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Biomedical subjects

F Deinhardt

Publications and source records attributed to F Deinhardt.

At least 289 records · Page 16Linked to original sources

Oncogenicity in marmosets of HL-23V, a type C oncornavirus isolated from human leukemic cells, and comparison with simian sarcoma virus type 1 (SSV-1/SSAV-1).

Type C virus produced by dog thymus cells (A7573) that were infected with virus (HL-23V), isolated from cultured leukocytes of an acute myelogenous leukemia patient, transformed marmoset and horse cells in vitro and induced virus-producing fibromas in marmosets. The tumors and transformed foci were indistinguishable morphologically from those induced by simian sarcoma virus, type 1 (SSV-1/SSAV-1). HL-23V was indistinguishable from SSV-1/SSAV-1 by immunofluorescence and neutralization tests, and the nontransforming virus associated with HL-23V completely inhibited SSV-1 focus induction in interference tests. Cell cultures established from a marmoset fibroma produced transforming and nontransforming virus biologically and antigenically indistinguishable from HL-23V and SSV-1/SSAV-1.

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Susceptibility of common marmosets (Callithrix jacchus) to oncogenic and attenuated strains of Herpesvirus saimiri.

Adult common marmosets, inoculated with either of 2 oncogenic Herpesvirus saimiri (HVS) strains, developed fatal lymphoproliferative disease within 23-25 days post inoculation (PI). The disease was identical to HVS-induced lymphoma in cotton-topped and white-lipped marmosets. Common marmosets inoculated with an attenuated HVS strain developed persistent infection; virus has been recovered from cocultivated lymphocytes of these animals for more than 384 days PI.

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Properties of a baboon lymphotropic herpesvirus related to Epstein-Barr virus.

Three lymphoblastoid cell lines were established from splenic lymphocytes of a lymphomatous baboon (Papio hamadryas) by co-cultivation of the lymphocytes with X-irradiated cells of marmoset or baboon lymphoblastoid cell cultures; the baboon splenic lymphocytes failed to grow when cultured alone. A herpesvirus, associated with each cell line, was identified by immunofluorescence, molecular hybridization and electron microscopy. Antigenic comparison with Epstein-Barr virus (EBV) showed that the baboon herpesvirus and EBV shared cross-reacting viral capsid antigens (VCA): 20 of 20 (100%) anti-VCA (EBV)-positive human sera and 55 of 62 (89%) baboon sera reacted with the baboon lymphoblastoid cells and baboon sera stained EBV VCA in P3HR-1 and EB-3 cells. No nuclear antigen, as assayed by anti-complement immunofluorescence tests, was detected in baboon lymphoblastoid cells when human or baboon anti-VCA positive sera were used. Baboon anti-VCA-positive sera also failed to stain EBV nuclear antigens (EBNA) in Raji or P3HR-1 cells. Preliminary molecular hybridization studies showed only approximately 40% homology between viral DNA of baboon cell lines and DNA of EBV derived from P3HR-1 cells.

Animals↗

[Hepatitis: an international problem (author's transl)].

Three kinds of virus hepatitis are recognized today: hepatitis A, B, and "non A-nonB". Hepatitis A is transmitted mainly by the anal-oral route, hepatitis B and probably also the third form of hepatitis principally by direct inoculation or close physical contact. Normal human immune serum globulin protects against hepatitis A, but only gives limited protection against hepatitis B and "non A-non B" hepatitis. Special immune serum globulin provides better protection but it is only available in small quantities and should be reserved for direct inoculation only. Vaccines for active immunization against hepatitis A and "non A- non B" hepatitis have not yet been developed and active immunization against hepatitis B with HBs-Ag is still in the experimental stage.

Adult↗

Epstein-Barr virus: experimental infection of Callithrix jacchus marmosets.

Eight common marmoset monkeys (Callithrix jacchus) were inoculated with about 10(4) transforming units of B95-8 virus; seven of the marmosets died 50-111 days post inoculation and all seven showed microscopic and/or macroscopic lesions compatible with a diagnosis of lymphoproliferative disease. Low levels of anti-VCA antibodies were detected in plasma from six marmosets. Attempts failed to establish continuous EBV-carrying lymphoblastoid cell cultures by cultivation in vitro of circulating lymphocytes or minced lymphoid tissues obtained at necropsy.

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Characteristics of three strains of feline fibrosarcoma virus grown in cat and marmoset monkey cells.

Two strains of feline fibrosarcoma virus (ST-FeSV and GA-FeSV) were found to induce tumors in cats and marmosets, and to transform feline and marmoset cells in vitro after primary inoculation. A third strain (SM-FeSV) failed to induce tumors or transform marmoset cells after primary inoculation; however, when SM-FeSV-injected marmoset cultures were passed 26 times in vitro, the cell cultures released infectious virus which transformed marmoset fibroblasts but still failed to induce tumors in marmosets. ST-FeSV induced mainly round-cell type transformation (r foci), GA-FeSV induced predominantly mixed round-fusiform cell type transformation (fr foci), and SM-FeSV induced r and fr type foci with a higher proportion of fusiform cells in the fr foci than seen with GA-FeSV. Transforming virus was obtained from r or mixed r/fr foci of ST-FeSV but not from fr foci; heat treatment changed the virus from producing almost exclusively r type foci to inducing an increased number of fr foci. Passage of FeSV in cat cells yielded viruses with a higher ratio of infectivity for feline vs marmoset cells, while passage of FeSV in marmoset cells yielded virus with a relatively higher infectivity ratio for marmoset cells; the three strains differed in the degree of change in the infectivity ratio. Despite the alteration of host range of SM-FeSV propagated in marmoset fibroblasts, the virus retained feline P-30 antigen by CF and FA assays. Neutralization tests did not indicate but also did not exclude an alteration of the surface antigens of ST-FeSV or SM-FeSV propagated in marmoset fibroblasts. The alteration of the relative infectivity of FeSV during passage in marmoset cells may be due to: (1) the selection of a variant present in the original heterogenous uncloned population; (2) mutation; or (3) recombination with some marmoset genetic material, possibly an as yet unidentified endogenous marmoset virus.

