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Biomedical subjects

O Jarrett

Publications and source records attributed to O Jarrett.

At least 109 records · Page 6Linked to original sources
PubMed1986

Histopathological and hematological findings in myeloid leukemia induced by a new feline leukemia virus isolate.

Myeloid leukemia was induced by a new feline leukemia virus isolate FeLV-AB/GM-1 in a high proportion of cats. The latency period was short. Three to 5 weeks after infection early changes were detectable in the bone marrow, and cats developed leukemia 5 to 8 weeks after infection. The results of the present histological and cytological studies suggested that there were two stages in the development of leukemia. The first stage appeared to be equivalent to the syndrome of bone marrow dysplasia or preleukemia which, however, converted rapidly to leukemia. Cytopenia(s) were the main hematological findings in all preleukemic and leukemic cats. White blood cell counts were low or normal, but the number of leukemic and abnormal cells increased in the peripheral blood with the progression of the disease. This reliable model system lends itself to further studies to elucidate the pathogenesis of myeloproliferative disorders.

Animals↗
PubMed1986

A possible maturation pathway of calicivirus particles.

The assembly process of feline calicivirus, a representative member of the Caliciviridae, from subunit components in infected cells was monitored by labelling the virus-specific proteins with 3H-leucine for different periods and harvesting cellular extracts at various phases of infection. A series of protein subunit components was detected and the virus assembly process appeared to have occurred in at least two stages. The first stage involved the very rapid aggregation of precursor polypeptides into 5S subunits which possible through several 'unstable' intermediates formed the stable 15S subunit component. The second stage was the association of 15S subunits with the synthesized viral genomes to form the mature infectious FCV particles which sedimented at 170S. Within 30 min of the initiation of protein synthesis, the process of assembly was complete and mature FCV particles appeared in infected cells.

Animals↗
PubMed1985

Feline calicivirus subunit vaccine--a prototype.

A vaccine was prepared from a subunit component, antigenically similar to the whole feline calicivirus (FCV) particles. Despite the limited number of animals available for this study we were able to demonstrate that the vaccine protected cats when challenged with a virulent strain of the virus while the non-vaccinates kept as controls developed clinical and histopathological symptoms of the calicivirus disease.

Animals↗
PubMed1985

Haemadsorption and haemagglutination by feline leukaemia viruses.

The interaction of feline leukaemia viruses (FeLV) with erythrocytes was investigated. Haemadsorption (HAd) was observed on the surface of feline embryonic fibroblast cells infected with FeLV. HAd was detected in various degrees when cat, hamster or horse erythrocytes were incubated with cells infected with viruses of subgroup C (FeLV-C) and on cells infected with some FeLV subgroup A viruses (FeLV-A), but not on cells infected with FeLV subgroup B viruses (FeLV-B). HAd of sheep erythrocytes was detected on cells infected with some FeLV-C viruses. The HAd of hamster erythrocytes on cells infected with FeLV-C/Sarma virus was inhibited by antisera against gp70 or p15(E) but not by sera to the other FeLV structural polypeptides. HAd inhibition was also exhibited by cat sera which had FeLV-neutralizing activity but not by sera of specific pathogen-free cats. Haemagglutination by FeLV-C viruses was demonstrated after the virus was treated with neuraminidase and phospholipase C, or Tween-80 and ether. Contrary to expectations from the pattern observed by HAd, all FeLV-A viruses had similar haemagglutinin (HA) activity to FeLV-C viruses. FeLV-B viruses did not possess an HA.

Animals↗
PubMed1985

Induction of protective immune response in cats by vaccination with feline leukemia virus iscom.

An effective candidate subunit vaccine consisting of the gp 70/85 of feline leukemia virus (FeLV) was prepared by using the immunostimulating complex (iscom) method for the presentation of membrane proteins of enveloped viruses. Two 32-wk-old specific pathogen-free (SPF) cats were immunized with a FeLV iscom vaccine prepared from the supernatant fluid of the FL74 tumor cell line without adjuvant. Both cats developed FeLV serum antibodies, as measured in an enzyme-linked immunosorbent assay (ELISA) and in a virus neutralization test. A proportion of the antibodies were directed to an epitope located on gp70/85, which was shown in competition ELISA with a peroxidase-labeled virus-neutralizing monoclonal antibody to be shared by all three subtypes of FeLV. The protective effect of FeLV iscom was studied by vaccinating six 8-wk-old SPF cats with iscom prepared from cell culture supernatant of another tumor cell line F422, followed by oronasal challenge with 10(6) ffu FeLV-A (strain Glasgow-1). Six unvaccinated cats were also challenged with the same dose of FeLV. The vaccinated cats developed FeLV serum antibodies, some of which were directed to the shared epitope on gp70/85. At 10 wk after challenge, none was viremic, whereas three of the control cats had developed FeLV viremia. The potential of FeLV iscom as a vaccine against FeLV-associated disease in cats, and of iscom vaccines for protection against mammalian retrovirus infections, is discussed.

