PubMed Health⌕ Search

Biomedical subjects

W Gerhard

Publications and source records attributed to W Gerhard.

At least 109 records · Page 6Linked to original sources
PubMed1978

Repertoire of antiviral antibodies expressed by somatic cell hybrids.

Fusion between P3 x 63 Ag8 mouse myeloma cells and spleen cells from BALB/c mice immunized with influenza type A or B or parainfluenza type 1 virus generated reproducibly antiviral antibody-producing somatic cell hybrids (hybridomas). Eleven hybridomas derived from spleen cells of mice immunized with influenza type A virus were directed against the viral hemagglutinin, one reacted with a host component derived from chickens, and one expressed a specificity not further characterized. The hybridoma antibodies tended to be highly specific for the hemagglutinin of the immunizing virus and seemed to express the same repertoire of strain-specific antibody reactivities as splenic precursor B cells, they did not express any of the frequently occurring crossreactive anti-hemagglutinin specificities. Hybridomas producing crossreactive antibodies against hemagglutinin could be obtained if priming and boosting virus were heterologous.

Animals↗
PubMed1978

The central nervous system-associated immune response to parainfluenza type I virus in mice.

The immune response in the cerebrospinal fluid (CSF) and serum of BALB/c mice was compared after intracerebral (i.c.) inoculation with inactivated parainfluenza type 1 virus. The antiviral antibody response in CSF peaked approximately 11 days after primary i.c. inoculation coinciding with or even slightly preceding the response in the serum. Prior extracerebral priming of the mice by the intranasal or i.v. route did not alter the kinetics of the response in CSF. However, the antibody response in CSF after i.c. inoculation was accelerated if the mice were primed previously by the i.c. route. In all instances, CSF and serum differed markedly with regard to the isotype composition, which was characterized by a 20- to 80-fold increase in IgA over IgG1 and IgG2 in CSF. Taken together, the results prove that part of the antiviral antibodies in CSF are locally produced. In addition, the results indicate that after primary i.c. inoculation with virus, the CNS acquired immunocompetence with regard to the secondary anti-parainfluenza response.

Animals↗
PubMed1978

The analysis of the monoclonal immune response to influenza virus. III. The relationship between stimulation of virus-primed precursor B cells by heterologous viruses and reactivity of secreted antibodies.

Individual splenic precursor B cells from BALB/c mice primed with influenza virus PR8[A/PR/8/34 (H0N1)] were stimulated in vitro in the splenic fragment culture system by homologous or various heterologous influenza viruses. The specificity of the stimulated precursor cells was determined by analysis of the antibodies secreted by the ensuing plasma cell clone in a radioimmunoassay (RIA). Viruses of the H2N2 and H3N2 subtypes were unable to stimulate hemagglutinin (HA)- or neuraminidase (NA)-committed precursor B cells but did efficiently stimulate chicken host component (ChHC)-committed precursors. Viruses of the H1N1 and H0N1 subtypes could stimulate precursors committed to any of the three viral surface components. Analysis of the fine specificity of HA-committed B cells showed that BEL(H0N1) and CAM(H1N1) stimulated almost exclusively precursors whose clonal antibody product reacted with the stimulating virus in the RIA. On the other hand, WSE and MEL (both H0N1) quite frequently were able to stimulate precursors whose clonal antibody product did not react with the stimulating virus in the RIA. These results suggest that the stimulatory interaction of viruses with the cell-bound immunoglobulin receptors is slightly less affinity dependent than the antigen-antibody interaction in the RIA.

Animals↗
PubMed1977

Generation of both cross-reactive and virus-specific T-cell populations after immunization with serologically distinct influenza A viruses.

Specificity of cytotoxic T-cell function was investigated for a range of different influenza viruses. T cells from mice immunized with A or B strain influenza viruses, or with vaccinia virus, showed reciprocal exclusion of cytotoxicity. Extensive cross-reactivity was, however, found for lymphocyte populations from mice infected with a variety of serologically distinct influenza A viruses, though serum antibodies did not cross-react when tested in a radioimmunoassay using comparable target cells as immunoadsorbents. This apparent lack of T-cell specificity was recognized for immune spleen cells generated after intraperitoneal inoculation of high titers of virus, and for mediastinal lymph node populations from mice with pneumonia due to infection with much less virus. The phenomenon could not be explained on the basis of exposure to the chicken host component, which is common to A and B strain viruses. However, not all of the virus-immune T-cell clones are cross-reactive. Competitive-inhibition experiments indicate that a considerable proportion of the lymphocyte response is restricted to the immunizing virus. Even so, the less specific component is significant. Also, exposure to one type A virus was found to prime for an enhanced cell-mediated immunity response after challenge with a second, serologically different A strain virus.

Animals↗
PubMed1977

Role of host immune response in the development of either encephalitic or paralytic disease after experimental rabies infection in mice.

