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Biomedical subjects

J Abb

Publications and source records attributed to J Abb.

At least 37 records · Page 2Linked to original sources

Treatment of HBsAg-,HBeAg-positive chronic active hepatitis with adenine arabinoside. A case report with clinical remission and seroconversion to anti-HBs.

A 26-year-old patient developed HBsAg-, HBeAg-positive chronic active hepatitis arising from an acute infection 6 months earlier. Treatment with adenine arabinoside (Ara-A), 15 mg/kg/day administered as overnight infusions for three weeks, resulted in clinical and complete biochemical remission with normalisation of aminotransferases, loss of HBsAg, HBeAg and DNA polymerase, and appearance of Anti-HBs during follow-up for 9 months. Treatment of chronic hepatitis B infection using Ara-A for several weeks may be especially effective when initiated early in the course of the disease.

Adult↗

[Prevention and therapy of herpesvirus infections].

The group of the human-pathogenic herpesviruses comprises five subgroups: Herpes simplex virus type 1 (HSV-1), Herpes simplex virus type 2 (HSV-2), varicella zoster virus (VZV), cytomegalovirus (CMV), and Epstein-Barr virus (EBV). Primary infection with these ubiquitous herpesviruses usually occurs in childhood or during adolescence and frequently remains inapparent. However, it can also give rise to a variety of clinical pictures. Important clinical manifestations of herpesvirus infections are mucocutaneous lesions (HSV-1, HSV-2, VZV) self-limited, lymphoproliferative diseases (CMV, EBV) and congenital malformations (CMV). Primary infection with herpesviruses leads to a persistent infection of the host. This clinically silent condition of latency can be interrupted and may cause pathological symptoms to recur by reactivation of latent herpesviruses. A classical example of the clinical manifestation of herpesvirus reactivation is herpes zoster following an overcome varicella disease. The mechanism of herpesvirus reactivation has not yet been fully clarified. Reactivation of herpesviruses might be attributable to a weakening of the cellular immunodefence. For the control of viral infections mainly two cellular effector systems are responsible: unspecific, cytotoxic, natural killer (NK) cells and specific cytotoxic thymus-dependent (T) lymphocytes. The functional impairment of these cytotoxic active cells my cause herpesvirus reactivation in immunodeficient or immunosuppressed persons. Interference with the immunological control function may also contribute to the genesis of herpesvirus-associated tumours. Such an association between herpesviruses and human tumours is assumed to exist especially in the case of EBV. The frequently life-endangering severity of local or disseminated herpesvirus infections calls for suitable measures ensuring efficient prophylaxis and therapy. However, the possibilities of a specific immunoprophylaxis (vaccine, special immunoglobulins) against herpesvirus infections are still rather limited. The development of antiviral substances has greatly benefited from the introduction of new agents (Acyclovir) and the production of sufficient quantities of interferon (IFN) preparations during the last few years. Impressive results were obtained with the nucleoside-related substance Acyclovir in the prevention and therapy of primary or reactivated HSV-1 or HSV-2 infections. The use of Acyclovir as prophylactic agent produced the effect that recipients of bone-marrow transplants were no longer afflicted by HSV-1 infections.(ABSTRACT TRUNCATED AT 400 WORDS)

Acyclovir↗

[Antibodies against human T-cell leukemia virus type III in acquired immunodeficiency syndrome and persistent lymphadenopathy].

HTLV III and LAV, retroviruses which have recently been described in the United States and France and which seem to be different isolates of the same virus, are closely associated with the acquired immune deficiency syndrome (AIDS) and the lymphadenopathy syndrome (LAS). Sera from male homosexuals from the Federal Republic of Germany with AIDS or LAS were examined for antibodies to HTLV III (anti-HTLV III) by means of the enzyme linked immunoadsorbent assay (ELISA) and by an indirect immunofluorescence assay. 53% of the patients were anti-HTLV III positive as were 20% of symptomless homosexual men.