Adjuvants, Immunologic↗
PubMed1984

Interaction between feline leukaemia virus subgroups in the pathogenesis of erythroid hypoplasia.

The interaction of feline leukaemia virus (FeLV) of subgroups A and C in the pathogenesis of erythroid hypoplasia in cats was studied. Weanling kittens infected with FeLV-A became permanently viraemic but remained haematologically normal over a period of 36 weeks. Similar kittens inoculated with FeLV-C, which produces erythroid hypoplasia when administered to newborn kittens, neither became viraemic nor developed the disease. However, weanling kittens inoculated with a mixture of FeLV-A and C became viraemic, first with FeLV-A and then additionally with FeLV-C, and the emergence of FeLV-C into the blood coincided with the advent of erythroid hypoplasia. When FeLV-C was inoculated into five older cats which had been viraemic with FeLV-A for several months previously, it appeared in the plasma of three of the cats and erythroid hypoplasia was diagnosed in two of these, 16-20 weeks after infection with FeLV-C. These results show that FeLV-A enhances the growth of FeLV-C in cats and overcomes their age-related resistance to FeLV-C. Also, the appearance of FeLV-C in the plasma of cats viraemic with FeLV-A indicates that erythroid hypoplasia will subsequently occur rapidly. These findings are relevant to the origin of FeLV-C isolates and their occurrence in nature.

Anemia, Aplastic↗
PubMed1983

Recovery of feline leukaemia virus from non-viraemic cats.

The persistence of virus in the bone marrow of cats which had ostensibly recovered from feline leukaemia virus (FeLV) infection was investigated. Nineteen cats were exposed to FeLV by natural, contact infection and 36 weeks later three were found to be persistently viraemic while the remainder were non-viraemic and had virus neutralising serum antibodies. Virus was isolated in bone marrow cultures established from nine of the 16 non-viraemic cats which were considered, therefore, to have latent infections. Cats infected soon after exposure to FeLV carrier cats were more likely to become persistently viraemic or develop a latent infection than those infected later, which tended to recover. There was no difference in serum antibody levels between the latently infected and recovered cats. Whether cats with latent infections spread virus or develop FeLV-negative haemopoietic tumours was considered. Six kittens housed together for eight months with a cat with a latent infection showed no signs of having been exposed to FeLV. Virus was not isolated from bone marrow cultures of two cats with FeLV-free lymphosarcoma or myelomonocytic leukaemia.

Animals↗
PubMed1983

Effect of hydrocortisone on osteoclasts generated in cat bone marrow cultures.

The generation of osteoclasts in cultures of cat bone marrow was completely inhibited for 4 weeks with 10(-6)M hydrocortisone (HC) and partially inhibited with 10(-7) to 10(-9)M in a dose-dependent fashion. This effect was completely reversible when cultures were exposed for only 2 weeks to 10(-9) or 10(-8)M HC. However, cultures in which higher concentrations (10(-7) to 10(-5)M) were maintained for the same period did not show complete recovery in terms of numbers of osteoclasts and number of nuclei per cell after withdrawal of HC, suggesting that precursor cells of osteoclasts were also damaged by HC. To study the effects of HC on osteoclasts already present in the cultures, 10(-6)M was added to 4-week-old untreated cultures. The number of osteoclasts decreased rapidly and a gross morphological response was also apparent (rounding of the cells leading to detachment from the substratum and inhibition of cell fusion), indicating that the generation as well as the survival of osteoclasts in vitro are sensitive to HC. The morphological changes observed under optical and electron microscopy correspond to those of the reported inactive form of osteoclasts, and suggest that their function may also be altered by HC.

Animals↗
PubMed1983

Haemopoietic colony formation (BFU-E, GM-CFC) during the development of pure red cell hypoplasia induced in the cat by feline leukaemia virus.

