The biological effects of ozone on representative members of five groups of animal viruses.
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Kinetics↗
Biomedical subjects
Y C Zee
Publications and source records attributed to Y C Zee.
Exposure to ozone reduces influenza disease severity and alters distribution of influenza viral antigens in murine lungs.
Exposure to ambient levels of ozone (0.5 ppm) was shown to alter the pathogenesis of respiratory infection after aerosol infection of mice with influenza A virus. A semiquantitative method for determination of the sites of virus replication by direct immunofluorescence indicated that exposure to ozone reduced the involvement of respiratory epithelium in the infectious process and resulted in a less widespread infection of the alveolar parenchyma. Furthermore, the ozone-mediated alteration in viral antigen distribution was consistent with significantly reduced influenza disease mortality and prolonged survival time, but only when the oxidant was present during the course of infection. Reduced disease severity in ozone-exposed animals appeared to be independent of peak pulmonary virus titers, pulmonary interferon titers, and pulmonary and serum-neutralizing antibody titers. These studies suggested that the distribution of influenza virus in the murine lung was a key factor in disease severity.
Animals↗
Dynamics of B-lymphocytes in the lungs of mice exposed to aerosolized influenza virus.
Immunoglobulin-containing cells were revealed by immunofluorescence in lung sections from mice infected with influenza virus by the aerosol route. The numbers of immunoglobulin A (IgA)- and IgM-containing cells were increasing by day 3 of the infection, whereas IgG-containing cells appeared a few days later. The responding B-cell populations appeared in two principal locations: along major airways and in consolidated lesions within lung parenchyma. IgA-containing cells were the most numerous isotype, occurring predominantly in the lamina propria of the airways. IgG-containing cells were the least frequently encountered class along airways and appeared most often within consolidated lung lesions in clustered groupings. Cells staining for mu chain appeared along the airways and in lung lesions. The population of IgM-containing cells declined approximately 30 days after infection. Cells producing alpha and gamma chains were still numerous on day 46. Assays for virus-reactive antibodies in lung secretions were positive on day 8 of the infection. The IgM titers were the first to decline, but virus-binding antibodies for all classes were still present on day 33. The implications of immune responses in viral pneumonitis were considered.
Animals↗
Immunoglobulin E-containing cells in mouse lung following allergen inhalation and ozone exposure.
Cells containing immunoglobulin E (IgE) were enumerated and their location in mouse lungs was determined by direct immunofluorescence. Lungs were studied from mice that had been immunized with aerosolized ovalbumin as well as from normal mice and from mice that were exposed to ozone (0.5 or 0.8 ppm) prior to receiving aerosolized antigen. In addition, some mice were immunized intraperitoneally with ovalbumin precipitated in alum. IgE-containing cells were primarily airway-related in normal mice and in mice immunized by the intraperitoneal route. Lungs from aerosol-immunized, and aerosol-immunized ozone-exposed mice showed a more disseminated distribution of IgE-containing cells. Fluorescent cells were counted and numbers were expressed as total cells per square millimeter of lung tissue and as airway-associated cells per millimeter of airway. Total IgE cells increased 9.4-fold in mice that received aerosolized ovalbumin as compared to normal mice. When ozone exposure was added to the effects from aerosolized ovalbumin, the increase of IgE cells over normal was 34.2-fold. IgE cell counts correlated well with anaphylactic sensitivity to intravenous challenge with ovalbumin. The observed enhancement of allergic sensitization by ozone exposure has important implications for human health.
Administration, Intranasal↗
Immunogenic collagen in induced ascitic fluid: concurrent preparation of anti-murine immunoglobulin E.
Antiserum to murine immunoglobulin (Ig) E was produced by inoculation of goats with a pool of partially purified IgE from serum and adjuvant-induced ascitic fluid. Antibodies to collagen were found to be present in the antiserum when the latter was conjugated with fluorescein isothiocyanate and applied to mouse pulmonic tissue. The intense connective tissue fluorescence was eliminated following absorption with mouse collagen. Immunogenic collagen components were presumed to arise in ascitic fluid as a consequence of the adjuvant-induced inflammation. Ascitic fluid is commonly used when large volumes of serum proteins are collected from small mammals. It is suggested that ascitic fluid may not be an ideal antigen source when antiserum is to be used for immunofluorescence studies on tissue.
Animals↗
Immunofluorescence determination of the pathogenesis of infection with influenza virus in mice following exposure to aerosolized virus.
