Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this report, we have investigated the contribution of primary sequence to the carbohydrate requirement for intracellular transport of two closely related glycoproteins, the G proteins of the San Juan and Orsay strains of vesicular stomatitis virus. We used site-directed mutagenesis of the coding sequence to eliminate the two consensus sites for glycosylation in the Orsay G protein. Whereas the nonglycosylated San Juan G protein required at least one of its two asparagine-linked oligosaccharides for transport to the plasma membrane at 37 degrees C, a fraction of the Orsay G protein was transported without carbohydrate. Of the 10 amino acid differences between these two proteins, residue 172 (tyrosine in San Juan, aspartic acid in Orsay) played the major role in determining the stringency for the carbohydrate requirement. The rates at which the glycosylated and nonglycosylated Orsay G proteins were transported to the cell surface were the same, although a smaller fraction of the nonglycosylated protein was transported. These results suggest that the carbohydrate does not promote intracellular transport directly but influences a polypeptide folding or oligomerization step which is critical for transport.
J Virol 1989 Sep
PMID:A single-amino-acid substitution eliminates the stringent carbohydrate requirement for intracellular transport of a viral glycoprotein. 276 Sep 84

An important mechanism used by the immune system in resisting infections by intracellular pathogens is the destruction of host cells by cytolytic lymphocytes. Whether these lymphocytes display a more direct antimicrobial action remains unclear. We have attempted to answer this question by testing extracts of cytolytic lymphocytes, prepared by cell fractionation, against three bacterial species - Escherichia coli, Salmonella typhimurium, and Listeria monocytogenes. We also tested these extracts against two viruses - pseudorabies virus and vesicular stomatitis virus. The extracts showed negligible activity against the test organisms under the conditions used.
Immunol Lett 1989 Sep
PMID:The absence of direct antimicrobial activity in extracts of cytotoxic lymphocytes. 280 99

A novel immunopotentiating agent, 5-amino-3-beta-D-ribofuranosylthiazolo [4,5-d]pyrimidine-2,7(3H,6H)-dione (7-thia-8-oxoguanosine), lacks virus-inhibitory properties in vitro but induces interferon and potentiates immune functions, such as natural killer cell activity. It was evaluated in rodent models to determine the spectrum of antiviral activity and effective treatment regimens. At 50 to 200 mg/kg given as single or divided intraperitoneal (i.p.) doses 1 day before virus inoculation, significant protection was afforded to mice infected i.p. with Semliki Forest, San Angelo, banzi, and encephalomyocarditis viruses. Similarly, suckling rats were protected from an intranasal challenge with rat coronavirus. Against San Angelo virus, treatments could be delayed to 1 day post-virus inoculation and still show a beneficial effect. The compound was moderately effective in mice infected i.p. with herpes simplex virus type 2 or intranasally with vesicular stomatitis virus. No activity was seen against influenza B virus in mice when the analog was administered one time pre-virus inoculation or in multiple doses given before and after the virus inoculation. Nor was there a prophylactic effect against herpetic skin lesions on mice. This immune modulator may have promise for the treatment of a variety of virus infections.
Antimicrob Agents Chemother 1989 Sep
PMID:Broad-spectrum in vivo antiviral activity of 7-thia-8-oxoguanosine, a novel immunopotentiating agent. 281 49

The P function of vesicular stomatitis virus (VSV) is defined as the viral function which results in a reduced rate of total protein synthesis (viral plus cellular) arising from a nonspecific reduction in the efficiency of the translational machinery in infected cells. The existence of P function has been challenged by Lodish and Porter who were unable to detect it in L-strain mouse cells infected with wild-type VSV (HR) or, as expected, with the P- mutant, T1026-R1. Although other groups have subsequently confirmed the existence of P function and the difference between HR and T1026-R1, we have sought an explanation for the difference between Lodish and Porter's results and those of other laboratories. We show that the VSV P function depends on the phase of the growth cycle of infected L-cell cultures. In very early exponential phase, as used by Lodish and Porter, HR has very little demonstrable P function; as the growth cycle proceeds toward stationary phase, P function becomes more and more manifest. Under the same conditions, T1026-R1 shows no P function throughout the growth cycle. Furthermore we show that the VSV M protein mutant tsG31 has a P++ phenotype reducing total protein synthesis below that seen with wild-type HR. P function can be observed in cells infected with tsG31, even early in the exponential phase of the cellular growth cycle.
Virology 1987 Sep
PMID:Vesicular stomatitis virus P function depends on cellular growth cycle. 282 Jan 32