Acquired Immunodeficiency Syndrome↗

Age-related decline of human interferon alpha and interferon gamma production.

The influence of donor age on the production of interferon (IFN) alpha and IFN gamma by human peripheral blood mononuclear cells in vitro has been studied. The results demonstrate an age-related decline of the capacity to synthesize and secrete antiviral activity. Yields of virus-induced IFN alpha and lectin-induced IFN gamma were significantly decreased in mononuclear cell cultures from older subjects (greater than 50 years) when compared to those of younger subjects (less than 50 years). The observed deficiency of IFN production may be involved in the increased susceptibility of aged humans to viral infections and malignant diseases.

Adult↗

Relationship between natural killer (NK) cells and interferon (IFN) alpha-producing cells in human peripheral blood. Studies with a monoclonal antibody with specificity for human natural killer cells.

The relationship between NK active and IFN alpha-producing cells in human peripheral blood was studied with a monoclonal antibody with specificity for NK cells (anti-Leu11b). Removal of Leu11b antigen expressing leukocytes with antibody-mediated complement-dependent lysis resulted in a marked reduction of NK activity. In contrast, the depletion of Leu11b positive cells did not affect the production of IFN alpha in response to influenza A/X31 virus, Corynebacterium parvum, or Molt 4 human leukemic cells. The results indicate that NK activity and synthesis of IFN alpha are mediated by different leukocyte subpopulations. The findings further suggest that the augmentation of the cytotoxic activity of NK cells by IFN may not be the consequence of positive self-regulation, but rather of cellular cooperation.

Antibodies, Monoclonal↗

Characterization of human interferon-gamma-producing leukocytes with monoclonal antileukocyte antibodies.

Monoclonal antibodies with specificities for subsets of human leukocytes have been used for the characterization of interferon (IFN) gamma-producing cells. The production of IFN gamma was demonstrated to be a function of OKT3+T lymphocytes. The capacity to secrete IFN gamma was not restricted to the OKT4+ or the OKT8+T-cell subset. BA-1+B lymphocytes and Leu7+ natural killer cells did not contribute to the production of IFN gamma. Ia+, OKM1+ monocytes served an auxiliary function in the production of IFN gamma. The requirement for accessory monocytes, however, was not absolute, because monocyte-free preparations of long-term cultured IL2-dependent T lymphocytes retained the capacity to secrete IFN gamma.

Antibodies, Monoclonal↗

Genetic influence on natural cytotoxicity and interferon production in multiple sclerosis studies in monozygotic discordant twins.

A dysfunction in natural killer (NK) cell activity has been assumed to play a substantial role in the pathogenesis of multiple sclerosis (MS). To investigate whether such a defect is genetically determined and thus in combination with a certain HLA status may represent an additional risk factor for contracting MS, spontaneous and interferon (IFN) induced NK cells activity against the K562 target cell were analyzed in nine pairs of monozygotic twins discordant for MS. In addition, IFN production was tested in nonadherent lymphocytes stimulated with PHA, influenza virus or leukemia cells. When compared to healthy controls, NK function appeared to be normal in healthy twins, whereas some MS patient displayed decreased activity. No difference in IFN induced NK cell activity and IFN production could be detected between normal controls, healthy twins, and MS patients. These data argue against a genetically determined dysfunction within the NK-IFN system in patients with MS.

Adult↗

Association of human leucocyte low responsiveness to inducers of interferon alpha with HLA-DR 2.

The influence of antigens of the major histocompatibility complex (MHC) on the production of interferon (IFN) alpha or IFN gamma by human peripheral blood leucocytes (PBL) in vitro has been studied. Synthesis of IFN gamma by PBL stimulated with purified phytohaemagglutinin (PHA-P) or protein A of Staphylococcus aureus (SpA) appeared not to be controlled by MHC antigens. The production of IFN alpha, however, was influenced by the HLA type of the donor. Low responsiveness of PBL to inducers of IFN alpha (influenza virus, Molt 4 cells) was associated with HLA-DR 2. Implications of these observations for studies of IFN production and natural killer (NK) cell activity are discussed.

