PubMed Health⌕ Search

Biomedical subjects

L Stitz

Publications and source records attributed to L Stitz.

70 records · Page 4Linked to original sources
PubMed1985

Influence of interferon on persistent infection caused by Borna disease virus in vitro.

The effect of interferon (IFN) on infection and maintenance of persistent infection of Borna disease (BD) virus in cell cultures was investigated. Acutely BD virus-infected primary rabbit brain and rat lung cells produced significant levels of interferon detectable 3 days post-infection in the culture supernatants. Rat brain and rat lung cells persistently infected with BD virus produced only moderate levels of IFN over a long period. In contrast, persistently infected Madin-Darby canine kidney (MDCK) cells did not produce detectable amounts of IFN. Exogenous homologous IFN completely inhibited the expression of BD virus antigen in acutely infected rabbit brain cells, when added during the first 24 h after infection. IFN added later (2 to 6 days post-infection) reduced virus titres to different degrees depending on the onset of treatment. However, IFN added to persistently infected rat lung cells did not appear to influence the degree or quality of BD virus antigen expression or the intracellular amount of infectious virus. Two facts indicate that IFN is not involved in the establishment or maintenance of persistent BD virus infection in vitro. Thus, MDCK cells, which could not be induced to produce IFN, can be readily persistently infected with BD virus in vitro, and exogenous IFN did not appear to influence persistent BD virus infection.

Animals↗
PubMed1985

Cytotoxic T cell lysis of target cells fused with liposomes containing influenza virus haemagglutinin and neuraminidase.

The lytic activity of secondary cytotoxic lymphocytes against influenza A virus was tested on cells which had been fused with liposomes containing the haemagglutinin and the neuraminidase of an avian influenza A virus (fowl plague virus, FPV). Fusion was obtained solely by the activity of the haemagglutinin and neuraminidase incorporated into the liposomes, without the need for any additional fusion factor. Highly reproducible lysis of these FPV-liposome target cells by influenza A-specific cytotoxic cells was found. In contrast, target cells containing the glycoproteins HN and F of Newcastle disease virus (NDV) were not lysed. In almost all experiments effector cell populations capable of lysing target cells also lysed the natural killer cell (NK)-sensitive cell line YAC-1. However, high NK activity alone was not sufficient to lyse target cells fused with liposomes containing the viral surface glycoproteins. To our knowledge this is the first report where after artificial introduction of viral surface components into cell membranes (either by fusion or by transfection) lysis of target cells was monitored also for non-specific lysis mediated by NK-like cells. Both the H-2 restriction and the virus specificity of lysis of FPV-liposome target cells indicate that influenza virus haemagglutinin and possibly neuraminidase do function as target antigens for influenza-specific T cells.

Animals↗
PubMed1985

Natural killer cells vs cytotoxic T cells in the peripheral blood of virus-infected mice.

The cell-mediated immune response of mice against various enveloped RNA and DNA viruses expressed by immune lymphocytes from the spleen and the peripheral blood (PBL) were compared. PBL from mice of various strains infected with vaccinia virus, vesicular stomatitis virus (VSV), or lymphocytic choriomeningitis virus (LCMV) were tested on histocompatible or incompatible target cells infected with the homologous virus. PBL from immune mice showed clear H-2 restriction, but additionally, they expressed high natural killing (NK) activity on YAC-1 cells. The high NK-cytolytic activity of PBL on YAC-1 differed significantly from that expressed by splenic lymphocytes. In both lymphocyte populations lysis was detected as early as 1 day after infection; NK activity decreased in the spleen after day 4 post infection, whereas that of PBL persisted at high levels for up to 10 days after infection. Treatment of mice with anti-asialo GM1 in vivo abrogated NK activity in PBL effector cells tested in vitro. These results may explain some of the difficulties to observe MHC-restricted cytotoxic T cells in PBL from humans or primates during primary infections with virus.

Animals↗
PubMed1984

Immune response against vaccinia virus in rhesus monkeys: no evidence for primary MHC-restricted cytolytic T cells.

