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)

An RNA polymerase activity has been demonstrated in purified rabies virions. Efficiency of the reaction is low since the rate of incorporation was equal to 3 to 5 pmol of uridine per hour, per mg of protein. As with other mammalian rhabdoviruses the optimal temperature was 31 degrees C. Unlike vesicular stomatitis virus, manganese could be substituted for magnesium as a divalent cation, at an optimum concentration of 10 to 20 mM.
J Gen Virol 1978 Jul
PMID:An RNA polymerase activity in purified rabies virions. 2 77

The effect of interferon on the replication of vesicular stomatitis virus (VSV) and type-C oncornavirus in two Balb/c mouse cell lines, JLS-V5 and JLS-V9R, infected with MuLV-R was examined. VSV replication was inhibited threefold (0-5 log10) in both cell lines by 10 to 20 units of interferon/ml. In JLS-V5 cells C-type virus yields, as measured by 3H-uridine incorporation and reverse transcriptase activity, were also reduced threefold by 10 to 20 units of interferon/ml. However, in JLS-V9R cells, C-type virus replication was refractory to interferon at concentrations up to 1 x 10(4) units/ml. Infectious C-type virus transmitted from JLS-V9R cells to Balb/3TS cells was as sensitive to interferon as virus transmitted from JLS-V5 cells, indicating that resistance of C-type virus in JLS-V9R cells is a feature of the cells rather than of the virus strain.
J Gen Virol 1976 Jun
PMID:Differential sensitivity of Rauscher murine leukaemia virus (MuLV-R) to interferons in two interferon-responsive cell lines. 5 65

Kethoxal bis (thiosemicarbazone) (KTS) inhibited replication of, and plaque formation by, vesicular stomatitis virus (VSV) in chick embryo cells. No other thiosemicarbazones tested were effective. Virus-specific m-RNA and protein synthesis were inhibited by KTS. However, virion RNA-dependent RNA synthesis was not inhibited by the drug. Treatment of VSV virions directly with KTS produced enhancement, rather than inactivation, of plaque formation. KTS inhibited cellular DNA and RNA synthesis by 67 and 25% respectively. Since cellular DNA and RNA synthesis are not required for VSV replication, the inhibition of these processes is probably unrelated to the antivirial activity of KTS. Cellular protein synthesis was inhibited 24% by KTS. Unexpectedly, synthesis of four proteins was induced in KTS-treated uninfected cells.
J Gen Virol 1977 Oct
PMID:Inhibition of vesicular stomatitis virus by kethoxal bis (thiosemicarbazone). 7 31

Human embryonic lung (MRC-5), feline embryo (FEA), mink lung (Mv1Lu) and monkey kidney (BSC-1) cells infected by respiratory syncytial virus showed characteristic morphological changes when viewed by scanning electron microscopy. The surfaces of respiratory syncytial virus-infected cells developed a profusion of slender filaments after 48 h incubation at 31 degrees C. Similar changes in surface morphology were observed in BSC-1 cells infected by murine pneumonia virus. Filament production therefore appears to be a common property of pneumo-viruses. Filaments were not observed in cells infected with either syncytial and non-syncytial herpes simplex virus, the cytocidal vesicular stomatitis and Batai (Bunyaviridae) viruses, or the focus-inducing rabbit fibroma virus. Filament production was not observed in cells infected with ts mutants of respiratory syncytial (RS) virus during incubation at the restrictive temperature, or in a persistently infected culture of BSC-1 cells at 37 degrees C. The persistently infected cells (the RS ts 1/BSC-1 line) had some of the characteristics of cells transformed by oncogenic viruses, namely ability to overlap adjacent cells and agglutination by a low concentration of concanavalin A. The pseudo-transformed phenotype was temperature-dependent, however, and suppressed by raising the temperature of incubation to 39 degrees C. The presence of virus antigen at the cell surface was similarly temperature-dependent in these cells, diminished at high temperature (39 degrees C) and enhanced at low temperature (31 degrees C), suggesting that the changes in the host cell were the result of insertion of virus protein into the cell membrane. Evidently, persistent infection by a cytoplasmic virus can produce alterations in the host cell usually associated with transformation by nuclear viruses.
J Gen Virol 1979 Aug
PMID:Pneumoviruses: the cell surface of lytically and persistently infected cells. 11 36

A non-virogenic African green monkey kidney cell line BGM/MV persistently infected with a neurotropic mouse brain-adapted strain of measles virus, was found to have undergone significant changes in the virus-host cell relationship between passages 35 and 119. Rather than the stable non-cytopathic relationship previously reported in which approximately 100% of the cells contained measles antigens and less than 1% of the cells expressed cell surface measles antigen, we observed cyclic manifestations of c.p.e. together with changes in the percentage of cells expressing intracellular and cell surface measles antigens. Treatment of BGM/MV cells with actinomycin D effected an increase in the percentage of cells expressing cell surface virus haemagglutinin (HA) at times when the percentage of cells with surface HA was less than the percentage of cells with intracellular measles antigens. Superinfection studies employing measles virus and vesicular stomatitis virus revealed a consonant cyclic refractivity and essentially no refractivity, respectively. Endogenous, infectious measles virus was not detected nor was interferon. It was concluded that a host cell factor other than interferon was modulating the cyclic expression of the measles virus infection.
J Gen Virol 1979 Oct
PMID:Changes in the virus-host cell relationship in a stable non-virogenic cell line persistently infected with measles virus (BGM/MV). 11 38

