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)

Cell cultures from the cutaneo-muscular tissue of fetuses (SE), and from lungs (SL), kidneys (SK), testes (STe) of adult spotted sousliks were obtained. Cells from lungs (SL) were viable at 4 degrees C three times longer than fibroblastic cells of human embryos (HEF). At 37 degrees C the growth rate of SL, HEF and L929 cells was similar. However, at 26 degrees C SL cells grew faster than HEF or L929 cells and their population doubling time was shorter. The cultures of SE, SL and SK cells were sensitive to vesicular stomatitis virus (VSV), Newcastle disease virus Radom (NDV-R) and Hertfordshire (NDV-H) strains, to vaccinia virus and herpes simplex virus type 1 and type 2. All these viruses were able to reproduce in souslik cell cultures and caused characteristic CPE.
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PMID:Cell cultures of spotted souslik--preliminary characterization of their growth and sensitivity to viruses. 608 65

The kinetics of intracellular transport of the vesicular stomatitis virus (VSV) glycoprotein (G) and the Newcastle disease virus (NDV) hemagglutinin-neuraminidase (HN) glycoprotein in chicken embryo cells were compared. To assay for the appearance of pulse-labelled glycoprotein at the cell surface, an antibody-binding assay was developed which allowed the precipitation of only those molecules on the outside surfaces of infected cells. Using this assay, it was found that pulse-labelled VSV G protein appeared at the cell surface with a half-time of approximately 27 min, while pulse-labelled NDV HN glycoprotein reached the cell surface with a half-time of approximately 78 min. To determine the transit time of these glycoproteins to trans-Golgi membranes, the kinetics of the acquisition of endoglycosidase H resistance was analyzed. The half-time of the transit of the G protein to the trans-Golgi membranes was found to be approximately 13 min while that of the HN glycoprotein was found to be approximately 60 min. Since the G protein migrates to the trans-Golgi membranes with a half-time of 13 min, and the cell surface with a half-time of 27 min, the half-time for the transit between the trans-Golgi membrane and the plasma membrane must be approximately 14 min. In a similar analysis, the half-time for the transit of the HN glycoprotein from the trans-Golgi membrane to the plasma membrane must be approximately 18 min, a time not significantly different from that of the G protein. Thus the difference in the kinetics of the intracellular transport of these two glycoproteins resides primarily in the transit from the rough endoplasmic reticulum to the trans-Golgi membranes. These results argue against a non-selective mechanism for the transport of plasma membrane glycoproteins to the cell surface.
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PMID:Intracellular processing of the vesicular stomatitis virus glycoprotein and the Newcastle disease virus hemagglutinin-neuraminidase glycoprotein. 609 58

Neutrophils collected from bovine mammary glands were placed in culture with virus-infected cell preparations that had been inactivated by ultraviolet light. Upon culture with infectious bovine rhinotracheitis (IBR) virus-infected Georgia bovine kidney cells, a material was released from the neutrophils that, like interferon, inhibited the replication of vesicular stomatitis virus and IBR virus. Cell-free IBR virus was a less effective inducer of the inhibitor produced by neutrophils. Other herpesviruses (including herpes simplex type 1), as well as equine rhinopneumonitis virus and pseudorabies virus, caused release of the inhibitor, but most other viruses tested, including Newcastle disease virus, a good inducer of type 1 interferon, failed to stimulate the production of inhibitor by polymorphonuclear neutrophils. Preliminary characterization studies revealed differences between the inhibitor produced by the polymorphonuclear neutrophils and type 1 and type II bovine interferons. The possible role of such an inhibitor in the recovery from herpesvirus infection is briefly discussed.
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PMID:Neutrophils in antiviral immunity: inhibition of virus replication by a mediator produced by bovine neutrophils. 615 12

An altered baby hamster kidney cell culture which resists the c.p.e. of HVJ (haemagglutinating virus of Japan - the Sendai strain of parainfluenza I virus) has been obtained and characterized. These cells, designated BHK-R, were originally obtained by prolonged cultivation of cells surviving HVJ infection; they have been subcultured in the presence of HVJ. No infectious virus was recovered from BHK-R cells and no evidence for the presence of HVJ antigens in the cells was demonstrated by immunofluorescent staining. When BHK-R cells were inoculated with HVJ the growth of challenge virus was suppressed and no obvious cytopathic changes were detected, while these cells normally supported the replication of mumps, influenza, Newcastle disease, vesicular stomatitis or Sindbis viruses. BHK-R cells became susceptible to HVJ infection after serial subculture in growth medium free of HVJ. It was suggested that sialic acid residues present in the surface of BHK-R cell membranes and responsible for adsorption of HVJ were split off by the action of neuraminidase of virus particles, resulting in inhibition of the attachment of challenge virus of HVJ.
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PMID:Characterization of altered BHK cells resistant to HVJ (Sendai virus) infection. 615 23

