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Biomedical subjects

R G Olsen

Publications and source records attributed to R G Olsen.

At least 145 records · Page 8Linked to original sources
PubMed1977

Inhibition of concanavalin A stimulation of feline lymphocytes by inactivated feline leukemia virus.

In a lymphocyte blast transformation assay, the response of feline lymphocytes to concanavalin A was suppressed 20 to 65 percent in the presence of inactivated feline leukemia virus. The decrease was not due to viral cytotoxicity, as determined by trypan blue viability counts, nor was the virus binding the concanavalin A and interfering with its mitogenic stimulation. The virus may be biochemically repressive in itself, interfering with cell-mediated immunity within the feline system.

Aged↗
PubMed1977

Abrogation of resistance to feline oncornavirus disease by immunization with killed feline leukemia virus.

Four-week-old specific-pathogen-free cats were immunized with a combined vaccine composed of killed feline leukemia virus and killed feline oncornavirus-associated cell membrane antigen-containing tumor cells. Immunization induced feline oncornavirus-associated cell membrane antigen antibody titers ranging from 1:32 to 1:256 but did not elicit detectable virus-neutralizing antibody titers. Kittens immunized with tumor cells alone developed higher feline oncornavirus-associated cell membrane antigen antibody titers (ranging from 1:512 to 1:2048) than those given the combined vaccine. All kittens were challenged with virulent Dynder-Theilen feline sarcoma virus at 12 weeks of age. Seventy-five % of the kittens vaccinated with combined vaccine and 67% of unvaccinated control kittens developed progressive fibrosarcomas after challenge. By contrast, none of the kittens vaccinated with killed tumor cells alone developed progressive fibrosarcomas after challenge. The combined vaccine did not, however, inhibit the induction of feline leukemia virus viremia.

Animals↗
PubMed1977

Erythrocyte rosette formation of equine peripheral blood lymphocytes.

Erythrocyte rosette (ER) formation of equine peripheral blood lymphocytes (PBL) was characterized. Guinea pig and, to a lesser extent, human erythrocytes formed ER; cat, cow, dog, hamster, mouse, rat, and sheep erythrocytes showed negligible rosetting properties. Conditions of the assay were varied to determine which procedure allowed the largest percentage of rosette formation. The PBL from 20 normal horses were then assayed, averaging 38 +/- 2% ER. To characterize the erythrocyte receptor as being on T or B cells, equine thymocytes from 6 foals were assayed; the thymocytes formed an average of 66 +/- 5% ER. Mixed ER and erythrocyte-antibody-complement rosette assays showed no PBL which bound both ER and erythrocyte-antibody-complement rosettes. The PBL which was stimulated with phytohemagglutinin formed more rosettes (69 +/- 2%) than nonstimulated, control PBL (42 +/- 3%).

Animals↗
PubMed1976

Influence of culture conditions of growth of FL-74 cells and feline oncornavirus cell membrane associated antigen production.

The FL-74 cell, a feline lymphoblastoid cell line derived from a tumor induced by leukemia virus, grows equally well in static suspension culture (plastic T-flask or silicone treated glass bottles) or in spinner culture. No growth was observed in unsiliconized glass bottles. Although feline leukemia virus production was nearly the same in FL-74 grown in each of the above types of vessel, the expression of the feline oncornavirus membrane associated antigen (FOCMA), as determined by membrane immunofluorescence, was more intense and more complete on cells grown in static suspension. Moreover, higher fluorescent antibody titer endpoints were observed with cells from static suspension cultures than with cells from spinner cultures, FL-74 cells grown in spinner culture, when subjected to partial synchrony by cold block or by deprivation of essential amino acids (arginine and/or isoleucine) for 12 hr, achieved a membrane fluorescent pattern for FOCMA similar to cells grown in static suspension. It is proposed that the expression of FOCMA on the cell membrane surface is cell-cycle dependent, and that the rate at which a cell passes through the cell cycle determines the pattern and intensity of the fluorescence of the cell membrane.

Antigens, Viral↗
PubMed1976

Feline oncornavirus-associated cell membrane antigen. VI. Cytotoxic antibody in cats exposed to feline leukemia virus.

Feline leukemia virus (FeLV)-infected specific pathogen-free (SPF) cats, normal uninfected SPF cats, and healthy cats from leukemic households were tested for antibody reactive to the feline oncornavirus-associated cell membrane antigen (FOCMA)-containing target cell line FL-74 by microcytotoxicity and indirect membrane immunofluorescence. Of the infected SPF animals, 81% showed concordant reactivity for the two tests. In contrast, only 55% of the healthy cats known to be naturally exposed to FeLV for long periods showed such concordance. FOCMA antibody could not be detected in normal SPF cats by either indirect membrane immunofluorescence or microcytotoxicity. Most cats in the FeLV-infected SPF group developed antibody detectable by both procedures by the fifth week post inoculation. Antibody detectable by membrane immunofluorescence persisted in a high percentage (75-90%) of the animals throughout the observation period of 19 weeks; after 9 weeks, fewer cats had antibody that was also detectable by microcytotoxicity.