Demethylchlortetracycline (DMCT), doxycycline and, to a lesser extent, chlortetracycline were capable of mediating the in vitro photoinactivation of Venezuelan equine encephalitis (VEE) virus. Other tetracyclines tested were found to be inactive in this respect. However, no correlation between chemical structure and photosensitizing activity could be established. The photoinactivation of VEE virus by DMCT proceeds through a photodynamic mechanism as shown by the absolute requirement of O2 for the inactivation to take place. The photoinactivating effect of DMCT was also exerted upon other animal viruses tested, i.e. vesicular stomatitis virus, herpes simplex virus and poliovirus, even when, in the case of poliovirus, the capsid seems to be impermeable to the tetracycline. The fact that the two most effective photosensitizing tetracyclines for VEE virus are also the drugs more frequently associated with drug-induced phototoxicity in humans, suggests that virus photoinactivation could be used as a screening procedure for potentially phototoxic drugs developed for human application.
J Gen Virol 1979 Nov
PMID:Tetracycline-mediated photodynamic inactivation of animal viruses. 12 Apr 11

A group of RNA viruses, echovirus, poliovirus, reovirus, respiratory syncytial virus and Semliki Forest virus have been examined for ability to grow in enucleate African green monkey kidney (BSCi) cells. Semliki Forest virus produced an almost normal yield of virus but poliovirus, echovirus, reovirus and respiratory syncytial virus, although showing clear evidence of virus replication when compared with a nuclear DNA virus (pseudorabies virus) gave much lower yields than those from nucleate cells. Analysis of enucleate cells infected with echovirus and reovirus showed no evidence of a specific block in the synthesis of any virus-specified polypeptide. Infection with vesicular stomatitis virus at intervals after enucleation demonstrated a diminishing ability to support virus growth with increasing time. It is suggested that the yield of virus obtained from an enucleate cell is related to the length of the growth cycle of the virus, the reduced yield obtained with some viruses reflecting the declining ability of the enucleate cell to support virus growth.
J Gen Virol 1975 Feb
PMID:Virus development in enucleate cells: echovirus, poliovirus, pseudorabies virus, reovirus, respiratory syncytial virus and Semliki Forest virus. 16 89

After an initial acute infection with cell killing, chicken or duck embryo fibroblasts infected in culture with reticuloendotheliosis viruses set up a chronic infection with no cell killing or morphological transformation. Essentially all of the chronically infected cells produced virus. The virus production was not sensitive to cytosine arabinoside or mitomycin C as was virus production in an acute infection. The chronically infected cells had a strong group-specific resistancto the c.p.e. of superinfecting reticuloendotheliosis viruses. However, they were sensitive to vesicular stomatitis virus and avian leukosis-sarcoma viruses. After double infection, single cells produced reticuloendotheliosis virus and avian leukosis-sarcoma virus.
J Gen Virol 1975 Jun
PMID:Replication of reticuloendotheliosis viruses in cell culture: chronic infection. 16 14

Treatment of L cells with 3 to 10 mM 3':5'-cyclic adenosine monophosphate (cAMP) in the presence of interferon was found to potentiate the development of antiviral activity. The dose response of interferon activity at various time periods in the presence and absence of cAMP indicated that potentiation of interferon activity by cAMP occurred at an early stage in the development of antiviral activity. Among the analogues of cAMP tested for interferon-potentiating activity, only the acylated derivatives were found to be active. Combined L-epinephrine and theophylline treatment of cells elevated cellular cAMP levels and also potentiated interferon-mediated antiviral activity. Interferon was also found to elevate cAMP levels in L cells. This activity was limited to biologically active interferon and antagonized the depression of cAMP associated with vesicular stomatitis virus (VSV) infection of L cells. These observations suggest that some aspects of interferon's biological activity is associated with an alteration in cellular levels of cAMP.
J Gen Virol 1975 Sep
PMID:Cyclic AMP potentiation of interferon antiviral activity and effect of interferon on cellular cyclic AMP levels. 17 Mar 77

The virulence of temperature-sensitive mutants of vesicular stomatitis virus (VSV) injected subcutaneously into newborn hamsters was positively correlated with their tendency to generate revertants and with their leakiness in cultured hamster embryo fibroblasts maintained at 37 degrees C, the measured body temperature of the animals under our experimental conditions. The complementation group of the mutants seemed important only in that it tended to determine reversion frequency and leakiness. One non-reverting group I mutant (T1026), however, was much less virulent than would be expected from its extreme leakiness at body temperature. The disease produced by the less virulent mutants was characterized by neurological symptoms and led to delayed death, unlike the rapid deatth produced by virulent mutants. Infectious virus could be found in higher titres in the brains than in peripheral organs of such animals (with ratios as high as 10(8)). This neurotropism was not correlated with the complementation group of the mutant but was shown to be the consequence of survival for more than 3 days after injection. Age was not responsible for the effect. Animals injected at birth with T1026 were completely resistant to subcutaneous superinfection with the highly virulent wildtype virus HR at 3 to 4 days, though non-T1026-protected animals were completely sensitive. When HR was injected intracerebrally at 3 to 4 days, the T1026-protected animals allowed replication to high titres in the brain but not in peripheral organs, whereas non-T1026-protected animals allowed replication to high titres in both brain and in peripheral organs. We suggest from these results that the observed neurotropism is produced by a resistance mechanism operative in peripheral organs but not in the brain; this resistance develops rapidly in newborn animals on exposure to virus and clears virus from the peripheral organs leaving it in the brain. It is possible that our effect represents a controlled and accelerated induction of the classical peripheral resistance of animals to various viruses which normally develops with age.
J Gen Virol 1975 Dec
PMID:On the mechanism of neurotropism of vesicular stomatitis virus in newborn hamsters. Studies with temperature-sensitive mutants. 17 95


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