The GM-CFC assay for granulocyte-macrophage progenitors and the BFU-E and CFU-E assay for early and late erythroid progenitors from cat bone marrow were characterized. GM-CFC gave 59 +/- 4 to 118 +/- 6 colonies per 10(5) bone marrow cells using colony stimulating factors (CSF) from cat, mouse or human sources. The CFU-E and BFU-E assays gave 114 +/- 7 and 58 +/- 7 colonies respectively with optimum doses of erythropoietin. Irradiated cat bone marrow cells were good sources of CSF and of burst promoting activity for these assays. Kittens infected with feline leukaemia virus, subgroup C (FeLV-C), which induces pure red cell hypoplasia, showed the incidence of BFU-E decreased to 25-35% of controls as early as one week postinfection, and even lower values at later times. In contrast, the incidence of GM-CFC remained normal for several weeks. No evidence of inhibitory cells or of lack of stimulatory cells in the infected marrows was seen when they were cultured together with normal marrow in the BFU-E assay. Conversely, normal marrow cells were not able to restore BFU-E growth from infected marrow. This suggests a direct action of FeLV-C on early erythroid precursors. Infection with FeLV, subgroup A, which induces only a mild transitory anaemia, produces only a moderate decrease in the incidence of BFU-E.

Anemia, Aplastic↗
PubMed1983

Feline leukemia virus envelope gp70 of subgroups B and C defined by monoclonal antibodies with cytotoxic and neutralizing functions.

Nine murine monoclonal antibodies (MAb) to the envelope proteins of feline leukemia virus (FeLV) are described. Eight MAb are directed to epitopes of the same molecular species of gp70 and the other MAb is directed to the p15E moiety. Six of the gp70 epitopes are discrete; two are closely associated or overlapping. Four anti-gp70 MAb (2 of IgG2A and 2 of IgG2B subclasses) were directly cytotoxic for FeLV-producer lymphoma cells with cat or with rabbit complement (C). Another MAb (IgG2B), which was not cytotoxic alone, specifically and synergistically increased the cytotoxic effects of both IgG2A MAb. Cytotoxic anti-gp70 MAb also had virus-neutralizing capacity; one MAb recognized a determinant common to all FeLV subgroups (A, B, and C), the others recognized gp70 epitopes not present on subgroup A but common to both B and C subgroups. Competitive inhibition of MAb binding was employed to map spatial distributions of the epitopes, and the results fitted a molecule shaped as an incomplete loop. According to the model, epitopes involved with cytotoxic and virus neutralizing antibody functions were closely associated; the region involved is approximately in the center of the molecule, and it contains epitopes that are variably expressed among individual isolates of FeLV derived from different cat lymphoma cell lines.

Animals↗
PubMed1982

A comparison of three methods of feline leukaemia virus diagnosis.

Samples of blood from pet cats were examined for evidence of feline leukaemia virus (FeLV) by three techniques: virus isolation, immunofluorescence and an enzyme-linked immunosorbent assay (ELISA) Leukassay F. There was good agreement between the results from virus isolation and immunofluorescence. However, about 30 per cent of cats which were positive for FeLV antigen by ELISA were negative by either of the other tests. The status of most of these cats was unchanged four or 12 weeks later.

Animals↗
PubMed1982

Detection of transient and persistent feline leukaemia virus infections.

A study was made of cats persistently or transiently viraemic with feline leukaemia virus (FeLV) following experimental oronasal infection. Cats of two ages were exposed to the virus. One group was infected when eight weeks old in the expectation that most of the cats would become persistently viraemic, and the second group when 16 weeks old, so that some would show signs of a transient infection and then recover. The periods following infection when virus was detectable in the blood and in the oropharynx were determined for each group. Three methods for detecting viraemia were compared: virus isolation, immunofluorescence on blood smears and an enzyme-linked immunosorbent assay (ELISA). There was good overall agreement among the three tests in detecting virus-positive cats. Virus was found sooner after infection by virus isolation than by the other methods, and virus appeared in the blood slightly sooner in cats which developed persistent viraemia than in transiently viraemic cats. Infectious FeLV was isolated from the oropharynx of all of the persistently viraemic cats, in most cases simultaneously with virus in the plasma. Virus was also isolated from the mouth of most transiently viraemic cats. Under field conditions such transient excretion of virus lasting only a few days would rarely be detected in a single sampling. This might explain how FeLV is maintained in free range urban cats in the absence of a large number of cats with persistent active FeLV infection. For routine diagnosis, immunofluorescence would appear to offer the best chance of differentiating transient and persistent infections by FeLV.

Age Factors↗