Female↗

Viral hepatitis.

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Adult↗

Phenotype of human alpha-interferon producing leucocytes identified by monoclonal antibodies.

Monoclonal antibodies with specificities for subsets of human leucocytes have been used for the characterization of alpha-interferon (alpha-IFN) producing cells. The production of alpha-IFN was demonstrated to be a function of Ia+ leucocytes. OKT3+ T lymphocytes, BA-1+ B lymphocytes and Leu 7+ natural killer (NK) cells did not contribute to the production of alpha-IFN. OKM1+ monocytes were essential for the production of alpha-IFN in response to bacterial products or leukaemia cells, but were not required for the synthesis of virus- or poly I:C-induced alpha-IFN. The results indicate that alpha-IFN producing cells represent a heterogenous population of cells of the myeloid lineage.

Antibodies, Monoclonal↗

Effect of retinoic acid on the spontaneous and interferon-induced activity of human natural killer cells.

Non-toxic concentrations of retinoic acid (RA) inhibited the spontaneous activity of human natural killer (NK) cells. RA also inhibited the activation of human NK cells by treatment with partially purified human leukocyte interferon (HulFN alpha) or with inducers of IFN alpha and IFN gamma. Full expression of the inhibitory action required prolonged exposure of human peripheral blood leukocytes to RA. Implications of these findings for the use of retinoids in the treatment of human malignancies are discussed.

Humans↗

Production and characterization of marmoset lymphoblastoid interferon.

We describe the production of marmoset lymphoblastoid cell interferon (IFN). Optimal yields of IFN were obtained when EBV-transformed lymphoblastoid cell lines (LCL) at a cell density of 1 X 10(6)/ml were incubated with 100 HAU Sendai virus/ml for 24 h. Sendai-virus-induced marmoset lymphoblastoid cell IFN was acid-stable and exerted antiviral activity on both homologous and heterologous human cells, thus allowing its classification as IFN alpha. Marmoset lymphoblastoid cell IFN did not inhibit the growth of herpesvirus-transformed marmoset T-or B-cell lines, but markedly enhanced marmoset NK-cell activity against human myeloid leukemia target cells. The use of lymphoblastoid cell IFN in marmosets in vivo may contribute to an understanding of the pathogenic role of IFN in herpesvirus-induced lymphoproliferative diseases.

Animals↗

Retinoic acid suppression of human leukocyte interferon production.

Retinoic acid (RA) suppressed the production of interferon (IFN) alpha and IFN gamma of human peripheral blood leukocytes in response to stimulation with lectin mitogens, bacterial products, synthetic polynucleotides, viruses, and tumor cell lines in vitro. Virus-induced secretion of IFN alpha of human lymphoblastoid cells was also inhibited. RA-mediated suppression was dose-dependent and required the near-concurrent addition of RA and inducers to human leukocyte cultures, thus suggesting that RA affects an early cellular function in the generation of IFN. Implications of these findings for the use of retinoids in the treatment of human malignancies are discussed.

Burkitt Lymphoma↗

Effect of cyclosporin A on the production of interferon by human peripheral blood leukocytes in vitro.

Cyclosporin A (CsA) was assessed for its effect on the production of antiviral activity by human peripheral blood leukocytes (PBL). CsA markedly reduced the production of interferon-gamma (IFN-gamma) in response to stimulation with lectin mitogens, bacterial products, alloantigens, or Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines (LCL). CsA-mediated suppression of IFN-gamma secretion was dose-dependent and did not result from a shift of kinetics of the production of antiviral activity. The production of IFN-alpha in response to stimulation with Corynebacterium parvum (CP), viruses, and synthetic polynucleotides was not affected by the addition of CsA. These findings confirm earlier observations that CsA predominantly acts on T lymphocyte function. CsA may prove a valuable agent to study the role of IFN-gamma in the pathogenesis of virus-associated malignant lymphoproliferative disease.

Cell Line↗