Animals↗
PubMed1976

Feline leukemia virus infection: age-related variation in response of cats to experimental infection.

Sixty-seven specific-pathogen-free cats of various ages (newborn, 2 wk, 1 mo, 2 mo, 4 mo, and 1 yr) were inoculated ip with either the Rickard (R) or the Kawakami-Theilen (KT) strain of feline leukemia virus (FeLV). Susceptibility to FeLV was judged by induction of a) FeLV group-specific antigens (gsa) in leukocytes, b) FeLV-related disease, c) antibody to feline oncornavirus-associated cell membrane antigen (FOCMA), and d) virus-neutralizing (VN) antibody. Susceptibility to FeLV-decreased with age. Persistent viremia and FeLV-related disease developed in 100% of cats inoculated as newborns, in 85% of cats inoculated at 2 weeks to 2 months of age, and in 15% of cats inoculated at 4 months or 1 year of age. Cats susceptible to FeLV leukemogenesis became persistently FeLV gsa-positive (viremic) at 4 weeks post inoculation and thereafter and produced little or no FOCMA or VN antibody. Cats that resisted leukemogenesis by FeLV all developed persistent FOCMA and VN titers and never became FeLV gsa-positive. The disease in inoculated cats was influenced by virus strain; FeLV-R induced predominantly thymic lymphosarcoma, whereas FeLV-KT caused fatal nonregenerative anemia without concurrent neoplasia.

Age Factors↗
PubMed1976

Characterization of feline T-and B-lymphocytes and identification of an experimentally induced T-cell neoplasm in the cat.

Membrane markers of feline T- and B-lymphocytes were identified for further investigation of leukemogenesis in the cat. Feline T-cells formed spontaneous erythrocyte rosettes with guinea pig (GPE) and rat erythrocytes (RE). The receptors for GPE and RE were separate entities and expressed independently on lymphoid cell membranes. The RE receptor appeared to be present only on more mature or differentiated T-cells, whereas the GPE receptor reacted with a broader population that included less differentiated T-cells. Feline B-cells bore a complement receptor that was detected by adherence of SE coated with antibody and complement. Malignant lymphoblasts obtained from thoracic fluid of cats with feline leukemia virus (FeLV)-induced thymic lymphosarcomas, as well as FL-74 cells (a FeLV-transformed feline lymphoblastoid cell line) expressed T-cell markers. These results provided definitive evidence for markers of feline T- and B-cells and identified an experimentally induced T-cell lymphosarcoma.

Animals↗
PubMed1976

Lymphocyte mitogen reactivity and enumeration of circulating B- and T-cells during feline leukemia virus infection in the cat.

Mitogen-induced blast transformation of peripheral blood lymphocytes and quantitative changes in circulating T- and B-cells were studied serially in cats inoculated with feline leukemia virus (FeLV). Concanavalin A-induced blast transformation sharply declined beginning at 5 weeks post inoculation (Pl) in FeLV-infected cats when compared to age-matched uninfected control cats. Similar but less consistent changes were seen in responses to pokeweed mitogen-induced stimulation. In most infected kittens this defect persisted until they died from thymic lymphosarcoma, 15-24 weeks Pl. An early lymphopenia, due primarily to a decrease in circulating B-cells, occurred in infected cats 5-8 weeks Pl. Following a return of total and B-lymphocytes to control values, infected cats developed increased numbers of T-cells at 16 or more weeks Pl, which correlated with circulating lymphoblastic lymphocytes bearing T-cell markers. These results correlated neoplasia arising in a thymus-derived lymphocyte population with mitogenic hyporeactivity in the preneoplastic period and suggested that FeLV-induced immune alterations may be a necessary antecedent of leukemogenesis in the cat.

Animals↗
PubMed1976

Influence of glucocorticoid, estrogen, and androgen hormones on transformation of human cells in vitro by feline sarcoma virus.

