a distinct resistance to various other strains of both types A and B influenza viruses. The growth of mumps, Sendai, or Newcastle disease virus was considerably restricted, but the cell line normally supported the replication of vesicular stomatitis virus. ESK-R cells were found to lack specific receptors for influenza virus as determined by fluorescence-activated cell sorter analyses. The membrane barrier of ESK-R cells was successfully overcome by nonspecific endocytosis of calcium-coprecipitated virus particles followed by production of an appreciable amount of progeny virus.
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PMID:Characterization of a porcine kidney cell line resistant to influenza virus infection. 397 72

The 3' end of the genomic RNA of Newcastle disease virus (NDV) has been sequenced and the leader RNA defined. Using hybridization to a 3'-end-labeled genome, leader RNA species from in vitro transcription reactions and from infected cell extracts were found to be 47 and 53 nucleotides long. In addition, the start site of the 3'-proximal mRNA was determined by sequence analysis of in vitro [beta-82P]GTP-labeled transcription products. The genomic sequence extending beyond the leader region demonstrated an open reading frame for at least 42 amino acids and probably represents the amino terminus of the nucleocapsid protein (NP). The terminal 8 nucleotides of the NDV genome were identical to those of measles virus and Sendai virus while the sequence of the distal half of the leader region was more similar to that of vesicular stomatitis virus. These data argue for strong evolutionary relatedness between the paramyxovirus and rhabdovirus groups.
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PMID:RNA sequence and transcriptional properties of the 3' end of the Newcastle disease virus genome. 402 52

Virazole (1-beta-d-ribofuranosyl-1,2,4-triazole-3-carboxamide) is a highly soluble new synthetic nucleoside having significant, reproducible activity against a broad spectrum of deoxyribonucleic acid and ribonucleic acid viruses in vitro. The drug inhibited viral cytopathogenic effects in monolayers of cells infected for 3 days with type 3 adeno, types 1 and 2 herpes, myxoma, cytomegalo, vaccinia, infectious bovine rhinotracheitis, types 1A, 2, 8, 13, and 56 rhino, types 1 and 3 parainfluenza, vesicular stomatitis, subacute sclerosing panencephalitis, Semliki Forest, Newcastle disease, and measles viruses. Hemagglutinin production by influenza A(2), influenza B, and type 1 parainfluenza viruses in chicken embryo cells was reduced by Virazole treatment. Recoverable intra- and extracellular virus titers were reduced by the drug in experiments with type 1 herpes, vaccinia, type 3 parainfluenza, and vesicular stomatitis viruses. Plaque formation by type 1 herpesvirus was also inhibited by exposure of the infected cells to Virazole. Pretreatment of cells with the compound, followed by its removal before addition of type 1 herpesvirus, severely lessened the antiviral activity; the compound was still moderately effective in reducing the viral effects on the cells when added as long as 22 hr after the virus. Parallel experiments, in which the antiviral activity of a number of known active drugs was compared, indicated Virazole to have at least a comparable degree of activity, and it was also active against a wider variety of viruses than any of these known active materials. The CCED(50) of Virazole to chicken embryo cells was approximately 1,000 mug/ml, although concentrations as low as 10 mug/ml caused slight (15%) inhibition in total cellular protein after 72 hr of incubation.
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PMID:In vitro effect of 1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide (virazole, ICN 1229) on deoxyribonucleic acid and ribonucleic acid viruses. 420 81

Presistent infections with rubella virus were established in baby hamster kidney, BSC-1, HeLa, RK-13, rabbit embryo chondrocyte, and Vero cell lines. All of the cultures except Vero continually produced rubella virus and interferon to which the virus was sensitive. Concurrently, only the Vero cells did not display interference against superinfection with Newcastle disease and vesicular stomatitis viruses. The addition of 1,000 U of exogenous interferon to the cultures cured only the rabbit embryo and Vero cells of the persistent infection. That the interferon is not required for the initiation and maintenance of rubella viral persistence in vitro is implied by the following. (1) Vero cells were persistently infected in the absence of interferon; (2) actinomycin D or cortisone inhibited interferon synthesis but not the rubella viral infection; and (3) cells continuously cultured in the presence of cortisone maintained a viral persistence without interferon synthesis. On the other hand, interferon seems to be responsible for the viral interference; Vero cells infected with rubella virus and cultures inoculated with rubella virus in the presence of actinomycin D or cortisone did not display interference against Newcastle disease or vesicular stomatitis viruses.
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PMID:Role of interferon in six cell lines persistently infected with rubella virus. 421 83

