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Biomedical subjects

F Rapp

Publications and source records attributed to F Rapp.

At least 199 records · Page 11Linked to original sources
PubMed1975

Chromosome aberrations in Syrian hamster embryo cells transformed after exposure to ultraviolet-irradiated herpes simplex virus type 1 or 2.

Six Syrian hamster embryo cell lines (14-012-8-1, KOS-6-1, 333-8-9, 333-2-29, MS-4-1, FR-6-1), developed after exposure of primary cultures to different strains of UV-irradiated herpes simplex virus (HSV) type 1 or 2, were analyzed for chromosome aberrations. All the cell lines showed chromosome stability (number of chromosomes were maintained within a narrow range of variation in the diploid region) and a low incidence of polyploids, endoreduplications, and metaphases with pulveration or extensively fragmented chromosomes. The cell lines, passaged over long periods of time in vitro, developed marker chromosomes that suggested a clonal-type evolution of the cell populations. Two cell lines, 333-8-9 and 14-012-8-1, showed two different marker chromosomes with large heterochromatic regions. Chromosomes with abnormal heterochromatic regions, which often appeared like prominent secondary constrictions, were found in all the cell lines we examined. The level of chromosome breakage was low in all the cell lines except the highly tumorigenic cell line 333-2-29, which had a high incidence of cells with single or double chromatinic bodies. The abnormal heterochromatic regions that occurred on marker chromosomes and prominent secondary constrictions were interpreted as a possible chromosomal effect of the HSV. The karyotypic stability and low incidence of open breaks might have been the result of UV irradiation of the HSV.

Animals↗
PubMed1975

Experimental measles encephalitis: a genetic analysis.

The encephalitogenic potential of nine temperature-sensitive mutants of measles virus was determined in newborn golden Syrian hamsters. The parental virus produced acute encephalitis without any prior adaptation. Six of the mutants were attenuated, two were virulent, and one was associated with hydrocephalus with acute onset. The attenuated mutants, blocked before measles virus antigen and ribonucleic acid synthesis at 39 C, were all members of one complementation group. The virulent temperature-sensitive mutants, defective in hemolysin antigen synthesis at 39 C, were members of a second complementation group. The hydrocephalus-inducing mutant was genetically distinct from the other mutants. The mechanism of attenuation most probably does not involve a temperature-induced inhibition of virus replication, but rather appears to be related to the partial defectiveness of the mutants under permissive conditions.

Acute Disease↗
PubMed1975

Stimulation of adenovirus replication in simian cells in the absence of a helper virus by pretreatment of the cells with iododeoxyuridine.

Pretreatment of African green monkey kidney cells with 50 mu g of 5'-iododeoxyruidine (IUdR) per ml can modify their susceptibility to the replication of human adenovirus type 7 in the absence of simian virus 40 (SV40) although this enhancement of adenovirus replication is not as efficient as that of the helper SV40 virus. Since the number of infectious centers remains unchanged after IUdR pretreatment whereas the burst size of virus from each infected cell increases, the IUdR appears to allow each infected cell to produce more virus. Cell DNA synthesis appears to be stimulated in IUdR pretreated cells infected with adenovirus 7, but the host cell DNA synthesized is small enough to remain in the Hirt supernatant fluid. The modification of susceptibility to adenovirus replication and the changed pattern of cell DNA synthesis is stable for at least two additional cell passages of the pretreated cells.

Adenoviridae↗
PubMed1975

Quantitative assay for transformation of 3T3 cells by herpes simplex virus type 2.

The interaction of herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) with Swiss/3T3 cells was investigated. Virus-induced cytopathic effects developed in the absence of production of infectious virus. HSV-2 inactivated with UV light (2, 4, 6, and 8 min) also induced cell death in the absence of virus replication. Cell death was not detectable after infection by HSV-2 that had been inactivated by UV irradiation for 10, 12, and 14 min. 3T3 cells infected with UV-inactivated virus (10 and 12 min) continued to replicate past the contact-inhibited monolayer normally associated with these cells. Infection of 3T3 cells with UV-irradiated USV-2 also induced the development of transformed foci. Transformed cells with an epithelioid of fibroblastoid morphology were identified and isolated. All HSV-2-transformed cell lines contained HSV-2-specific antigens detectable by immunofluorescence techniques. The maximum frequency of HSV-2-induced transformation was 3 times 105 PFU per transformed focus, and the observed transformation could be inhibited by pretreatment of the virus with specific antiserum. No type C particles were detected within five cell culture passages after transformation by HSV-2. Type C virus particles were detected after 10 cell culture passages of the HSV-2-transformed cell lines.

Animals↗
PubMed1975

Temperature-sensitive host range mutants of herpes simplex virus type 2.