Infection of human foreskin cells (D-550) by the Snyder-Theilen strain of feline sarcoma virus produced small but countable foci and demonstrated "single-hit" dose-response kinetics. Significant quantitative and qualitative enhancement of focus formation was observed when the glucocorticoid hormones, dexamethasone, hydrocortisone, cortisol acetate, and prednisolone were added to cell cultures (1.0 mug/ml) 24 hr postinfection. However, aldosterone, while inducing qualitatively larger foci, did not bring about a quantitative enhancement in total foci number. By contrast, 17beta-estradiol, progesterone, cortisone acetate, methyltestosterone, and estrone elicited little or no effect on focus induction by Snyder-Theilen feline sarcoma virus. Evidence is suggestive of a posttranscriptional effect possibly modulating viral genome expression resulting in an increased efficiency of viral transformation, and an increased proliferation of transformed cells.

Aldosterone↗
PubMed1976

Inactivation of tumor cell-associated feline oncornavirus for preparation of an infectious virus-free tumor cell immunogen.

Ultraviolet (UV) and thermal methods of inactivating the oncogenic potential of C-type particle-producing feline oncornavirus-induced tumor cells were developed. The techniques were evaluated by several parameters for their use in preparation of cellular immunogens. The UV inactivation dose required to reduce the number of focus-forming units per ml by 1 log10 for FL-74 lymphoblastoid cell-associated feline leukemia virus was 44,000 ergs/sq mm, and the thermal inactivation dose required to reduce the number of focus-forming units per ml by 1 log10 at 45 degrees was 16 min. Inactivation of greater than 6 log10 of virus per ml associated with 4 x 10(8) cells required a UV dose of 270,000 ergs/sq mm, 100 min at 45 degrees or 3 min at 56 degrees. All three treatments concomitantly destroyed the replicating potential of FL-74 cells as shown by their inability to propagate under normal growth conditions and to incorporate [3H]thymidine into nuclear DNA. UV inactivation and thermal inactivation at 45 degrees allowed the best retention of feline oncornavirus-associated cell membrane antigen. A 50% loss in antigenic activity was observed as a result of 56 degrees treatment, but this method was the only one that did not destroy the surface structural integrity of FL-74 cells.

Antibodies, Viral↗
PubMed1976

Immunization against feline oncarnavirus disease using a killed tumor cell vaccine.

Specific pathogen-free cats were immunized with an inactivated feline oncornavirus tumor cell vaccine. Immunized cats produced high antibody titers to the feline oncornavirus-associated cell membrane antigen and were protected from oncogenic feline sarcoma virus challenge. However, immunization did not produce virus-neutralizing antibody nor did it prevent viremia.

Animals↗
PubMed1976

Experimental oncornavirus vaccines in the cat.

An experimental approach to the immunoprophylatic control of feline oncornavirus-mediated diseases has included induction of antivirus immunity and antibodies to the feline oncornavirus-associated membrane (tumor) antigens. A suitable model for exploring the effectiveness of killed oncornavirus vaccines in the cat has been provided by the use of feline sarcoma virus. Immunization of seven pregnant queens over a 6-week period with ultraviolet light-inactivated Gardner-Arnstein feline sarcoma virus resulted in significant protection among 12 kittens challenged with a tumor-forming Dose 90 at 7 days of age. This immunity was not present in kittens challenged at 35 days of age. Among 12 kittens born of queens immunized during pregnancy with ultraviolet light-inactivated Kawakami-Theilen feline leukemia virus and challenged with the same live virus at 4 days of age, significant protection was noted, ranging from prolongation of survival time to complete protection in 3 kittens. In general, the higher the antibody titer in the mother, the more effective the protection afforded the kittens. Immunization of 43 kittens during their first 5 weeks of life with the same vaccines used in adult cats did not immunize sufficiently to protect against feline sarcoma virus challenge at 5 weeks of age. Neutralizing antibody responses in these kittens were significantly lower than in pregnant queens. That kittens of this age are immunologically responsive was established, since complete protection of 9 kittens to feline sarcoma virus was obtained by immunization with a crude tumor extract inactivated with 5 to 7 megarads of gamma-irradiation. All these kittens developed feline oncornavirus-associated membrane antibodies while 3 developed demonstrable levels of virus-neutralizing antibodies. The results of these studies are believed indicative that killed virus vaccines and tumor vaccines can be effective immunoprophylatic measures in the control of RNA tumor virus oncogenesis in the cat. Developments in this model system should be relevant to any consideration given similar vaccines in humans.

Age Factors↗
PubMed1975

Feline oncornavirus-associated cell membrane antigen. V. Humoral immune response to virus and cell membrane antigens in cats inoculated with Gardner-Arnstein feline sarcoma virus.