The pathogenesis of infection with influenza A virus in mice was studied by exposure of specific pathogen-free mice to aerosols of influenza virus and by monitoring of mortality, viral titers in lung homogenates, and presence of viral antigens in respiratory cells as determined by immunofluorescence. In two experiments with different death rates (100% and 43%), viral antigen accumulated in the epithelial cells lining the airways, in alveolar macrophages, in alveolar cells, and in visceral pleura. By enumeration of the number of airways, alveolar macrophages, and alveolar cells containing influenza viral antigens at different intervals after exposure to the viral aerosol, it was determined that viral replication occurred initially in the epithelial cells lining the airways and later extended to the alveolar macrophages and alveolar cells. This semiquantitative survey of the dynamics of influenza viral infection by aerosol indicated that the viral infection in mice was a descending process.
Aerosols↗
Antibody responses and interferon titers in the respiratory tracts of mice after aerosolized exposure to influenza virus.
We studied the temporal appearance of immunoglobulins (immunoglobulins G1, G2, M, and A) and interferon in lung lavage fluids of mice after aerosol exposure to influenza virus in six animal groups in which mortality rates ranged from 0 to 24%. Immunoglobulin levels in the lung lavage fluids were markedly higher in mouse groups with higher mortality rates (16, 20, and 24%) than in those with low mortality rates (0, 2.5, and 7.5%). Analysis of serum albumin in the respiratory secretions as an index of edema indicated that increased immunoglobulin G levels during the early phase of infection were due to increased vascular permeability. The detection of virus-neutralizing antibodies and antibodies reactive with influenza virus antigens in the lavage fluids at 6 to 8 days postinfection suggested local immunoglobulin synthesis as a result of antigenic stimulation. Both systemic and local antibody productions contributed to immunoglobulin levels in the respiratory secretions after aerosolized influenza virus infection. Peak levels of interferon in the lavage fluids were reached before detection of significant levels of virus-neutralizing antibody in the serum or the lung lavage.
Aerosols↗
The effects of ozone on the respiratory epithelium of mice II. Ultrastructural alterations.
Ultrastructural alterations in the tracheal and bronchial epithelium of mice exposed to 0.8 ppm ozone for varying periods of time were examined with scanning electron microscopy. The lesions were apparent in the ciliated cells. Examination of tissue from control mice showed that the ciliated cells were arranged in groups and the cilia were uniform in length. After six days of exposure to ozone, shortened cilia were occasionally observed by day 10, more pronounced changes were observed. Cilia were either absent or became short and blunt. The lesions observed after 20 days in ozone were similar to those seen on day 10. After ozone-exposed mice had been returned to ambient air for 10 days, ciliary regeneration occurred and, the major airways had a surface appearance approaching the normal state.
Animals↗
Effect of amphotericin B methyl ester on vesicular stomatitis virus morphology.
The water-soluble methyl ester of amphotericin B inactivates vesicular stomatitis virus in association with morphological alterations of the envelope.
Amphotericin B↗
The pathogenesis of vesicular stomatitis virus, serotype Indiana, in Aedes aegypti mosquitoes, after imbibition of a viremic blood meal.
This study showed that Vesicular Stomatitis Virus (Indiana) in most instances was not capable of replicating in Aedes aegypti when imbibed by the mosquitoes on a viremic host. Rapid inactivation of the virus was observed in some cases within 24 hours after imbibition. Attempts to demonstrate virus inactivation by midgut contents in vitro were not successful.
Aedes↗
Purification and buoyant density of infectious bovine rhinotracheitis virus.
A purification scheme for infectious bovine rhinotracheitis virus utilizing rate-zonal centrifugation in a 10-40% potassium tartrate gradient was described. The density of IBRV in the potassium tartrate gradient was found to be 1.22 g/cm3. Electron microscopic examination of purified virus preparations revealed homogeneous populations of enveloped virions with minute projections on the envelope surface.
Centrifugation, Isopycnic↗
The effects of ozone on the respiratory epithelium and alveolar macrophages of mice. I. Interferon production.
The effects of 0.8 ppm ozone on the capacity of the tracheal epithelium and alveolar macrophages of mice to produce interferon in vitro was studied. Exposure of mice to ozone for a period of 11 days or more affected the capacity of the tracheal epithelial cells in vitro to produce interferon. The inability of the tracheal epithelium in vitro to produce interferon was not due to the inhibition in the release of intracellular interferon but to an inhibition in the production of interferon. There was a complete recovery of the ability of tracheal epithelium to respond to interferon inducers after the mice were returned to ambient air 24 days post ozone exposure. However, ozone did not seem to have any affect on the capacity of the alveolar macrophages to produce interferon in vitro.
