Search PubMed⌕ Search

Biomedical subjects

R C Wardley

Publications and source records attributed to R C Wardley.

69 records · Page 4Linked to original sources
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↗
PubMed1976

Observations on recovery mechanisms from feline viral rhinotracheitis.

Experiments were designed to determine immunological mechanisms responsible for controlling dissemination of feline rhinotracheitis virus in feline cell cultures. Virus infected cells could be destroyed by three mechanisms--antibody and complement mediated lysis, direct lymphocyte cytotoxicity and antibody dependent cell-mediated cytotoxicity. This latter immune parameter was mediated by both lymphocytes and macrophages and varied in extent in different cats. To ascertain the potential importance of the immunological parameters in curtailing viral spread, the time when virus infected cells could be destroyed by each component was related to the chronological events of viral replication and dissemination. Intracellular infectious virus and intracellular spread occurred at six to seven hours postinfection and extracellular spread at nine to ten hours postinfection. Antibody complement lysis and antibody dependent cell-mediated cytotoxicity occurred at six hours postinfection and direct cytotoxicity at eight hours postinfection. The relevance that these findings might have in relation to the occurrence and frequency of recrudescent disease is discussed.

Animals↗
PubMed1975

Defense mechanisms against bovine herpesvirus: relationship of virus-host cell events to susceptibility to antibody-complement cell lysis.

The interaction of infectious bovine rhinotracheitis virus and susceptible host cells was examined to determine whether an infected cell could be destroyed by humoral immune mechanisms before or after the transmission of virus to susceptible adjacent cells. Viral antigens were detectable on cell membranes at 6 h postinfection, but cells were not susceptible to antibody-complement lysis until 10 h postinfection. Intracellular infectious virus was also detectable at 10 h postinfection, and transmission to adjacent cells by the intracellular route began at this time. Extracellular virus was not detectable until 12 to 13 h postinfection. By the continual addition of antibody and complement, virus dissemination could be reduced more than 50-fold. These results support the hypothesis that the humoral immune mechanism may be involved in the recovery from herpesvirus infections.

Animals↗