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)

Human CD4 was expressed on a range of mammalian cell lines. CD4+ non-primate cells, derived from rat, hamster, mink, cat, and rabbit, bind recombinant gp120 of human immunodeficiency virus type 1 (HIV-1) but are resistant to HIV-1 infection. CD4 expression on various human, rhesus, and African green monkey cell lines confers differential susceptibilities for HIV-1, HIV-2, and simian immunodeficiency (SIV) strains. For example, CD4+ TE671 rhabdomyosarcoma cells are sensitive to HIV-1 and HIV-2 but resistant to SIV, whereas CD4+ U87 glioma cells are resistant to HIV-1 infection but sensitive to HIV-2 and SIV. HIV-1 infection was not dependent on human major histocompatibility class I expression. Studies of cell fusion and of infection by vesicular stomatitis virus pseudotypes bearing HIV-1 and HIV-2 envelopes showed that the differential cell tropisms of HIV-1, HIV-2, and SIV are determined at the cell surface.
 ...
PMID:Specific cell surface requirements for the infection of CD4-positive cells by human immunodeficiency virus types 1 and 2 and by Simian immunodeficiency virus. 167 40

Theiler's murine encephalomyelitis virus (TMEV) induces demyelinating disease which is associated with persistent virus infection of the central nervous system. To study the interaction between TMEV and host cells, we infected the G26-20 glioma cell line in vitro, and this resulted in a lytic infection in which most, but not all, cells were killed. Surviving cells divided and formed a viable monolayer in which a small proportion of cells displayed viral cytopathic effects. Levels of virus produced by these cultures over a 6 month period fluctuated between 6 and 8 log10 p.f.u./ml as measured by viral plaque assay. Similarly, the percentage of cells producing both viral antigen and viral RNA, as measured by a simultaneous immunoperoxidase/in situ hybridization technique, varied between 5 and 30%. Although persistently infected cultures were susceptible to challenge by both vesicular stomatitis virus and herpes simplex virus, they were resistant to infection by homologous viruses. Interferon activity was not identified. TMEV isolated from passage 12 produced smaller plaques than wild-type Daniels strain virus (wt-DAV) on L-2 cell monolayers. In contrast to demyelination induced in SJL/J mice after intracerebral inoculation with wt-DAV, mice infected with the small plaque variant virus failed to develop viral persistence or chronic demyelination. However, following immunosuppression by total body irradiation, SJL/J mice infected with the small plaque variant developed viral persistence but no demyelination. Characterization of the biochemical and molecular determinants of the variant will lead to a better understanding of determinants important in viral persistence.
 ...
PMID:Persistent infection of a glioma cell line generates a Theiler's virus variant which fails to induce demyelinating disease in SJL/J mice. 221 94

Mouse L-929 cells (L cells), human oligodendroglioma cells, and rat glioma cells were persistently infected with vesicular stomatitis virus (VSV) mutant tsG31 and maintained for at least 4 years at 37 degrees C. The striking observation in this study was that there is a marked difference in neurovirulence among the persistent infections (PIs) derived from the three cell lines. tsG31 VSV derived from persistently infected L cells and oligodendroglioma cells remained highly virulent as assayed by intracerebral (i.c.) inoculation into 3-week-old Swiss mice. In contrast, tsG31 VSV isolated from glioma cells lost neurovirulence by passage 20. Persistently infected glioma cells were carried through more than 180 passages without reemergence of neurovirulent virus. Importantly, glioma PI virus neurovirulence was restored quickly by i.c. passage in mice and more slowly by passage through normal L cells. In contrast, the neurovirulence of L-cell PI virus was enhanced by i.c. passage in mice and slowly reduced by passage through normal glioma cells. Furthermore, no alteration in neurovirulence was observed in the case of oligodendroglioma PI virus. Although the mechanism(s) underlying the loss of virulence in glioma cells is unclear, our studies suggest that either strict temperature sensitivity or the presence of a heat-labile transcriptase or both play a major role in this phenomenon.
 ...
PMID:Persistent infection of a temperature-sensitive G31 vesicular stomatitis virus mutant in neural and nonneural cells: biological and virological characteristics. 242 95