The intergenic sequences of vesicular stomatitis virus of the New Jersey serotype [VSV (NJ): Ogden strain] have been determined by dideoxy sequencing across the gene junctions of the viral RNA genome using deoxyoligonucleotide primers. The N-NS, NS-M, and M-G intergenic sequences of VSV (NJ) are identical to the consensus intergenic sequence for VSV of the Indiana serotype [VSV (IND)]: 3'-AUACU7GAUUGUCNNNAG-5' (genome sense; N denotes any nucleotide), where 3'-AUACU7-5' encodes the 3' terminus and the start of the polyadenylate tract of the preceding mRNA, 3'-UUGUCNNNAG-5' encodes the 5' terminus of the succeeding mRNA, and 3'-GA-5' is a nontranscribed dinucleotide. Notably, the NS-M junction of VSV (NJ) does not contain the anomalous dinucleotide 3'-CA-5' which is found at the NS-M junction of VSV (IND). In striking contrast to VSV (IND), the G-L intergenic sequence of VSV (NJ) contains a 19-base insertion between the nontranscribed dinucleotide and the consensus mRNA start sequence. During in vitro transcription, the L mRNA of VSV (NJ) may initiate at two distinct sites: the first start site (3'-CCUUAUCUUC-5') is that flanking the nontranscribed dinucleotide, and the second start site is a consensus mRNA start sequence located 20 bases downstream from the nontranscribed dinucleotide. However, the L mRNA isolated form VSV (NJ)-infected cells appears to initiate only at the consensus start sequence. The possible role of these start sites in L mRNA synthesis is discussed.
Virology 1987 Sep
PMID:Intergenic sequences of the vesicular stomatitis virus genome (New Jersey serotype): evidence for two transcription initiation sites within the L gene. 282 Jan 43

We have used monospecific antisera to two lysosomal membrane glycoproteins, lgp120 and a similar protein, lgp110, to compare the biosynthesis and intracellular transport of lysosomal membrane components, plasma membrane proteins, and lysosomal enzymes. In J774 cells and NRK cells, newly synthesized lysosomal membrane and plasma membrane proteins (the IgG1/IgG2b Fc receptor or influenza virus hemagglutinin) were transported through the Golgi apparatus (defined by acquisition of resistance to endo-beta-N-acetylglucosaminidase H) with the same kinetics (t1/2 = 11-14 min). In addition, immunoelectron microscopy of normal rat kidney cells showed that lgp120 and vesicular stomatitis virus G-protein were present in the same Golgi cisternae demonstrating that lysosomal and plasma membrane proteins were not sorted either before or during transport through the Golgi apparatus. To define the site at which sorting occurred, we compared the kinetics of transport of lysosomal and plasma membrane proteins and a lysosomal enzyme to their respective destinations. Newly synthesized proteins were detected in dense lysosomes (lgp's and beta-glucuronidase) or on the cell surface (Fc receptor or hemagglutinin) after the same lag period (20-25 min), and accumulated at their final destinations with similar kinetics (t1/2 = 30-45 min), suggesting that these two lgp's are not transported to the plasma membrane before reaching lysosomes. This was further supported by measurements of the transport of membrane-bound endocytic markers from the cell surface to lysosomes, which exhibited additional lag periods of 5-15 min and half-times of 1.5-2 h. The time required for transport of newly synthesized plasma membrane proteins to the cell surface, and for the transport of plasma membrane markers from the cell surface to lysosomes would appear too long to account for the rapid transport of lgp's from the Golgi apparatus to lysosomes. Thus, the observed kinetics suggest that lysosomal membrane proteins are sorted from plasma membrane proteins at a post-Golgi intracellular site, possibly the trans Golgi network, before their delivery to lysosomes.
J Cell Biol 1987 Sep
PMID:Kinetics of intracellular transport and sorting of lysosomal membrane and plasma membrane proteins. 282 Oct 12