The clinical and histopathological manifestations of the infection of immunosuppressed (cyclophosphamide-treated) and immunocompetent (control) adult mice with the CVS ts 2 strain of fixed rabies virus were correlated with the kinetics of virus multiplication in the central nervous system and with the development of serum antibody. In immunocompetent mice severe paralytic disease causing 80% mortality was accompanied by marked inflammation and degeneration of the central nervous system parenchymatous tissue. Antirabies antibody was detected in all immunocompetent mice severely paralyzed from postinoculation day 6 on; virus was rarely isolated. In contrast, immunosuppressed mice developed encephalitic symptoms with only minor paralysis; the infection was 100% fatal. Histopathological changes in immunosuppressed mice were confined to degeneration and necrosis of individual neurons and mild microglial reaction; virus was isolated from all of these mice. No significant level of antibody was detected. Similar manifestations were seen after infection of immunodeficient (athymic) mice except that the athymic mice developed levels of antibody similar to those of control mice on day 6; antibodies in athymic mice were predominantly of immunoglobulin class M.

Animals↗
PubMed1976

The analysis of the monoclonal immune response to influenza virus. II. The antigenicity of the viral hemagglutinin.

The antigenicity of the hemagglutinins (HA) of five influenza viruses of the A0 and A1 subtypes has been analyzed by means of monoclonal antibodies of murine origin produced in vitro. Secondary monoclonal anti-HA(PR8) antibodies were able to differentiate 14 antigenic determinants (or groups of determinants) on the HA of five influenza virus strains of the A0 and A1 subtypes. Taking into account that certain pairs of determinants delineated on heterologous HA may reflect the heterogeneity of the humoral immune response to a single homologous determinant, the presence of at least eight determinants (host cell-derived determinants not included) on the homologous HA of PR8 and probably on the HA of influenza viruses in general is postulated. Three types of HA-determinants of A0 and A1 influenza virus strains could be distinguished: strain-specific, partially shared, and determinant(s) common to all five virus strains tested. Roughly 40, 55, and 5%, respectively, of the secondary anti-PR8 antibodies of BALB/c mice were directed against determinants belonging to either of the three types.

Animals↗
PubMed1976

Analysis of the humoral immune response to influenza virus in vitro.

The induction of in vitro primary and secondary humoral immune responses to influenza virus in murine splenic explant culture is described. Anti-influenza antibody synthesized in vitro was detected and quantitated by a radioimmunoassay which utilized influenza coupled to bromoacetylcellulose. Both in vitro primary and secondary responses could be stimulated over a large range of virus doses. In vitro secondary responses were maximal when spleen donors had been immunized by the parenteral route although secondary type responses could be demonstrated as well after primary immunization by pulmonary infection. In vitro stimulation with influenza virus was relatively insensitive to inhibition at high antigen doses. The results are discussed in terms of the response of other antigens in spleen fragment culture.

Animals↗
PubMed1975

The analysis of the monoclonal immune response to influenza virus. I. Production of monoclonal anti-viral antibodies in vitro.

Limiting numbers of spleen cells from mice primed with influenza virus were transferred into lethally irradiated syngeneic recipients. Upon antigenic stimulation of fragment cultures of the recipient spleens it was observed that a linear relationship existed between the number of transferred spleen cells and the number of responding fragments. The antibody product of individual fragments exhibited a highly restricted heterogeneity in isoelectric focusing as well as in its reactivity against various viral antigenic determinants. It was concluded that the limiting cell type in this adoptive transfer system corresponds to the virus-primed B cell which, upon antigenic stimulation, gives rise to a clone of antibody-producing cells. PR8-specific precursor B cells occurred at a frequency of at least 1/4000 splenic B cells in PR8-primed BALB/c mice. Approximately 25% of the stimulated cell clones produced sufficient quantities of antibody (200 ng) to render feasible an analysis of closely related viral antigens.

Adoptive Transfer↗
PubMed1969

Morphogenesis of influenza A virus in Ehrlich ascites tumor cells as revealed by thin-sectioning and freeze-etching.

The budding of a tumor-adapted strain of influenza A(0) virus at the surface of Ehrlich ascites tumor cells was studied by electron microscopy. Thin sections of budding sites showed the formation of a fuzzy coat on the outside of the cell membrane and simultaneously the apposition of a dark layer on the inner side. The continuity of cellular and viral membrane seemed to be preserved up to the point where the virion remained attached by only a thin stalk. Freeze-etching of virus budding sites yielded pictures in which a clear differentiation between the viral membrane and the host cell membrane was visible. The breaks across the fuzzy coat revealed striations corresponding to the "spikes" seen in negative contrast, whereas tangentially broken virus particles were best interpreted by assuming that splitting occurred midway between the two outer layers of the envelope.

Animals↗