Previous work in our laboratory has demonstrated that only certain temperature-sensitive (ts) mutants of vesicular stomatitis virus (VSV) appear capable of producing central nervous system (CNS) infection in a mouse model system. Considerable effort has been devoted to studies directed at unraveling the mechanisms underlying host virulence with these tsVSV mutants. With the previous demonstration that certain neuropeptides, capable of lowering body temperature, alter avirulent into virulent infection, we explored the role of one of these neuropeptides, bombesin, in CNS infection induced by normally avirulent tsG11 VSV, as well as certain tsVSV mutants derived from persistently infected (pi) carrier cultures. Our observations indicate that bombesin dramatically alters CNS infection with either tsG11 VSV as well as tsVSV mutants derived from persistent carrier cultures. When virus alone was inoculated intracerebrally, no sign of illness was observed and no animal died. When bombesin was injected along with normally avirulent tsG11 VSV, or glioma derived tsG31 VSV, 50% of mice died within 6-8 days after inoculation. Moreover, mice infected with virus and neuropeptide demonstrated striking pathological alterations in the CNS. These studies are in agreement with previously published results from others as well as our own laboratory and strongly suggest a direct correlation between CNS temperature and the capacity of certain tsVSV mutants to induce clinical and pathological disease.
 ...
PMID:Altered neurovirulence of temperature-sensitive vesicular stomatitis virus mutants in a murine model by inoculation of bombesin: a neuropeptide. I. Clinical, virological and pathological observations. 253 76

Thymidine kinase negative (dTK-) mutants of herpes simplex virus type 1 (HSV-1) multiplied well in rat brain glioma cells. A proportion (less than 1%) of glioma cells survived the infection with HSV and were designated "survivor" glioma cells. Survivor cells of dTK- mutant virus infection ceased to produce infectious virus after two passages and were highly resistant to both HSV-1 and HSV-2 but not to vesicular stomatitis virus (VSV). Flow cytometric studies indicated morphological differences between parental and survivor glioma cells, and HSV-1 specific antigens as well as DNA were detected in the survivor glioma cells, but only in early passages. Sensitivity to superinfection with HSV appears to correlate to loss of HSV-specific viral DNA in the survivor glioma cells. Survivor glioma cells after several subcultures lost their ability to resist superinfecting HSV, reverted morphologically to the appearance of parental glioma cells and also lost significant amount of HSV-1 specific DNA. These transient survivor glioma cells became persistently infected-virus producer cells upon HSV infection.
 ...
PMID:Studies on interactions of dTK-HSV mutants with neurons in vitro. 287 27

Rat brain glioma cells were semipermissive for herpes simplex virus (HSV) replication, because the growth of HSV was multiplicity-dependent in these cells. By using this property, we successfully isolated 'survivor' glioma cells following HSV infection at low multiplicity and without using any special treatment (such as UV irradiation) either of the cells or of the virus. Under the same conditions there were no survivor BHK or 3T3 cells, which suggests the uniqueness of the glioma cell-HSV interaction. The survivor cells ceased to produce infectious virus after two subcultures, but were highly resistant to superinfection for at least 20 subcultures. Parental cells were significantly more permissive for homologous virus growth than survivor cells. Interferon was apparently not induced in the survivor cells, because they were as susceptible as the parental cells to infection with vesicular stomatitis virus. The survivor cells produced HSV-specific antigens and contained HSV-specific DNA.
 ...
PMID:Herpes simplex virus type 1 and neuronal cells--a special cell-virus interaction. 298 13

N-Phosphonacetyl-L-aspartic acid (PALA) is new synthetic antimetabolite which inhibits de novo pyrimidine biosynthesis. Its significant activity against Lewis lung carcinoma, B16 melanoma, and glioma 26 suggested that it might be useful in the treatment of human solid tumors. Phase I trials revealed that dose-limiting toxicity included skin reactions, diarrhea, and stomatitis. Pharmacologic studies demonstrated rapid renal excretion of more than 70% of the unmetabolized drug in 24 h. Peak plasma levels correlated with dose of PALA administered. Partial responses to PALA were seen in one patient with melanoma, one with chondrosarcoma, and one with colon carcinoma. The potential for PALA's use in combination chemotherapy, particularly with 5-fluorouracil, is discussed.
 ...
PMID:An overview of the clinical pharmacology of N-phosphonacetyl-L-aspartate (PALA), a new antimetabolite. 744 50