Tumor growth responses in 5- to 6-week-old kittens inoculated with the Gardner-Arnstein strain of feline sarcoma virus exhibited three distinct pattern: 1) complete tumor regression or no detectable tumor growth in approximately one-third of 43 inoculated kittens, 2) rapid tumor progression which led to debilitation and death within 16.2 +/- 4.2 weeks following infection in an additional one-third, and 3) slow tumor growth or temporary regressions in the remaining third. The feline oncornavirus-associated cell membrane antigen (FOCMA) antibody response was closely correlated with tumor progression; rapid progressors had the lowest antibody titers, whereas those in the "no tumor or permanent regression" categories had the highest titers. These results agreed with those previously observed with another virus strain, the Snyder-Theilen feline sarcoma virus. Cats in the intermediate categories of tumor growth also had intermediate levels of FOCMA antibody. The presence of virus-neutralizing (VN) activity was not always correlated with anti-FOCMA activity. Animals in the rapid-progressor category, compared to the regressors or slow progressors, were more likely to have detectable VN antibody during early periods. Conversely, animals in the regressor group or group with no tumors were more likely to show an early rise in detectable anti-FOCMA activity than animals in either of the progressor groups.

Animals↗
PubMed1975

Determination of subgroup-specific feline oncornavirus-neutralizing antibody.

A microneutralization assay was developed for antibody-to-subgroup-specific feline oncornaviruses. This study combines the economic advantage of a microtiter system and the quantitative focus reduction method which permits contruction of multiplicity curves for determination of virus-neutralizing titers. A twofold increase in Synder-Theilen feline sarcoma virus (ST-FeSV) on feline embryo cells decreased by approximately twofold the titer of reference goat serum prepared against Kawakami-Theilen feline leukemia virus. Similar dose effects with FeLV serotype virus preparations were not observed. An assay system utilizing FeLV serotypes on sarcoma-positive leukemia-negative cells demonstrated slightly greater sensitivity than one employing ST-FeSV on FE cells. Differential antibody responses to the three subgroup-specific feline oncornaviruses (A, B ,and C) were observed in reference goat sera. This test demonstrated good reproducibility as well as sensitivity and constitutes a significant improvement over end point dilution assay systems.

Animals↗
PubMed1975

Evidence of respiratory tract infection induced by equine herpesvirus, type 2, in the horse.

Five horses were experimentally exposed to equine herpesvirus 2 strain LK. Two young foals developed chronic pharyngitis (98 and 232 days, respectively). Growth characteristics, cytopathic effects (CPE), inclusion body formation, ether sensitivity, and immunofluorescent analysis indicated that the virus recovered from infected animals was a herpesvirus serologically identical with, or at least antigenically related to EHV-2 strain LK. No significant complement-fixing (CF) or virus-neutralizing (VN) antibody responses were observed in adult horses while both foals demonstrated a rise in CF antibody titer. One of the two foals demonstrated a rise in VN antibody only. The results suggest that EHV-2 virus induced chronic pharyngitis, primarily the result of lymphoid proliferation, with no overt clinical signs.

Animals↗
PubMed1975

Complement-fixation-inhibition as a test for antibodies in cats and humans to C-type RNA tumor virus antigen.

The complement-fixation-inhibition (CFI) test was evaluated as a means of detecting humoral antibodies in cat sera and in human sera to mammalian C-type RNA virus interspecies antigen(s). CFI antibody titers of greater than or equal 1:2 were detected in sera from all tumor bearing (23) and normal cats (23), however, sera from most germ free cats were negative. When the same cat sera were tested for blocking antibody by the paired radioiodine labeled antibody technique the correlation between the radioimmune assay and CFI tests was 85%. Sera from 378 cancer patients and 193 normal people were tested for antibodies to the mammalian oncornavirus interspecies-specific antigen in the CFI test. This test used a rabbit antiserum prepared toward a purified feline leukemia virus (FeLV) interspecies antigen. Disrupted Rauscher murine leukemia virus (RLV) was used as source of interspecies antigen in the CFI test. A significantly (P=0.01) higher number of reactions occurred with sera from patients with lymphosarcoma (70.4%), osteosarcoma (41.0%), reticulum cell sarcoma (56.7%), and rhabdomyosarcoma (31.8%) as opposed to sera from normal individuals (6.2%). Of 51 sera from patients with acute lymphocytic leukemia 23.5% (P=0.05) were reactive. Of the sera from 88 breast cancer patients 22.7% reacted, as opposed to 7.8% of 116 normal females and 13.9% of 43 patients with benign breast disease. CFI antibody titers were shown to be dependent on RLV antigen concentration. Absorption with human A and B red blood cell (RBC) and Forssman antigen did not reduce the CFI titers in human sera whereas absorption with RLV reduced them significantly. By indirect radioimmunoelectrophoresis the antibody in selected human sera was shown to be an IgG.

Animals↗