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Biomedical subjects

R C Wardley

Publications and source records attributed to R C Wardley.

At least 19 recordsLinked to original sources
PubMed1992

The use of feline herpesvirus and baculovirus as vaccine vectors for the gag and env genes of feline leukaemia virus.

The env and gag genes from feline leukaemia virus were expressed in a thymidine kinase-negative feline herpes-virus and a baculovirus. Cats were vaccinated with various combinations of these recombinant viruses and 100% protection against feline leukaemia virus challenge was achieved using an immunization schedule which utilized both env and gag products delivered at both a mucosal and systemic site.

Animals↗
PubMed1979

The replication of virulent and attenuated strains of African swine fever virus in porcine macrophages.

The replication of virulent and attenuated strains of African swine fever virus (ASFV) was studied in pure cultures of swine macrophages. To ensure complete destruction of the macrophage monolayers about 50--100 times more virulent ASFV was needed than attenuated virus although both isolates could be used to establish persistently infected cultures. Interferon did not appear to influence virus yields from such cultures. Fluorescent and electron microscopy studies of infected macrophages suggested that the cycle of infection of the two isolates was different.

African Swine Fever Virus↗
PubMed1979

Solid-phase radioimmunoassay techniques for the detection of African swine fever antigen and antibody.

A solid phase radioimmunoassay (RIA) has been successfully developed to measure both African swine fever virus (ASFV) antigen and antibody. Studies show that the assay is reproducible and will detect limiting antigen concentrations equivalent to 50--500 HAD50/ml. Both direct and indirect antibody RIA have been developed and have proved to be approximately 100 times fore sensitive than the complement fixation test at present available and 1000 times more sensitive than the immuno-electro-osmophoresis test for the detection of ASFV antibody.

African Swine Fever Virus↗
PubMed1979

A solid-phase enzyme linked immunosorbent assay for the detection of African swine fever virus antigen and antibody.

A solid-phase enzyme-linked immunosorbent assay was developed to measure both African swine fever virus (ASFV) antigen and antibody. Experiments showed it to be reproducible and able to detect limiting antigen concentrations of 50--500 HAD50/ml. The assay was more sensitive than those used at present to detect ASFV antibody and it is suggested that it might be of great diagnostic use in countries where African swine fever has recently appeared.

African Swine Fever Virus↗
PubMed1979

A blastogenic test for foot-and-mouth disease.

A blastogenic test to detect peripheral blood leukocytes specifically sensitized to foot-and-mouth disease virus antigen is described. The test is carried out in microtitre plates and optimum conditions were found by titration. These employed 7.5 x 10(5) cells/well and 20 complement fixing units of antigen. Peak [3H]thymidine incorporation was found to take place at 2-3 days.

Animals↗
PubMed1978

The growth of virulent African swine fever virus in pig monocytes and macrophages.

The replication of virulent African swine fever virus (ASFV) in cultures of monocytes and macrophages derived from pig bone marrow (PBM) and pig leukocyte (PL) cells was investigated by light microscopy, immunofluorescence, haemadsorption and infective virus release. Monocytes showed a high rate of infection and complete destruction within 2 to 3 days, whereas macrophages had only a very low level of infection and survived to form persistently infected cultures. These observations may explain the decrease in sensitivity of PBM and PL cells for ASFV assay after extended periods of incubation and suggest that the macrophage may be one of the cell types concerned with virus persistence in the pig.

African Swine Fever Virus↗
PubMed1977

The association of African swine fever virus with blood components of infected pigs.

The distribution of African swine fever virus (ASFV) in whole blood, plasma, red blood cells (RBC) and white blood cell (WbC) sub-populations was determined in pigs infected with virulent virus. Changes in the RBC and WBC populations were also examined. Total WBC counts decreased and RBC numbers remained unchanged during the course of the disease. The number of circulating lymphocytes decreased whilst neutrophil numbers increased owing to the replacement of mature forms by juveniles. Virus was present in all major blood fractions and was associated with equivalent numbers of both RBC and WBC. However, 90 per cent of the virus in whole blood was associated with RBC. Of the WBC subpopulations, virus was definitely associated with lymphocytes and possibly neutrophils.

African Swine Fever↗
PubMed1977

African swine fever virus replication in porcine lymphocytes.

Purified preparation of porcine lymphocytes were infected with three isolates of virulent African swine fever virus (ASFV). Electron microscopy showed the presence of small numbers of mature virus particles in degenerating cells. The titres of infective virus released were low and reached a maximum by 24 h after infection.

African Swine Fever Virus↗
PubMed1977

The role of neutrophils in antiviral defense--in vitro studies on the mechanism of antiviral inhibition.

Highly enriched populations of bovine neutrophils were added, in the presence of antiviral antibody, to herpesvirus-infected bovine cell cultures. A cell dose-dependent reduction in virus-induced cytopathology was observed. The mechanism of inhibition was presumed to be mediated by a subcellular neutrophil product and not the result of either direct cytotoxicity or antibody-dependent cell-mediated cytotoxicity (ADCC). Thus, inhibition of comparable magnitude was observed when neutrophils and virus-infected cells were separated by cell impermeable membranes. In addition, plaque reduction occurred when antiviral immunoglobulins or fragments unable to mediate ADCC were used in the assays. Killed neutrophils and sonicates were unable to mediate plaque inhibition. Speculations were made as to the origin of the virus-inhibitory substances and the role that neutrophils might assume in mediating recovery from virus infection.

