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)

Two xenotropic murine leukaemia virus (XMuLV)-related proteins--a major envelope glycoprotein gp70 and a 90K protein (probably corresponding to the uncleaved envelope precursor)--were expressed on the surface of mouse L cells as demonstrated by lactoperoxidase-catalysed iodination and immunoprecipitation with anti-XMuLV serum. These two proteins out of many labelled cell surface proteins were selectively incorporated into vesicular stomatitis virus (VSV) virions. Significant differences were found in the amounts of labelled XMuLV-related proteins between L cells and two cell lines infected with XMuLV (rabbit SIRC and lamb LKC cells). The two viral antigens represented only a small proportion of radioactivity on L cells. While in XMuLV-infected SIRC and LKC cells, the gp70 was the major labelled surface protein no detectable amounts of XMuLV-related 90K protein or of cell-specific proteins were found in these cells.
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PMID:Assembly of xenotropic murine leukaemia virus-related antigens from the surface of mouse L cells by vesicular stomatitis virus. 613 28

We tried to transmit human T-cell leukemia virus type I (HTLV-I) into non-lymphoid cells and found that S+L- CCC cat cells were permissive for HTLV-I. Using these HTLV-positive cat cells, vesicular stomatitis virus (VSV) pseudotypes bearing envelope antigens of Japanese isolates of HTLVs were prepared and their reactivities with human or rabbit serum were examined. Japanese HTLV2M, HTLV10Y, and HTLVMT-2 pseudotypes and American HTLVPL pseudotype were neutralized by sera of Japanese and American patients with adult T-cell leukemia/lymphoma (ATL) and rabbit antisera against HTLV. Each serum showed similar antibody titers against different pseudotypes. Thus, envelope antigens of four HTLVs that reacted with the human and rabbit sera were considered to belong to a single serotype.
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PMID:Pseudotype viruses bearing envelope antigens of Japanese isolates of human T-cell leukemia viruses type I. 615 58

The mechanisms by which interferon inhibits viral growth are only partially understood. Several enzymatic activities increase in cells shortly after treatment with interferon. One of these enzymes, oligo-isoadenylate synthetase, synthesizes (2'-5') isoadenylate oligomers which strongly stimulate the activity of a cellular ribonuclease, RNase F (ref. 7). Interferon also significantly increases the activity of a protein kinase which phosphorylates the initiation factor eIF-2 and can inhibit in vitro protein synthesis. Such interferon-induced enzymes, which affect RNA and protein metabolism, might be responsible for many of its effects on viruses. Indeed, inhibition of viral protein and RNA synthesis appears to have a major role in the antiviral state. We have now investigated possible interactions of the two enzymes with viral constituents during the course of infection and found that in two different membrane-coated RNA viruses, vesicular stomatitis virus (VSV) and Moloney murine leukaemia virus (M-MuLV), there is an accumulation of the 2'-5') oligo-isoadenylate synthetase (E) in the virions. Most of the enzyme is bound to the virion ribonucleoprotein core. The incorporation of E into the virions suggests a direct involvement of the enzyme in regulation of virus functions.
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PMID:An interferon-induced cellular enzyme is incorporated into virions. 615 96

The pseudotype particles vesicular stomatitis virus (bovine leukaemia virus) [VSV (BLV)] contain a surface antigenic mosaic, composed of both VSV- and BLV-specific antigens, as demonstrated by increased neutralization by anti-VSV serum after addition of complement or of "second antibody". All the pseudotype infectivity was precipitated by VSV-specific antibody: it could be pelleted by low-speed centrifugation and its infectivity recovered without any loss by sonication. Polycations present during adsorption had little effect on infectivity of the pseudotype for Vero cells, but markedly increased its titre for chicken fibroblasts.
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PMID:Pseudotypes of vesicular stomatitis virus with coat antigen of bovine leukaemia virus--VSV (BLV): antigenic surface mosaic and the roles of precipitating antibodies and polycations. 615 52

A mouse cell line, NIH 3T3, does not respond to some of the activities of interferon. Even after treatment with high concentrations of interferon the replication of lytic viruses, such as encephalomyocarditis virus (EMCV) and vesicular stomatitis virus (VSV) is not inhibited in these cells. In contrast, interferon treatment of these same cells results in the inhibition of Moloney murine leukemia virus (MMuLV) production. We have analyzed enzymatic pathways which are induced by interferon in these cells. After interferon treatment, the level of the (2'-5')oligoadenylate [(2'-5)An] synthetase activity and the phosphorylation of the 67000-dalton protein (P1) are enhanced in NIH 3T3 cells to approximately the same level as interferon-sensitive mouse L-cells. Moreover, NIH 3T3 and L-cells, contain approximately the same levels of enzymes which inactivate (2'-5')An. Both exogenously added (2'-5')A3 or double-stranded RNA (dsRNA) failed to inhibit protein synthesis in NIH 3T3 extracts even though they were potent inhibitors of L-cell extract-directed protein synthesis. Direct measurements of the (2'-5')An-dependent ribonuclease F (RNase F) failed to detect such activity in NIH 3T3 cells. Our results, therefore, suggest that the presence of RNase F activity is necessary for the interferon-induced antiviral activity against EMCV and against VSV. The induction of protein kinase activity by interferon treatment of NIH 3T3 cells appears to have no direct effect on EMCV and VSV replication.
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PMID:A mouse cell line, which is unprotected by interferon against lytic virus infection, lacks ribonuclease F activity. 616 26