Herpesviruses are capable of several types of infection of a host cell. To investigate the early events which ultimately determine the nature of the virus-host cell interaction, a system was established utilizing temperature-sensitive mutants of herpes simplex virus type 2. Four mutants have been isolated which fail to induce cytopathic effects and do not replicate at 39 C in hamster embryo fibroblast cells. At least one mutant is virus DNA negative. Since intracellular complementation is detectable between pairs of mutants, a virus function is known to be temperature sensitive. However, all four mutants induce cytopathic effects and replicate to parental virus levels in rabbit kidney cells at 39 C. This suggests that a host cell function, lacking or nonfunctional in HEF cells but present in rabbit kidney cells at 39 C, is required for the replication of these mutants in hamster embryo fibroblasts cells at 39 C. Therefore, we conclude that these mutants are both temperature sensitive and exhibit host range properties.

Animals↗
PubMed1975

Isolation and preliminary characterization of temperature-sensitive mutants of measles virus.

Twenty-four genetically stable temperature-sensitive mutants of measles virus were isolated after mutangenesis by 5-azacytidine, 5 fluorouracil, or proflavine. The restricted replication of all mutants at 39 C was blocked subsequent to cell penetration and could not be attributed to heat inactivation of virus infectivity. Complementation analysis was made possible through the use of poly-L-ornithine. The members of one complementation group exhibited wild-type RNA synthesis at the nonpermissive temperature and induced the synthesis of virus antigens. These mutants were found defective in both hemolysin antigen synthesis and cell fusion "from within," supporting the unitary hypothesis for these functions. The members of the other two complementation groups synthesized neither virion RNA nor detectable virus antigens at the nonpermissive temperature.

Antigens, Viral↗
PubMed1975

Long-term persistence of cytomegalovirus genome in cultured human cells of prostatic origin.

Cells from prostatic tissue obtained from a 3-year-old male donor exhibited scattered foci of cytopathology on primary culture. A virus was isolated and shown by serological analysis to be cytomegalovirus (CMV). After a number of cell culture passages, a cell line (disignated CMV-Mj-P) was obtained in which foci of infection could no longer be demonstrated, nor could virus be rescued. On continued passage the doubling time of the cells decreased markedly, and the fibroblastoid cells ceased to demonstrate contact inhibition. CMV-specific antigen(s) was detected on the surface of the cells by indirect immunofluorescence techniques after exposure of the cultures to iododeoxyuridine. Microcytotoxocity tests established that CMV-Mj-P cells, but not control human prostate cells or human embryonic lung cells, share a membrane antigen with hamster cells transformed by CMV. Nucleic acid hybridization studies revealed that virus genetic information was carried by the human prostate cells and that the cells contained an average of about 10 to 15 genome equivalents of CMV DNA. Karyotypic analysis confirmed that the CMV-Mj-P cells were of human male origin. These results indicate that the cells either have been transformed by CMV or are chronically infected with CMV and releasing virus at levels below detection.

Antigens, Viral↗
PubMed1975

In vivo characteristics of temperature-sensitive host range mutants of herpes simplex virus type 2.

The in vivo properties of four host range temperature-sensitive (ts) mutants of herpes simplex virus type 2 (HSV-2) were correlated with known in vitro characteristics. Mutants and parental virus were inoculated into newborn and weanling mice and weanling hamsters by intracranial and subcutaneous routes, and into weanling rabbits by corneal scarification. In all cases the pattern of attenuation of mutants in vivo correlated with their stability in vitro at 39 degrees. The most attenuated mutant (mutant 69) was also the most consistent in its inability to induce cytopathic effects (CPE) in vitro or to replicate under nonpermissive conditions. Conversely, the most virulent mutant (mutant 41) was the least stable under nonpermissive conditions.

Animals↗
PubMed1975

Spleen cell-mediated cytotoxicity of hamster cells transformed by Herpes simplex virus: evidence for virus-specific membrane antigen.

The nature of the host's immune response to isografts of hamster embryo fibroblasts (HEF) transformed by herpes simplex virus type 1 (HSV-1) was investigated by the microcytotoxicity assay. It was found that spleen cells from tumor-bearing hamsters killed homologous tumor cells but not HEF transformed by cytomegalovirus or PARA-(defective SV40)-adenovirus 7 (PARA-7). Cytotoxicity was lost as the tumor increased in size. Spleen cells from animals bearing isografts of HSV type 2 (HSV-2) transformed cells also killed HSV-1 target cells whereas spleen cells from PARA-7 tumor bearers did not. Further studies showed that animals immunized with HSV-1 or HSV-1-infected rabbit kidney cells produced spleen cells specifically cytotoxic for HSV-transformed cells. On the other hand, sera from virus-immunized hosts or tumor bearers had no effect on the cells in the presence of guinea pig complement. However, in blocking experiments such sera could significantly reduce spleen cell cytotoxicity. These experiments established that cells transformed by HSV could elicit a cellular immune response in the syngeneic host, and provided evidence that the immunity was directed against virus-specific antigens on the cell surface.

Adenoviridae↗