A system for studying the effects of relative humidity (RH) and temperature on biological aerosols, utilizing a modified toroid for a static aerosol chamber, is described. Studies were conducted at 23 C and at three RH levels (10, 35, and 90%) with four viruses (Newcastle disease virus, infectious bovine rhinotracheitis virus, vesicular stomatitis virus, and Escherichia coli B T3 bacteriophage). Virus loss on aerosol generation was consistently lower at 90% than at 10 or 35% RH. When stored at 23 C, Newcastle disease virus and vesicular stomatitis virus survived best at 10% RH. Infectious bovine rhinotracheitis virus and E. coli B T3 bacteriophage survived storage at 23 C best at 90% RH.
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PMID:Influence of relative humidity on the survival of some airborne viruses. 429 70

Vero cells, a line of African green monkey kidney cells, failed to produce interferon when infected with Newcastle disease, Sendai, Sindbis, and rubella viruses, although the cells were sensitive to interferon. Further, infection of Vero cells with rubella virus did not result in interference with the replication of echovirus 11, Newcastle disease virus, or vesicular stomatitis virus, even in cultures where virtually every cell was infected with rubella virus. Under the same conditions, BSC-1 cells and other cells of primate origin produced interferon and showed rubella virus interference. The results indicate that the presence of rubella virus in the cell does not in itself exclude multiplication of other viruses and that rubella virus interference appears to be linked to the capability of the cell to produce interferon.
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PMID:Defectiveness of interferon production and of rubella virus interference in a line of African green monkey kidney cells (Vero). 430 13

A method is described for the detection of interferon production by individual spleen cells of mice after intravenous virus infection. Although mouse spleen plays a major role in the total interferon response to Newcastle disease virus, the number of spleen cells participating is a small fraction of the total, suggesting that interferon formation is to some extent a specialized cell function. Monolayers of mouse embryo cells, after brief contact with agar-suspended spleen cells from interferon-producing mice, have roughly circular foci of cells remaining after removal of agar and vesicular stomatitis virus challenge. The numbers of such foci correlate directly with the number of spleen cells, concentration of inducing virus in the inoculum, duration of contact of cells with mouse-embryo indicator monolayers, time after interferon induction, and serum interferon titer. With this technique, evolution of the interferon-forming cell response in spleens of virus-infected mice has been studied.
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PMID:The role of individual spleen cells in the interferon response of the intact mouse. 430 72

Incubation of Sindbis virus-infected cultures in medium with an ionic strength of 0.105 reduced the virus yield more than 99%. This inhibition was rapidly reversed by exposing the cultures to normal medium: within 20 min the previously inhibited cultures had released as much infectious virus as normal controls had produced during hours of incubation. The following intracellular processes were essentially normal in inhibited, infected monolayers: protein and phospholipid synthesis, the synthesis of infectious viral ribonucleic acid and its incorporation into nucleocapsids, and viral modification of the cell membrane. Accelerated virus production was detected within 20 sec after exposure of inhibited cultures to normal medium. It required an ionic strength greater than 0.145, a pH above 6.7, and a temperature above 21 C. It was not dependent on osmotic pressure, de novo protein synthesis, or a functional energy metabolism. Virus release also occurred in sonic-treated materials of inhibited cells under the same conditions as in living cells. Potential applications of the inhibition to concentration of virus stocks or to obtaining virus in nonphysiological solutions are noted. Preliminary studies with Semiliki Forest virus, Newcastle disease virus, and vesicular stomatitis virus suggest that this phenomenon may be limited to arboviruses.
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PMID:Inhibition of Sindbis virus production by media of low ionic strength: intracellular events and requirements for reversal. 431 61

Shope fibroma virus establishes a persistent cytoplasmic infection in primary (RK) and serially cultivated (DRK(3)) rabbit kidney cells which is accompanied by a morphological alteration of the cells. The response of such cells to superinfection by other viruses was compared with that of control cells by determining plaque production and virus yield of superinfecting viruses. It was found that the growth of other poxviruses, myxoma and vaccinia, was greatly inhibited in the fibroma virus-infected cells, but that of pseudorabies and herpes simplex viruses, which are unrelated deoxyribonucleic acid viruses, was virtually unaffected. The ribonucleic acid (RNA) viruses, poliovirus 1 and coxsackievirus B1, did not produce plaques on either RK or fibroma virus-infected (F-RK) monolayers. However, the growth of several other RNA viruses, vesicular stomatitis virus, encephalomyocarditis virus, Sindbis virus, and Newcastle disease virus, was enhanced in F-RK cells. None of these latter RNA viruses produced any infectious progeny in DRK(3) cells, but they all plaqued on and produced good yields in DRK(3) cells persistently infected with fibroma virus. This phenomenon is termed facilitation. Facilitation results from the infection of DRK(3) cells by fibroma virus. Neither interference nor facilitation were due to changes in the adsorption or eclipse of the superinfecting virus.
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PMID:Effect of persistent fibroma virus infection on susceptibility of cells to other viruses. 431 46


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