Neither indomethacin nor aspirin, at concentrations which inhibited the formation of prostaglandins and prevented the interferon-induced increase in the intracellular concentration of cyclic GMP, had any significant effect on the development of the interferon-induced antiviral state either in mouse L1210 cells challenged with vesicular stomatitis virus or in mice infected with encephalomyocarditis virus. Furthermore, neither drug had any significant effect on the interferon-induced inhibition of cell multiplication in cultures of mouse leukaemia L1210 cells. The differences in the effects of these cyclo-oxygenase inhibitors on different interferon effects may provide some insight into the different pathways of interferon action.
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PMID:Indomethacin and aspirin do not inhibit the antiviral or anti-proliferative actions of interferon. 618 29

Infectious leukemia virus production by two chronically infected NIH/MOL lines was strongly inhibited by interferon treatment of the cells. The corresponding degree of inhibition in JLSV-11 cells was much lower. Multiplication of encephalomyocarditis virus in all three cell lines was barely affected by interferon treatment. Replication of vesicular stomatitis virus, on the other hand, was highly sensitive to interferon in the JLSV-11 line and in one NIH/MOL line but was practically insensitive in the other NIH/MOL line. Anticellular actions of interferon were more pronounced in the JLSV-11 line than in the others. In response to interferon treatment, 2',5'-oligoadenylate synthetase activity was induced to a high level in JLSV-11 cells and to lower levels in the NIH/MOL lines. We failed to detect any 2',5'-oligoadenylate-dependent endonuclease activity in extracts of these cells. Double-stranded RNA-dependent protein kinase activity was present in extracts of interferon-treated NIH/MOL cells, but it was barely detectable in extracts of interferon-treated JLSV-11 cells. The above studies demonstrated that interferon could differentially affect the replication of three different viruses in three different cell lines, including two seemingly identical NIH/MOL lines, and that certain tentative conclusions can be drawn regarding the roles of different interferon-inducible enzyme markers in the different antiviral actions of interferons.
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PMID:Differential antiviral effects of interferon in three murine cell lines. 618 40

Treatment of murine NIH/MOL, C cells which are chronically infected with Moloney murine leukemia virus (MuLV), with mouse interferon (IFN), causes inhibition of extracellular MuLV production. We tested the effect of procaine, a drug that is known to expand cellular membranes and to increase their fluidity, on IFN-mediated inhibition of MuLV production. We observed that procaine did not alleviate this inhibition when IFN was present during procaine treatment. However, if IFN was removed from the culture medium before procaine treatment, the inhibition of MuLV production was partially reversed. We also observed that procaine treatment caused an increase in the amount of MuLV production by cells which had not been treated with IFN. Oxyphenylbutazone (OPB) is an inhibitor of cyclooxygenase, a key enzyme in prostaglandin biosynthesis. New synthesis of prostaglandins is thought to be needed for the antiviral actions of IFN. We observed that OPB did not prevent the antiretroviral action of IFN on NIH/MOL, C cells. OPB also failed to alleviate the IFN-mediated inhibition of replication of vesicular stomatitis virus either in NIH/MOL, C cells or in the L929 cells.
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PMID:Effects of procaine and oxyphenylbutazone on interferon-mediated inhibition of murine leukemia virus production. 619 28

A 200-fold inhibition in the titer of infectious vesicular stomatitis virus (VSV) was produced in cultures of Ly cells treated with 30 reference units of interferon per milliliter. Virus particle production, as measured by VSV particle-associated transcriptase, or nucleocapsid protein was inhibited by a maximum of tenfold. The glycoprotein and membrane protein content was reduced in VSV derived from interferon-treated cells. Thus interferon-treated cells may have produced VSV particles with low infectivity, which may be related to the reduced amount of glycoprotein incorporated into such particles. These findings resemble those reported in interferon-treated cells infected with murine leukemia viruses.
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PMID:Selective inhibition of glycoprotein and membrane protein of vesicular stomatitis virus from interferon-treated cells. 624 16

Forty-one pediatric patients with advanced cancer (24 with acute leukemia and 17 with diverse solid tumors) received 74 courses of therapy with a new chemotherapeutic agent, 4'-(9-acridinylamino)methanesulfon-m-anisidide (AMSA: NSC 249992). Treatments were given by slow i.v. injection daily for five days every two to three weeks. In patients with leukemia: (a) dosages were escalated from 1.3 to 150 mg/sq m/day; (b) toxicity in the form of stomatitis, vomiting, and phlebitis occurred at dosage levels of 125 to 150 mg/sq m/day; and (c) oncolytic effects were observed in 13 of 24 patients. In patients with solid tumors: (a) dosages were escalated from 5 to 50 mg/sq m/day; (b) toxicity (stomatitis, myelosuppression, and phlebitis) occurred at the dosage level of 50 mg/sq m/day; and (c) no oncolytic responses were noted. Serum concentrations of total and free AMSA were assayed by a fluorescence technique and declined in a biphasic manner with free AMSA declining more rapidly than total AMSA. Dosages of greater than 100 mg/sq m/day were required to maintain serum concentrations of total and free AMSA greater than 0.2 microM for the entire five-day schedule. The results suggest that maximum tolerated dosages of AMSA may differ in children with leukemia and solid tumors; however, hematopoietic toxicity could not be fully evaluated in the patients with leukemia. AMSA has clear antileukemic activity that warrants future Phase II trials.
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PMID:Phase I clinical and pharmacokinetic study of 4'-(9-acridinylamino)-methanesulfon-m-anisidide in children with cancer. 625 75


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