Animals↗
PubMed1977

The pathology and sites of persistence associated with three different strains of feline calicivirus.

The pathology and sites of multiplication associated with three different strains of feline caliciviruses are described. The main pathological lesions were found in the tongue, soft palate and lungs and like the clinical signs were of mild nature. Virus multiplication was associated mainly with the tissues of the mouth and tonsils and in asymptomatic carrier animals the tonsil appeared to be preferred organ of viral persistence.

Animals↗
PubMed1977

The clinical disease and patterns of excretion associated with three different strains of feline caliciviruses.

Three groups of cats were infected intranasally with three different feline calicivirus strains: A3, 68/40 and M8. Each strain produced a uniformly muld upper respiratory tract disease, with glossal ulceration being the most prominent clinical sign. Virus was most consistently isolated from the oro-pharyngeal region and, in non-euthanised animals, excretion continued long after clinical signs had disappeared. It is suggested that an asymptomatic phase of excretion may be a normal sequel to FCV infections.

Animals↗
PubMed1976

Feline calicivirus carrier state. A study of the host/virus relationship.

The inter-epidemic phase of feline calicivirus was studied in a number of cats. During this period animals asymptomatically shed infective virus which was monitored at a number of sites and during different environmental conditions. Analysis of the amounts of virus shed by different cats showed that excretion occurred almost exclusively from the oropharynx, fluctuated with time, but was not influenced by periods of natural or artificial stress. Viral excretion from one individual cat was fairly constant although it appears that cats might be divided into high, medium or low level excretors. This variation in levels of excretion appears to have epidemiological importance in that high-level excretors more easily infect susceptible individuals.

Animals↗
PubMed1976

Antibody-dependent cell-mediated cytotoxicity in cows: comparison of effector cell activity against heterologous erthrocyte and herpesvirus-infected bovine target cells.

Bovine peripheral blood leukocytes (PBL) and cells collected from the bovine mammary gland were assayed for antibody-dependent cell-mediated cytotoxicity (ADCC) against chicken erythrocyte (CRBC) and bovine herpesvirus-infected bovine kidney cell targets. Bovine antisera were used to sensitize target cells. Both PBL and mammary leukocytes expressed ADCC, with the latter cell population having greater activity against both target cells. Only the CRBC target cells were killed by nonadherent PBL and phagocyte-depleted PBL. Nonadherent mammary leukocytes, rich in monocytes and macrophages, did kill virus-infected target cells. Carbonyl iron-treated mammary leukocytes failed to kill virus-infected targets but could destroy CRBC targets. Antimacrophage serum inhibited lysis of both CRBC and virus-infected targets, but antilymphocyte serum only inhibited CRBC killing. These observations indicated that at least two kinds of cells could mediate ADCC against CRBC but only cells of the mononuclear phagocytic series could kill virus-infected target cells. The herpesvirus-infected target cells became susceptible to ADCC 9 h after virus infection. A case is made for investigating the phenomenon of ADCC using in vitro systems that closely mimic the in vivo situation. The possible role of the ADCC mechanism as instrumental in causing recovery from herpesvirus infections is discussed.

Animals↗
PubMed1976

Polymorph-mediated antibody-dependent cytoxicity--modulation of activity by drugs and immune interferon.

Bovine polymorphonuclear leukocytes (PMN) mediated antibody-dependent cell cytotoxicity (ADCC) against erythrocyte and herpes virus-infected target cells. The extent of cytotoxicity was not affected by drugs that inhibited DNA, RNA, or protein synthesis. The effect did not occur in the absence of divalent cations, was suppressed by pretreatment of PMN with silica and cytochalasin B, and was subject to the bidirectional control by cyclic nucleotides; drugs decreasing cyclic AMP or elevating cyclic GMP levels enhanced ADCC. The ADCC phenomena was also enhanced by supernates containing immune interferon activity from antigen-stimulated-immune lymphocyte-macrophage cultures. The possibility that immune interferon(s) might be causing the elevation of ADCC and the relevance of this observation in terms of the part interferon might play in modulating recovery from herpes virus infections was discussed.

Animals↗
PubMed1976

Lymphocyte activation by cell separation procedures.

Cell separation techniques normally used to obtain subpopulations of lymphocytes were shown, under certain conditions, to render the cells cytotoxic towards a number of target-cells including autologous lymphocytes. To cause cytotoxicity, it was necessary to pass cells through glass wool and/or nylon wool columns equilibrated with media containing fresh plasma or serum. Cells lost activation upon overnight in vitro culture or treatment with trypsin. In addition to direct cell cytotoxicity, cells released heat labile cytotoxic factors and antibody during the separation procedures. The implications of the results for the interpretation of cell separation studies designed to attribute immunological effects to one or another cell type were discussed.

Animals↗