Goose erythrocyte membranes were isolated and tested for their ability to compete with red cell receptors for vesicular stomatitis virus (VSV) attachment and fusion at acidic pH. Crude membranes, solubilized with Triton X-100, Tween 80 and octyl-beta-D-glucopyranoside, showed a dose-dependent inhibitory effect on virus binding and haemolysis. The chemical nature of the active molecules was investigated by enzyme digestion and by separation of purified components. Only the lipid moiety, specifically phospholipid and glycolipid, was found to inhibit VSV attachment; a more detailed analysis of these molecules showed that phosphatidylinositol, phosphatidylserine and GM3 ganglioside were responsible for the inhibitory activity and could therefore represent VSV binding sites on goose erythrocyte membranes. Removal of negatively charged groups from these molecules by enzymic treatment significantly reduced their activity, suggesting that electrostatic interactions play an important role in the binding of VSV to the cell surface. Enzymic digestion of whole erythrocytes confirmed the involvement of membrane lipid molecules in the cell surface receptor for VSV.
J Gen Virol 1987 Sep
PMID:Characterization of membrane components of the erythrocyte involved in vesicular stomatitis virus attachment and fusion at acidic pH. 282 Nov 75

A modified passive cutaneous anaphylaxis test and an ELISA were used to identify IgE in calves vaccinated (sensitized) with chlorine dioxide-inactivated bluetongue virus (BTV) and in calves inoculated with infectious BTV. The levels of IgE were greatest in the vaccinated calves after challenge with infectious virus, which correlated with development of clinically apparent dermatitis and stomatitis. These findings suggest that some aspects of clinical bluetongue disease in cattle may have an immunopathological mechanism mediated by IgE (type I hypersensitivity).
J Gen Virol 1987 Sep
PMID:Identification of bluetongue virus-specific immunoglobulin E in cattle. 282 Nov 88

Interferons inhibit the replication of vesicular stomatitis virus (VSV), but not of encephalomyocarditis virus (EMCV), in mouse JLSV-11 cells. We report the isolation of clonal derivatives from this cell line in which the replication of both viruses is impaired by interferons. These clones were selected from the parental line by virtue of their rescue by interferon treatment from the cytopathic effects of EMCV infection. In one such clone, RK8, the replication of VSV and EMCV and the production of resident murine leukemia virus were inhibited by interferon. On the other hand, in clone RK6, which was isolated without any selection, the replication of VSV, but not of EMCV, was impaired by interferons. The levels of 2'-5'-oligoadenylate synthetase mRNA and enzyme activity were similarly elevated upon interferon treatment in the two clones. However, the level of RNase L, as determined by binding and cross-linking of a radiolabeled 2'-5'-oligoadenylate derivative, was much lower in RK6 cells than in RK8 cells. In accord with this observation, the introduction of 2'-5'-oligoadenylates into cells inhibited protein synthesis much less strongly in RK6 cells than in RK8 cells. These results are consistent with the notion that the 2'-5'-oligoadenylate-dependent RNase L may be a mediator of the inhibition of EMCV replication by interferons.
J Virol 1988 Sep
PMID:Studies on the role of the 2'-5'-oligoadenylate synthetase-RNase L pathway in beta interferon-mediated inhibition of encephalomyocarditis virus replication. 284 70

NK cells mediate their cytotoxicity against tumor cells through abroad array of cytotoxic and cytostatic proteins. We investigated whether specific proteins could also be identified that contributed to NK cell-mediated antiviral immunity. Human CD16+/CD3- NK cells were obtained by using FACS and subsequently cloned by using limiting dilution. These NK cell lines, which were cytotoxic against NK-sensitive tumor targets and virally infected cells, also generated supernatants that selectively killed vesicular stomatitis virus-infected cells while sparing noninfected cells. This soluble antiviral activity was completely neutralized by antibodies specific for TNF and lymphotoxin. Purified human rTNF also duplicated this specific cytotoxicity against vesicular stomatitis virus-infected cells, as well as against CMV-, Theiler's murine encephalomyelitis virus-, and HSV-infected cells. The degree of cytotoxicity varied for the different viruses and depended on the cell type infected. These results suggest that NK cells can mediate selective and direct cytotoxicity against virally infected cells by the secretion of TNF and lymphotoxin.
J Immunol 1988 Sep 15
PMID:Tumor necrosis factor and lymphotoxin secretion by human natural killer cells leads to antiviral cytotoxicity. 284 93


<< Previous 1 2 3 4 5 6 7 8 9 10