Publications by authors named "Lage-Stehr J"

BERNA-YF (Flavimun) is a live, attenuated yellow fever (YF) vaccine of the 17D strain produced by Berna Biotech Ltd. following a transfer of technology from the Robert Koch Institute (RKI) in Berlin, Germany. In this phase 3 bridging study, the immunogenicity and safety of BERNA-YF were compared with the original RKI YF vaccine (RKI-YF) and to a current, commercially available YF vaccine, Stamaril (AP-YF; Aventis Pasteur, Lyon, France), in 304 healthy, adult volunteers.

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Dengue fever is recognized as one of the most frequent imported acute febrile illnesses affecting European tourists returning from the tropics. In order to assess the value of virus isolation for the diagnosis of dengue fever, 70 cases of dengue fever confirmed in German travelers during the period 1993-2001 were analyzed retrospectively. In 26 patients who had developed acute febrile illness within 2 weeks following their return from a trip to a dengue-endemic area, 9 of 13 attempts to isolate the virus were successful in sera drawn 1-5 days and 2 of 13 sera drawn 6-10 days after the onset of illness.

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To monitor early and late events of immune system activation after primary and secondary flavivirus infection, 17 healthy persons were vaccinated with the standard 17D vaccine virus strain of yellow fever (YF). Twelve of these persons had not received YF vaccine previously and 5 had been vaccinated once at least 10 years before. Viremia and various parameters of humoral and cellular immune activation were followed daily for 7 days and weekly thereafter.

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A simple device for laboratory scale production of monoclonal antibodies has been developed. Hybridomas were cultured in four individual dialysis tubes containing 40-50 ml medium with 10% foetal calf serum, surrounded by 1.5-2 litres supply medium without any serum supplement.

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A key factor causing immunodeficiency in HIV infection seems to be defective antigen presentation. Consequently, CD4+ T-cell populations, initially those expressing CD45RO, decrease in number not because of their destruction, but because they fail to expand in response to antigenic stimulation. This view implies that it would be mistaken to aim therapies only at correcting T-cell function or preventing infection of T cells.

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Peripheral blood and tissue mononuclear phagocytes serve as major viral reservoirs in HIV-infected individuals. We investigated the role of complement receptors CR1 (CD35) and CR3 (CD11b/CD18) in mediating productive infection with complement-opsonized HIV-1 and HIV-2 of cultured normal human peripheral blood monocytes, the promonocytic cell line THP-1, the monocytic cell line Mono Mac 6 and the glial cell line U251-MG. Cells were infected with the HTLV-IIIB strain of HIV-1 or the LAV-2 strain of HIV-2 that had been preopsonized with fresh human normal HIV seronegative serum.

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Two women and two men were infected with the human immunodeficiency virus type 1 (HIV-1) transmitted by renal transplantation from i.v. drug-addicted donors in 1984.

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The recently established human monocytic cell line Mono Mac6 expressing distinct characteristics of mature monocytes/macrophages was tested for its susceptibility to infection with human immunodeficiency virus. Inoculation of the cells with the T-cell-tropic human immunodeficiency virus strains human T-lymphotropic virus type IIIB and lymphadenopathy-associated virus type 2 led to a noncytopathic productive infection becoming apparent only after a latency period of up to 56 days. The infectibility of the Mono Mac6 cells was dependent on low levels of CD4 expression, as demonstrated by blocking experiments with various CD4-specific antibodies.

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Murine monoclonal antibodies directed against the structural proteins p17 and p24 of human immunodeficiency virus type 1 were investigated in an epitope mapping system. Overlapping peptides consisting of 15 amino acids of the p17 and p24 protein, respectively, were used as competitors in an enzyme-linked immunosorbent assay. Three different immunogenic regions (A, B, and C) could be defined, one on p17 and two on p24.

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Monoclonal antibodies (MAbs) were raised against gag proteins of human immunodeficiency virus type 1 (HIV-1), strain HTLV-IIIB. One of 29 antibodies was specific for p17 of HIV-1. Twenty of 28 MAbs reactive with the major core protein p24 of HIV-1 showed cross-reactivity with HIV-2, and five of these also detected the corresponding antigens of simian immunodeficiency virus (SIVmac).

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The human immunodeficiency virus (HIV) is reportedly transmitted by sexual contact, sharing of infected needles among intravenous drug abusers, blood and blood products, artificial insemination, and kidney transplantation. This study reports on cornea and kidney recipients of two HIV-infected donors. HIV was transmitted to two kidney recipients who developed symptoms of acute HIV infection (i.

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To study the intra- and extracellular distribution of yellow fever virus 17D (YFV)-specific antigens, pre-embedding immunoelectron microscopy (IEM) and IEM on ultrathin frozen sections were carried out comparatively using monoclonal antibodies (MAB) and YFV-infected cells. In addition, three electron-dense marker systems (IgG-ferritin and IgG-gold and protein A-gold) were compared for their efficiency in detecting bound MAB. Pre-embedding immuno-labelling was performed in microtest plates followed by in situ embedding and immunocryoultramicrotomy was performed using pellets of sucrose-infused cells.

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Activated B cells isolated shortly after primary immunization of BALB/c donor mice with sheep erythrocytes (SRBC), were transferred to normal syngeneic recipients or to low-dose cyclophosphamide-pretreated syngeneic recipients. In pretreated recipients, the transfer of activated B cells, but not of T cells or macrophages, resulted in an augmented production of indirect plaque-forming cells in the primary immune response to SRBC but not to horse erythrocytes. It was shown in double-transfer experiments that T helper cells (Lyt-1+) had been stimulated by the transfer of antigen-activated B cells.

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An immunoregulatory circuit is described in which B cell blasts activate syngeneic Ly-1+2-3- T cells to (a) start a reaction which is indistinguishable from a graft-vs.-host reaction (syngeneic GvH) and (b) induce suppressor cell activity which abrogates the syngeneic GvH. Since capping the surface immunoglobulin (Ig) on B cell blasts blocks their ability to activate the circuit, it is likely that the relevant cell surface structure "seen" on the B cell by the Ly-1 T cell is either Ig itself or another molecule in association with Ig.

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