Susceptibility of eight strains of influenza A and B viruses to interferon and to poly(I) . poly(C) were determined by the plaque reduction method. All strains tested were slightly less susceptible than vesicular stomatitis virus (VSV) in an established line of canine kidney (MDCK) cells. The 50% plaque depression doses (PD50) of poly(I) . poly(C) for influenza A and B viruses were as high as 3.0- to 4.5-fold and 6- to 18-fold that for VSV, respectively. The amounts of interferon required to inhibit plaque formation of influenza A and B viruses by 50% were 3.0-6.2 and 7.3-15.2 units/ml, respectively. The ratio of PD50 of poly(I) . poly(C) for each strain of influenza viruses tested to that for VSV in chick embryo cells was almost the same as in MDCK cells. Furthermore, in chick embryo cells, the strains of influenza virus tested were demonstrated to be much more susceptible to poly(I) . poly(C) than both Newcastle disease virus and vaccinia virus. It is suggested that influenza viruses may be relatively susceptible to interferon and to poly(I) . poly(C).
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PMID:Susceptibility of influenza viruses to interferon and to poly(I) . Poly(C) determined by the plaque reduction method. 615 60

Adult Beagles failed to respond to high concentrations of interferon (IF) when they were injected with a nuclease-resistant complex poly I:C with poly-L-lysine and carboxymethylcellulose (PICLC), by the IV or intrathecal route. An IV dose of 1 mg of PICLC/kg of body weight was lethal to 1 of 3 adult dogs, but induced IF in only 2 dogs. Smaller doses were less toxic, but also were less effective. The injection of a high dose of a known IF inducer (3 X 10(8) egg LD50 of Newcastle disease virus) also failed to induce IF in Beagles. Interferon could not be induced in vitro when primary cultures of neonatal dog lung or kidney were treated with cultures of neonatal dog lung or kidney were treated with PICLC. When these primary cell cultures were compared with the cell line Madin-Darby canine kidney in an IF assay, no difference in sensitivity to IF-induced protection from infection with vesicular stomatitis virus could be shown. This indicated that the sensitivity of the Madin-Darby cell line was not the only factor in determining the lack of IF response in dogs and indicates that the dogs are poor responders to IF induction.
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PMID:Minimal interferon induction in dogs, using a modified polyriboinosinic-polyribocytidylic acid complex. 616 81

In response to antigenic stimulation, spleen cells from Toxoplasma-infected mice produce a factor showing inhibitory activity against vesicular stomatitis virus infection in L cell cultures. When BALB/C and ICR mice were inoculated intraperitoneally with the low-virulent S-273 strain of T. gondii, such activity was first detected in 4 and 7 days and reached maximum levels at 10 and 14 days respectively, and retained these levels for at least three weeks. However, BALB/C mice, which are considerably more sensitive to Toxoplasma infection than ICR mice, produced significantly smaller amounts of interferon (IF) after challenge with the high virulent strain. The IF produced in this system possessed certain known properties of immune (type II) IF and was not neutralized by rabbit antiserum against mouse type I IF. The immune IF preparation also inhibited multiplication of Toxoplasma within nonphagocytic L cells in an IF-like fashion, whereas Newcastle disease virus-induced (type I) IF had no effect on this parasite. The antiviral and anti-Toxoplasma activity in immune IF preparations could not be distinguished solely on the bases of their molecular weight and isoelectric point. The experiments with anti-theta serum plus complement and with nylon wool column effluent cells strongly suggest that immune IF was produced by T lymphocytes and required the assistance of macrophages.
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PMID:Production and properties of immune interferon from spleen cell cultures of Toxoplasma-infected mice. 616 46