Rhesus monkeys were tested in vitro for their cellular immune response after infection with vaccinia virus, employing lymphocyte preparations from various lymphoid tissues. Although virus-infected target cells were lysed by lymphoid cells from immunized, but not from uninfected, rhesus monkeys, we could neither find evidence for MHC-restricted T cells nor for antibody-dependent cellular cytotoxicity. Kinetics of target cell lysis, the killing patterns of immune lymphocytes measured on syngeneic, allogeneic, and xenogeneic target cells, and the influence of protein A on cytotoxic activity in vitro suggest induction predominantly of natural killer cells in vivo which exhibit lytic activity on virus-infected target cells in vitro.

Animals↗
PubMed1984

Immunological tolerance to a non-cytopathic virus is not inheritable in mice.

Male lymphocytic choriomeningitis (LCM) virus-carrier mice were mated to uninfected females and their offsprings tested for (i) LCMV virus and (ii) their potential to generate LCM virus-specific cytotoxic T cells. Among about 500 offspring tested no example of antigen-independent inheritance of tolerance to LCM virus was detected. Therefore inheritance of acquired tolerance cannot be observed in this murine infectious disease model.

Animals↗
PubMed1983

Characterization of cloned cytotoxic lymphocytes with NK-like activity.

Cloned H-2b-restricted male antigen-specific cytotoxic T cells were kept in culture in the presence of IL 2 for over 2 yr. During this time, they lost their antigenic specificity and now exhibit high NK-like activity. Three separate clones HY 1, HY 2, and HY 3 and their subclones, when tested on a panel of NK-sensitive and NK-insensitive target cells, showed typical lysis patterns of NK cells. Three cytotoxicity-loss mutants were obtained by subcloning. At least one of these cytotoxicity-loss mutants still exhibited binding to NK-sensitive target cells. The various HY clones were compared with cloned alloreactive cytotoxic T cells of B10 anti-B10.D2 specificity with respect to surface markers, target specificity, kinetics of lysis, morphology, and influence of monoclonal antibodies and chemicals on cytotoxicity. Only one major difference between cloned NK-like and alloreactive T cells was detected: monoclonal anti-Lyt-2 antibodies inhibited cytotoxic activity of alloreactive T cells but not of NK-like cells, although both expressed Lyt-2 on their surface. Morphologically, HY cells were characterized by numerous lysosomal granules in their cytoplasm. Clones with NK-like activity differed from cytotoxicity-loss mutants by both ultrastructural appearance and enzyme histochemistry of lysosomes. Interaction of NK-like cells with YAC-1 cells induced membrane lesions of variable size in target cells. Effects of chemicals influencing lysosomal pathways such as monensin, NH4Cl, and chloroquine on cytotoxicity were investigated. Monensin as well as NH4Cl inhibited cytotoxicity of NK as well as alloreactive clones, whereas chloroquine did not. Spleen cells from acutely virus-infected mice with high NK reactivity showed the same behavior except for chloroquine, which was slightly inhibitory. The addition of monensin to the cells resulted in morphologic changes in the lysosomal granules. These data strongly suggest that NK-like killing is triggered by unknown substance(s) released from lysosomes of effector cells. Cloning of antigen-specific cytotoxic T cells under conditions of limiting dilution and continuous growing in medium containing Con A supernatant but not the relevant antigen often leads to loss of specificity and appearance of NK-like activity. The results presented are representative of a great amount of work in this and probably many other laboratories attempting to clone cytotoxic effector T cells.

Animals↗
PubMed1982

Prevention of interferon-induced augmentation of cellular antitumor effector mechanisms by phorbol esters.

Both natural killer cell- and macrophage-mediated spontaneous in vitro cytotoxicity for tumor targets is rapidly and strongly augmented by interferon. Macrophage-activating lymphokines considerably enhance macrophage-tumoricidal activity but did not affect natural killer cell-type cytotoxicity. Augmentation of cytolytic capacity by interferon and by macrophage-activating lymphokines is prevented by the tumor-promoting phorbol ester, 12-O-tetradecanoylphorbol-13-acetate. However, the classical antiviral activity and the specific binding of interferon to cell surface receptors remains unaffected by 12-O-tetradecanoylphorbol-13-acetate.

Animals↗
PubMed1981

Borna disease in rhesus monkeys as a models for uveo-cerebral symptoms.