We have developed a cell-free infection system to titrate neutralizing antibodies against human T-cell leukemia virus type 1 (HTLV-1) using the polymerase chain reaction (PCR). S+L-CCC (8C) feline kidney or U-251 MG human glioma cells were infected with a cell-free culture supernatant derived from HTLV-1-infected c77 feline cells. DNA was extracted from 8C or U-251 MG cells after incubation for 24 hr and amplified by PCR. The c77 cell supernatant gave discrete bands, whereas those of HTLV-1-positive T cells did not. When the inocula were treated with HTLV-1 antibody-positive human sera or the monoclonal or polyclonal antibody against the peptide 190-199 of HTLV-1 envelope protein gp46, the subsequent formation of HTLV-1 proviral DNA was inhibited. We determined the titers of neutralizing antibodies by densitometrically scanning the intensity of the PCR bands. These titers correlated well with those determined by the plaque assay using a pseudotype of vesicular stomatitis virus bearing the envelope antigens of HTLV-1. At high serum concentrations, many seronegative samples markedly inhibited the plating of the HTLV-1 pseudotype whereas they barely affected results obtained by PCR. Thus, the c77-PCR system can detect neutralizing antibodies against HTLV-1 even at low titers.
 ...
PMID:Detection of neutralizing antibodies against human T-cell leukemia virus type 1 using a cell-free infection system and polymerase chain reaction. 792 51

Thirty-six lectins that recognize various sugar chains were examined for inhibitory activities against infection with human T-cell leukemia virus type I (HTLV-I). Wheat-germ agglutinin (WGA) was the most inhibitory among them: plating of the pseudotype of vesicular-stomatitis virus (VSV) bearing envelope antigens of HTLV-I was markedly inhibited by treatment of indicator cells with WGA just before adsorption, but not by treatment after virus adsorption. Treatment with WGA before adsorption, however, could not inhibit the plating of VSV, VSV pseudotypes of bovine leukemia virus, Moloney murine leukemia virus and human immunodeficiency virus type I. Syncytium formation induced by HTLV-I was also inhibited by WGA upon co-cultivation of U-251 MG human glioma cells or MOLT-4 human T-cells with HTLV-I-producing C91/PL cells. Formation of proviral DNA detected one day after infection was also inhibited when indicator cells had been treated with WGA before adsorption of HTLV-I, but not after its adsorption. These findings indicated that WGA specifically inhibits plating of HTLV-I when added to culture just before adsorption and suggested that a substance(s) containing sugar chains recognized by WGA might be involved in an adsorption step of HTLV-I.
 ...
PMID:Inhibition of adsorption of human T-cell-leukemia virus type 1 by a plant lectin, wheat-germ agglutinin. 826 63

The existence of specific rabies virus (RV) glycoprotein (G) binding sites on the surfaces of neuroblastoma cells is demonstrated. Spodoptera frugiperda (Sf21) cells expressing G of the RV strain CVS (Gcvs-Sf21 cells) bind specifically to neuroblastoma cells of different species but not to any other cell type (fibroblast, myoblast, epithelial, or glioma). Attachment to mouse neuroblastoma NG108-15 cells is abolished by previous treatment of Gcvs-Sf2 cells with anti-G antibody. Substitutions for lysine at position 330 and for arginine at position 333 in RV G greatly reduce interaction between Gcvs-Sf21 cells and NG108-15 cells. These data are consistent with in vivo results: an avirulent RV mutant bearing the same double mutation is not able to infect sensory neurons or motoneurons (P. Coulon, J.-P. Ternaux, A. Flamand, and C. Tuffereau, J. Virol. 72:273-278, 1998) after intramuscular inoculation into a mouse. Furthermore, infection of NG108-15 cells by RV but not by vesicular stomatitis virus leads to a reduction of the number of binding sites at the neuronal-cell surface. Our data strongly suggest that these specific attachment sites on neuroblastoma cells represent a neuronal receptor(s) used by RV to infect certain types of neurons in vivo.
 ...
PMID:Neuronal cell surface molecules mediate specific binding to rabies virus glycoprotein expressed by a recombinant baculovirus on the surfaces of lepidopteran cells. 944 3


1 2 3 Next >>