Animals↗
The pathogenesis of vesicular stomatitis virus, serotype Indiana, in Aedes aegypti mosquitoes. I. Intrathoracic injection.
Analysis of infectious virus particles after intrathoracic injection revealed that Aedes aegypti mosquito tissues are capable of supporting the growth of vesicular stomatitis virus (VSV), serotype Indiana. Although all tissues assayed (salivary gland, midgut, diverticulum, malphigian tubules, and ovary) were capable of supporting VSV growth, the salivary gland was the only organ capable of maintaining an appreciable amount of virus for periods longer than 9 days postinfection. Electron microscopic studies of infected tissues showed virus particles consistently within the cell cytoplasm of all organs with no evidence of nuclear involvement. Direct evidence of crystalline formation of VSV in the apical cavities of salivary gland tissue was demonstrated.
Aedes↗
A procedure for pulmonary lavage in mice.
A method for the pulmonary lavage of mice is described. The procedure includes exsanguination of anesthetized mice by severting the renal artery, inserting a tracheal catheter in situ, and repeatedly injecting and aspirating 0.9% sodium chloride solution. Protein was recovered from the cell-free lavage fluid even after a given mouse was lavaged several times. The major part of the protein, however, was obtained with 1-ml washes repeated 3 times. Approximately 0.563 mg of protein was recovered by the procedure from a 29-g mouse. Four lavages per mouse yielded approximately 2.9 x 106 free cells.
Animals↗
Immunochemical analysis of serum-related proteins in the respiratory tract secretions of normal mice.
Normal mouse lung lavage fluid was analyzed for its content of serum-related proteins by the methods of gel filtration, immunoelectrophoresis, and double immunodiffusion. Lavage samples were collected from exsanguinated mice using three repeated infusions of 0.9% sodium chloride solution. Cells were removed, and the lavage fluid was concentrated. Approximately 0.23 mg of protein per mouse was present in the concentrated solution. Albumin, transferrin, and immunoglobulin G (IgG) were among the proteins in greatest concentration. Albumin, IgG1, IgG2, IgA, and IgM were quantitated by single radial diffusion. Although immunoglobulins could be synthesized locally, albumin and transferrin were assumed to come from plasma. The albumin content was used to estimate the amount of transudated plasma as 0.0027 ml per mouse. The IgA levels were low with an IgA/IgG1 ratio of 0.58 and an IgA/IgG2 ratio of 0.43. IgM was not detected. Goat anti-lung lavage serum revealed the presence of additional lung-related proteins.
Animals↗
Characterization of bovine viral diarrhea virus RNA.
RNA extracted from isopycnically banded [3-H]uridine-labeled bovine viral diarrhea virus with sodium dodecyl sulfate was resolved into one major and two minor components by both sedimentation analysis and electrophoresis in polyacrylamide gels. The major RNA component was estimated to have a 38S sedimentation coefficient. The minor RNA components were estimated to have S values of 31 and 24. The approximate colecular weights were calculated to be 3.22 times 10-6 (38S), 2.09 times 10-6 (31S), and 1.22 times 10-6 (24S). A single broad peak of radioactivity, maximum at 24S, was obtained when sedimentation was conducted under conditions of low ionic strength. All three RNA components were found to be susceptible to digestion with RNase. The presence of multiple RNA components in heterogeneous populations of infectious virus is discussed.
Animals↗
Structural proteins of bovine viral diarrhea virus.
A procedure for the purification of radioactively labeled bovine viral diarrhea virus was critically evaluated. Purification of virus from artificial mixtures of unlabeled infected and labeled noninfected cells indicated that the extent of purification was approximately 100-fold with respect to host proteins. Residual host proteins were found to contaminate the viral preparation even after extensive purification by differential and isopycnic zonal centrifugation. Co-electrophoresis of 3H-labeled virus with 14C-labeled host cell material in neutral sodium dodecyl sulfate-7.5% polyacrylamide gels provided a means to distinguish viral specific proteins from host cell protein contaminants. Four major electrophoretic components were identified as being of viral origin; molecular weights of the components were estimated from their migration rates relative to protein markers of known molecular weight. Two viral components (VC), VC 1 and VC 3, migrated heterogeneously and had molecular weights of 93,000 to 110,000 and 50,000 to 59,000 daltons, respectively. Molecular weights of VC 2 and VC 4 were 70,000 and 25,000 daltons, respectively.
Animals↗
Histologic, immunofluorescent, and electron microscopic studies of equine dermis cells infected with an equine adenovirus.
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Adenoviridae↗