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)

MaTu is a quasi-viral agent presumably derived from a human mammary tumor. In some respects it resembles classical viruses and in some the "slow viruses," and in others it is different from both. Using monoclonal antibodies (Mabs), we showed that it is a two-component system. One part of the complex, MX, is exogenous; it is manifested by a protein, p58X, which is a cytoplasmic antigen and it reacts with some natural sera of man and of various animals. The other component, MN, is endogenous to human cells. This is manifested by a twin protein(s), p54/58N, localized on the cell surface and in the nucleus. This protein is absent in rapidly growing, sparse cultures of HeLa, but it is inducible either by keeping the cells in dense cultures or, more efficiently, by infecting them with MX. Both inducing factors are synergistic. Only p54/58N is associated with virions of vesicular stomatitis virus (VSV), reproduced in MaTu-infected HeLa. This suggests that MN is responsible for complementation of VSV mutants and for the formation of the VSV (MaTu) pseudotype. Both p54/58N peptides are glycosylated and they form oligomers linked by disulfidic bonds; p58X is not glycosylated and it does not form S-S-linked oligomers.
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PMID:A novel quasi-viral agent, MaTu, is a two-component system. 131 72

Cyclopentenylcytosine (CPE-C, 2), a pyrimidine analogue of the fermentation derived carbocyclic nucleoside neplanocin A, has been synthesized from the optically active cyclopentenylamine 3b by two synthetic routes. CPE-C demonstrates significant antitumor activity against both the sensitive and ara-C resistant lines of L1210 leukemia in vivo. Multiple long term survivors are produced in both tumor models. The compound also gives 100% growth inhibition of the solid human A549 lung and MX-1 mammary tumor xenografts grown in athymic mice. Good activity is also observed against a third human tumor xenograft model, metastatic LOX melanoma. CPE-C has significant activity against both DNA and RNA viruses in vitro. Potent activity is observed against HSV-1 (TK+ and TK-), HSV-2, vaccinia, cytomegalovirus, and varicella-zoster virus. Good activity is also found against a strain of influenza virus (Hong Kong flu), vesicular stomatitis virus, Japanese encephalitis virus, and Punta Toro virus.
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PMID:Cyclopentenylcytosine. A carbocyclic nucleoside with antitumor and antiviral properties. 341 97

The ability of a mouse mammary tumor cell line to abrogate antibody neutralization of vesicular stomatitis virus was shown to be due to the presence of mycoplasma. The mycoplasma was isolated from the cell line and typed as Mycoplasma orale. Colonies of this mycoplasma were used to deliberately infect cell cultures which then gained the capacity to reactivate antibody-neutralized virus. The extent of the reactivation depended on the source of neutralizing antiserum. Other species of mycoplasma were tested and were found to reactivate neutralized virus, indicating that this may be a general phenomenon of mycoplasma contamination.
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PMID:Antibody-mediated neutralization of virus is abrogated by mycoplasma. 624 48

We have found that various sorts of virus particles, including avian leukosis and sarcoma viruses, Sendai virus, Friend leukemia virus and murine mammary tumor virus, are able, upon coincubation with chicken peripheral lymphocytes and either Concanavalin A (Con A) or phytohemagglutinin (PHA), to inhibit the mitogenic responses that normally follow. Such inhibition is not dependent on the use of infectious virus, and can be documented by using particles whose infectivity has been abolished by irradiation with ultraviolet light. Lymphoid cells that had been preincubated with viruses at concentrations approximating 10 particles per cell and for only 2 hours were inhibited by as much as 83% in ability to respond to the lectins employed. These results appear to be mediated, at least in part, by a virus-induced factor with the capacity to abrogate the responsiveness of freshly obtained lymphocytes to mitogenic stimulus. This factor is devoid of interferon activity, as tested in a vesicular-stomatitis-virus plaque reduction assay.
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PMID:Virus-mediated abrogation of chicken lymphocyte responsiveness to mitogenic stimulus. 625 23

Pseudotypes of vesicular stomatitis virus (VSV) containing envelope glycoproteins provided by C3H mammary tumor virus (MTV) instead of the normal VSV G-proteins were prepared and used to assay the presence of an MTV receptor on cells. The assay was specific as demonstrated by competition studies with excess MTV particles and neutralization of the pseudotypes with anti-MTV serum or monoclonal antibodies directed against MTV gp52. The MTV receptor was abundantly present on mouse cells but hardly detectable on nonmurine cells, including the Chinese hamster cell line E36. Somatic cell hybrids between E36 cells and GRS/A spontaneous leukemia cells (GRSL cells) and between E36 and GRS/A primary mammary tumor cells were made. The hybrids retained all Chinese hamster chromosomes but segregated mouse chromosomes. From the analysis of the isoenzymes and chromosomes of the hybrid cell lines we conclude that the gene for the receptor (MTVR-1) is located on mouse chromosome 16.
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PMID:Identification of a cellular receptor for mouse mammary tumor virus and mapping of its gene to chromosome 16. 629 28

Enveloped viruses enter cells by binding to their entry receptors and fusing with the membrane at the cell surface or after trafficking through acidic endosomal compartments. Species-specific virus tropism is usually determined by these entry receptors. Because mouse mammary tumor virus (MMTV) is unable to infect Chinese hamster cells, we used phenotypic screening of the T31 mouse/hamster radiation hybrid panel to map the MMTV cell entry receptor gene and subsequently found that it is transferrin receptor 1. MMTV-resistant human cells that expressed mouse transferrin receptor 1 became susceptible to MMTV infection, and treatment of mouse cells with a monoclonal antibody that down-regulated cell surface expression of the receptor blocked infection. MMTV, like vesicular stomatitis virus, depended on acid pH for infection. MMTV may use transferrin receptor 1, a membrane protein that is endocytosed via clathrin-coated pits and traffics through the acidic endosomes, to rapidly get to a compartment where acid pH triggers the conformational changes in envelope protein required for membrane fusion.
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PMID:Mouse transferrin receptor 1 is the cell entry receptor for mouse mammary tumor virus. 1221 82

APOBEC3 proteins are important cellular factors that restrict infection by a number of viruses, including human immunodeficiency virus type 1 (HIV-1). Previously, we found that the mouse APOBEC3 (mA3) restricts infection by mouse mammary tumor virus (MMTV) in its natural host. Dendritic cells (DCs) are the first in vivo targets of MMTV infection. In this study, we demonstrate that mA3 expressed in target cells restricts MMTV infection in DCs ex vivo and in vivo. By comparing infection of DCs from mA3(+/+) and mA3(-/-) mice with one-hit viruses, we show that mA3 expression in target cells blocked MMTV infection at a postentry step and acted together with virion-packaged mA3 to inhibit infection. Similar results were obtained upon infection of mouse DCs with HIV-1 cores pseudotyped with vesicular stomatitis virus G protein. In addition, treatment of cells or mice with lipopolysaccharide (LPS) caused increased levels of mA3 expression and rendered them resistant to MMTV infection. Alpha interferon treatment had a similar effect. This LPS-induced resistance to infection was seen only in mA3(+/+) mice and not in mA3(-/-) mice, arguing that mA3 is the major anti-MMTV restriction factor that is induced upon DC maturation. Thus, increasing the levels of this intrinsic antiretroviral factor in vivo can lead to increased levels of restriction because of higher levels of both cell-intrinsic as well as virion-packaged APOBEC3.
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PMID:Induction of APOBEC3 in vivo causes increased restriction of retrovirus infection. 1915 38