Borna disease, a naturally occurring encephalomyelitis of horses and sheep, was induced in rhesus monkeys after intracerebral infection with virus containing rabbit brain suspension. The animals developed neurological disorders followed by a severe encephalomyelitis which was accompanied by a retinopathy. In all the analyzed brain and retina tissue pieces, virus-specific antigen could be demonstrated by immunoelectrophoretic techniques. Antibodies could be demonstrated by the intermediate gel technique as well as by the immunofluorescence test in the serum and the cerebrospinal fluid of all the monkeys. The histopathological findings in the brain and the eye might be comparable to certain types of encephalitis in man and to pathological changes in the eye of human patients, the etiologies of which are still obscure. An attempt was also made to study cell-mediated immunity by a chromium release assay in infected animals, the results of which might provide, together with the histopathological observations, strong evidence for the role of lymphocytes in the pathogenesis of BD infection in rhesus monkeys.

Animals↗
PubMed1981

Absence of a correlation between humoral and cellular responses to a vaccinia virus and products of the major histocompatibility complex in rhesus monkeys.

Sixty-two Rhesus monkeys were tested at different times after vaccinia virus infection for virus-specific induction of lymphocyte proliferation in vitro or antibody production in vivo. No association was found between identifiable RhLA-controlled antigens and the strength of the cellular proliferative and/of humoral response.

Animals↗
PubMed1980

Influence of input multiplicity of infection on the antiviral activity of interferon.

The antiviral activity of interferon was shown to be dependent on the input m.o.i. Cells could not be protected against the cytopathogenic effect of vaccinia, herpes, Echo or vesicular stomatitis virus at m.o.i. greater than 1. At a m.o.i. of less than or equal to 1, cells could be protected but the amount of interferon necessary to yield protection was inversely related to the m.o.i. When protection was afforded, it was only transient. The duration of the antiviral effect of interferon was also inversely related to the m.o.i. The dependence of the antiviral effect on the m.o.i. could not be explained by assuming the viruses to be mixtures of subtypes with different interferon sensitivity. Also, selection by interferon treatment of interferon-insensitive subtypes could not be shown. The greater antiviral effect of interferon at low m.o.i. was probably not caused by induction of interferon by the infecting virus. A direct inactivation by the virus of the antiviral effect of interferon could not be demonstrated. These results indicate that when interferon-treated cells are infected, they will not survive the infection. The only result of the interferon treatment will be to inhibit virus replication to some extent, leading only to a delay in cell death.

Animals↗
PubMed1980

Prevention of vaccinia lesions in Rhesus monkeys by human leucocyte and fibroblast interferon.

The prophylactic antiviral activity of systemically administered human interferon preparations was tested in 36 rhesus monkeys against vaccinia virus injected into the skin. All nine control monkeys developed typical vaccinia skin lesions. Eight of nine monkeys treated with daily intramuscular injections of leucocyte interferon (5 x 10(5) units/kg) from day -1 to day +7 after vaccination were completely protected. No lesions developed after discontinuation of therapy. Administration of the same amounts of leucocytic interferon intravenously (i.v.) was equally effective. Daily intramuscular (i.m.) injections of lower doses of leucocyte interferon (1.25 c 10(5) units/kg; 0.5 x 10(5) units/kg) decreased the severity of the skin lesions. Lesion scores correlated inversely with the dose of interferon. Four of six animals receiving daily i.m. injections of fibroblast interferon (5 x 10(5) units/kg) and one of three animals treated i.v. with the same dose were protected against vaccinia virus, and the lesions in the other monkeys were smaller. Intramuscular injections of 5 x 10(5) units/kg of fibroblast interferon or 1.25 x 10(5) units/kg of leucocyte interferon resulted in comparable serum levels and had comparable efficacy in reducing lesion scores.

Animals↗
PubMed1977

Studies on the inhibitory effect of lectins on myxo-virus release.

Lectins of different specificities do not interfere with the maturation of myxo-viruses; their inhibitory effect on virus replication is mainly due to prevention of the detachment of infectious virus particles from the host cell. In chick embryo fibroblasts infected with an influenza virus and treated with concanavalin A, budding occurs into intracytoplasmic vacuoles, but this phenomenon is not observed with a parainfluenza virus and with different cells.

Animals↗