The induction of phosphorylation of both protein P1 and protein synthesis initiation factor eIF-2 alpha and the inhibition of virus replication were examined in mouse L929 fibroblasts treated with either natural mouse or individual cloned human interferons (IFN). Natural mouse IFN synthesized in Newcastle disease virus-induced L929 cells and two cloned human leukocyte IFN subspecies synthesized in Escherichia coli, IFN-alpha D and IFN-alpha A/D, possessed antiviral activity in L929 cells as measured by single cycle virus yield reduction with both vesicular stomatitis virus and reovirus. Natural L929 IFN and cloned IFNs, alpha D and alpha A/D, also induced the protein kinase that catalyzed the phosphorylation of endogenous ribosome-associated protein P1 and the alpha subunit of purified initiation factor eIF-2. Two other cloned human IFNs, alpha A and alpha D/A, were poor inducers of both the antiviral state and the phosphorylation of P1 and eIF-2 alpha in mouse L929 cells. The ability of individual human IFN-alpha subspecies to induce P1 and eIF-2 alpha phosphorylation in mouse L929 cells correlated with their ability to induce an antiviral state. Furthermore, the detailed kinetics of induction, in mouse L929 cells, of P1 and eIF-2 alpha phosphorylation and of the antiviral state by the heterologous cloned human IFN-alpha A/D were equivalent to the kinetics of induction by the homologous natural mouse L929 IFN. These results suggest that different subspecies of biologically active IFN induce equivalent antiviral activities and biochemical changes in mouse L929 cells, and that protein phosphorylation may play a major role in the antiviral mechanism of IFN action in mouse L929 fibroblasts.
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PMID:Mechanism of interferon action. Kinetics of induction of the antiviral state and protein phosphorylation in mouse fibroblasts treated with natural and cloned interferons. 618 Oct 59

The kinetics of decay of the antiviral state and protein phosphorylation induced with natural mouse interferon (IFN) and with cloned human IFN were examined in monolayer cultures of mouse Ll929 fibroblast cells. The antiviral state measured by single cycle virus yield reduction with either vesicular stomatitis virus or reovirus decayed significantly within 2 to 3 days following removal of IFN and by 5 to 8 days virus yields had returned to the level of untreated control cells. Trypsinization of IFN-treated cells did not detectably alter the rate of decay of the antiviral state; however, the decay occurred slightly more rapidly in actively growing as compared to stationary cell cultures. The decay of the IFN-induced protein kinase which catalyzes the phosphorylation of endogenous protein P1 and purified initiation factor eIF-2 alpha correlated with the decay of the antiviral state. The decay rates of the antiviral state and protein kinase observed in mouse L929 cells that had been treated with natural mouse IFN synthesized in Newcastle disease virus-induced L929 cells were comparable to the decay rates observed in L929 cells that had been treated with recombinant human IFN-alpha A/D synthesized in Escherichia coli. The induction and decay of the antiviral state and protein kinase following treatment with a single dose of IFN did not significantly affect the sensitivity of the cell population to a subsequent treatment with a single dose of IFN. However, continuous treatment of L929 cells with natural mouse IFN or recombinant human IFN prevented the decay of both the antiviral state and protein kinase but also ultimately lead to cell death. The results suggest that protein phosphorylation may play an important role in the mechanism of IFN action in mouse L929 fibroblasts.
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PMID:Mechanism of interferon action. Kinetics of decay of the antiviral state and protein phosphorylation in mouse fibroblasts treated with natural and cloned interferons. 618 Oct 60

The interferon (IFN) system of human cornea cells in culture was studied. IFN produced by these cells by infection with Newcastle disease virus (NDV) was shown, by neutralization studies with specific antisera against human alpha interferon (HuIFN-alpha) and human beta interferon (HuIFN-beta), to contain 90-95% antiviral activity characteristic of the HuIFN-beta and 5-10% that of HuIFN-alpha. The chromatographic behavior of human cornea IFN on Con A-Sepharose and zinc chelate agarose columns was identical to that of HuIFN-beta produced by human foreskin cells. The cornea cells developed marked resistance when exposed to either HuIFN-beta or human gamma interferon (HuIFN-gamma) against vesicular stomatitis virus (VSV), but to a much lesser degree against HSV-1. Both the laboratory-adapted strain and a clinical isolate of HSV-1 were found to be resistant to HuIFN-beta and HuIFN-gamma as compared with VSV. The clinical isolate of HSV-1 was, however, more sensitive to HuIFN-gamma than the laboratory-adapted strain. Furthermore, a combination of HuIFN-beta and HuIFN-gamma did not significantly increase the level of antiviral state induced in cornea cells against HSV-1. These results suggest that in-vitro culture of human cornea cells can be a valuable system to evaluate the potential of chemotherapeutic agents against common ophthalmic viral infections.
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PMID:Interferon system of human cornea cells: interferon production, characterization, and development of antiviral state. 618 55


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