0000000000054910
AUTHOR
D. Falke
showing 9 related works from this author
Infection of murine hepatocyte cultures by herpes simplex virus (HSV) 1 and 2
1984
A study was undertaken of the interaction between liver cells and Herpes Simplex Virus (HSV) in vitro. Hepatocytes were obtained from HSV-resistant (C57/B16) and from HSV-susceptible (BALB/c, A/J, C3H) mouse strains and cultured according to standard methods. Each culture was infected with several strains of HSV-type 1 or of HSV-type 2, respectively. The multiplicity of infection was 5. The cytopathic effect was evaluated by light- and electron-microscopy. The number of infectious particles was determined using rabbit kidney or Vero cell cultures. All evaluations were made at different time intervals after infection. No difference concerning the replication rate of HSV-1 and 2 in isolated h…
Translocation of the nuclear autoantigen La to the cell surface of herpes simplex virus type 1 infected cells.
1992
Recently we developed a procedure to translocalize one of the extractable nuclear antigens (ENAs), the La protein, to the cell surface of CV-1 cells. Here we report that herpes simplex virus type 1 infection can also induce a translocation of the autoantigen to the cell surface. On the cell surface we detected La protein assembled with large protrusions. Within these protrusions La protein colocalized with virus particles. These protrusions are known to be released from the cell after virus infections. Such complexes consisting of self and virus could provide helper determinants for an anti-self response, and therefore be important in generation of autoimmunity.
HSV hepatitis in the mouse: A light and electron microscopic study with immunohistology and in situ hybridization
1988
In order to characterize better the morphology and immune response in acute necrotizing HSV infection, murine HSV hepatitis was examined. BALB/c mice were inoculated intraperitoneally with 10(6) plaque-forming units (PFU) of HSV-1 (Lenette) and HSV-2 (D316). In both groups half the animals were pretreated with silica particles to block macrophage function. Up to 6 days after infection four mice from each group were sacrificed at daily intervals and the livers were examined by light and electron microscopy, immunohistology, in situ hybridization, combined immunohistology/in situ hybridization and titration of viral PFU. HSV-2 infected mice developed severe necrotizing hepatitis with persiste…
Immun-Adhärenz zum Nachweis virusspezifischer Antigene und Antikörper
1968
Es wurde eine Methode zum Nachweis herpesspezifischer Antikorper mit Hilfe der Immun-Adharenz-Reaktion ausgearbeitet und beschrieben. Nach Ermittlung der optimalen Versuchsbedingungen ergeben vergleichende Versuche mit der Komplementbindungsreaktion und dem Neutralisationstest, das die Immun-Adharenz-Reaktion etwa zehnfach hohere Endtiter als die KBR und etwa gleich hohe wie der Neutralisationstest erbringt. Die Immun-Adharenz-Reaktion reagiert antigenspezifisch.
Ca++, Histidin und Zn++ als Faktoren bei der Riesenzellbildung durch das Herpes-Virus hominis
1967
Es wird uber den Ionen- und Aminosaurebedarf der herpesinfizierten Zelle berichtet. Als Merkmal der Wirksamkeit pruften wir die Lebensfahigkeit der Zellen und die Befahigung zur Riesenzellbildung.
Epidemiologie der Infektionskrankheiten
2006
Epidemiologie behandelt die Verbreitung von Krankheitserregern nach ihrer Freisetzung aus dem Organismus, gleichgultig, ob der Organismus erkrankt oder nicht. Sie verfolgt ihren Ubergang in die unbelebte Umwelt einerseits (Wasser, Staub, Luft, Lebensrnittel, so genannte Vektoren und alle denkbaren “Vehikel„) sowie die RuckUbertragung in tierische und menschliche Organismen. Sie zeigt die Notwendigkeit von Impfungen auf und erfasst die Wirkung von Impfmasnahmen oder der Chemotherapie. Sie liefert Hinweise fur das Auftreten von bestimmten Infektionskrankheiten und definiert Ubertragungsrisiken. Ziel ist die Ausrottung von Infektionskrankheiten durch Impfungen (z. B. Pocken, Poliomyelitis), de…
T-cell-mediated cytotoxicity against herpes simplex virus-infected target cells
1977
THE control of herpes simplex virus (HSV) infection by immunological mechanisms seems to be complex and is poorly understood. Neutralising antibodies to HSV plus complement seem to have no effect on the propagation of HSV infection, because HSV spreads to adjacent cells by passing through intercellular bridges1–3. Anti-HSV antibodies plus complement, however, destroy virus-infected cells, but cannot prevent the spread of HSV, suggesting that the virus must be transferred to neighbouring cells before immune lysis occurs1,5. Therefore if lymphocyte-mediated cytolytic mechanisms are instrumental in blocking the spread of HSV in vivo, they ought to destroy infected cells at a very early stage i…
In Vivo Protective Effect of Tumour Necrosis Factor Against Experimental Infection with Herpes Simplex Virus Type 1
1991
C57BL/6 mice, which differ genetically from other strains by their resistance to herpes simplex virus type 1 (HSV-1) infection, were inoculated intraperitoneally with different doses of tumour necrosis factor alpha (TNF-alpha). Mice pretreated with 100 ng, or even 10 ng, of TNF-alpha showed prolonged survival compared to control mice that were infected with 10(7) p.f.u. of HSV-1. Significant protection was observed in mice injected 4 or 8 h prior to or after HSV-1 inoculation, respectively. Protection was also observed when mice which differed at their H-2 locus were treated with TNF-alpha after infection with HSV-1. Interferon could not be detected in the sera of mice at different time poi…
Electron microscopic observations on primary hepatocyte cultures infected with herpes simplex virus Types I and II
1984
The replication cycle of the Herpes simplex virus (HSV) strains I and II has so far been described mainly in established proliferative cell cultures. Most of the biochemical data and ultrastructural cell changes regarding the virus-cell interaction have been obtained from ‘permissive’ cells which allow almost unrestricted viral multiplication. It seems obvious, however, that the in vivo viral infections are not represented adequately by these experiments. In order to achieve a more realistic view of the ultrastructural events during HSV infection of adult tissue, cell cultures were prepared from adult mouse and rat livers and infected with several HSV strains. Established ‘permissive’ cell …