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Mononuclear cell fraction carrying Herpesvirus saimiri in persistently infected squirrel monkeys.

Circulating lymphocytes from squirrel monkeys persistently infected with Herpesvirus saimiri (HVS) were separated into B- and T-lymphocyte fractions by a rosette-enrichment technique. HVS was isolated only from lymphocyte fractions forming rosettes or from unseparated lymphocytes; this indicated that T-lymphocytes were the target cells for HVS in the natural host, squirrel monkeys.

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Experimental infection of squirrel and marmoset monkeys with attenuated Herpesvirus saimiri.

Herpesvirus saimiri (HVS) was propagated in vero cells for 3 passages at 39 degrees and cloned 3 times at 34 degrees. This virus was inoculated into cotton-topped marmoset and squirrel monkeys; all inoculated monkeys became infected as HVS was reisolated after their circulating lymphocytes were cultured with vero cells and measurable levels of antiviral antibodies developed that were measured by immunofluorescence and/or neutralization tests. None of the inoculated monkeys developed any signs of overt disease and all inoculated monkeys have survived 9 to 14 months postinoculation. The attenuated virus appears to be genetically stable as virus isolated from an infected marmoset was passed 3 times in vitro and then inoculated into other marmosets, which became infected and remained clinically well. Marmosets latently infected with attenuated HVS were not protected when challenged with a large dose (770 plaque-forming units) of oncogenic HVS, although these marmosets survived about 3 times longer than did inoculated control marmosets.

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Epidemiology and mode of transmission of viral hepatitis A and B.

Viral hepatitis is now subdivided into three forms: hepatitis A (HA), epidemic or short-incubation-period hepatitis; hepatitis B (HB), homologous serum or posttransfusion hepatitis; and a third form, for which the term "hepatitis C" (HC) or "non-A-non-B hepatitis" has been proposed. Hepatitis A is usually transmitted by the anal-oral route and occurs endemically and epidemically; hepatitis B is transmitted by direct inoculation but probably almost as frequently by nonparenteral routes and is usually endemic; hepatitis C occurs after transfusion and may account for more cases of posttransfusion hepatitis than HA and HB together. Both HA and HB can be diagnosed accurately by their respective antigens and corresponding antibodies; in contrast, little is known yet about the characteristics of HC.

Adolescent↗

Experimental infection of marmosets with a cytomegalovirus of human origin.

Two adult and two neonatal cotton-topped marmosets and two neonatal white-lipped marmosets (Saguinus species) were inoculated with 10(7) plaque-forming units of cytomegalovirus (Colburn strain). No overt clinical disease developed in four marmosets during observation for eight months; one adult and one neonatal cotton-topped marmoset died from nonspecific causes 63 and 259 days after inoculation, respectively. By days 7-16 after inoculation, all marmosets developed plasma antibodies, which were detectable by neutralization and immunofluorescence assays (peak titers, 1:128-1:256 and 1:64-1:256, respectively). Attempts to isolate virus from whole blood, peripheral lymphocytes, oropharyngeal swabs, or vaginal swabs by cocultivation with permissive cell cultures were unsuccessful. Virus was recovered, however, by cocultivation from the kidney tissues of the adult marmoset that died. Immunosuppressive treatment with azathioprine resulted in a fourfold increase in antibody levels in plasma of two of three marmosets.

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Immunization of Rous sarcoma virus-inoculated marmosets with BCG and transformed allogeneic cells.

The effects of specific immunotherapy with allogeneic cells transformed by Schmidt-Ruppin Rous sarcoma virus (SR-RSV), of treatment with BCG, and of surgery on the growth of SR-RSV-induced sarcomas in white-lipped marmosets were studied. Tumor incidence, tumor progression, and survival did not differ between control and treated animals. Animals immunized with BCG developed lymphocyte reactivity to tuberculin, which remained until the animals died. BCG was isolated from the spleen of one tumor-bearing animal.

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Immunological control of virus-induced tumors in primates.

Cells infected by oncogenic viruses may transform, may develop a latent carrier state, or may be destroyed but understanding of the control of the results of infection is incomplete. Even if cells transform, ultimate development of a tumor may be immunologically controlled. For example, cells of some marmoset species transform after infection with RNA tumor viruses, and animals react to the transformed cells with cell-mediated and humoral immune responses. Both virus specific and cross-reacting cell membrane antigens have been demonstrated. Immune deficiency accelerates tumor growth or causes recurrence of a regressing tumor. In contrast certain simian herpesvirus (Herpesvirus saimiri, HVS and Herpesvirus ateles, HVA), which cause no or minor disease in their natural hosts, induce lymphomas or lymphoblastic leukemias in other primate species. The immune response of the natural host species to HVS is greater than that of animals developing malignancies after experimental infection. HVS and HVA share many properties with Epstein-Barr virus (EBV) of man, including antigens appearing early and late during infection and their related antibody responses but no evidence exists that they induce malignancies in their natural hosts. However, if induction is as infrequent as that with EBV and Burkitt's lymphoma (BL), we have not observed sufficient numbers of squirrel or spider monkeys to have seen a BL-like tumor. Interference with the immune systems of animals carrying HVS or HVA may induce tumor development, and clarify our understanding of the relationships between EBV and BL.

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