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At least 1,135 records · Page 63Linked to original sources
PubMed1991

Changes in phospholipids of alveolar lining material in calves after aerosol exposure to bovine herpesvirus-1 or parainfluenza-3 virus.

Pulmonary lavage samples were collected from 90- to 130-day-old calves before and 6 days after aerosol inoculation with bovine herpesvirus-1 (BHV-1) or parainfluenza-3 (PI3) virus. Alveolar lining material was separated from lavage fluids by high-speed centrifugation and phospholipids were extracted from alveolar lining material and analyzed by high-performance liquid chromatography. Phosphatidylcholine and phosphatidylethanolamine were 74.2 +/- 6.5% and 13.3 +/- 2.8%, respectively, of the total phospholipid content in the surfactant obtained from calves before virus inoculation. Other phospholipids were represented by substantially lower percentages. Infection with either of the 2 viruses caused a significant (P less than or equal to 0.05) decrease in the percentage of phosphatidylcholine to 66.0 +/- 8.0% and 65.1 +/- 10.8% in the calves inoculated with BHV-1 and PI3 virus, respectively. A significant (P less than or equal to 0.05) increase in the percentage of phosphatidylethanolamine to 18.1 +/- 2.2% and 17.8 +/- 4.5% developed in calves inoculated with BHV-1 and PI3 virus, respectively. Infection with BHV-1 also induced an increase (not significant) in the percentage of phosphatidylinositol from 5.5 +/- 2.8% to 7.8 +/- 2.2%. A similar, but not significant, increase in the percentage of phosphatidylinositol was also seen in the calves inoculated with PI3 virus. Less substantial changes in the percentage of other phospholipids were detected after virus infection.

Aerosols↗
PubMed1985

Impaired function of bovine alveolar macrophages infected with parainfluenza-3 virus.

Bovine alveolar macrophages (BAM) were harvested from nonsedated cattle, adhered to glass or plastic surfaces, and infected with parainfluenza-3 (PI-3) virus at a multiplicity of infection of 10. Control and PI-3 virus-infected BAM were compared at 24-hour intervals up to 168 hours for their ability to phagocytize antibody-coated sheep erythrocytes (EAC) and latex particles, to kill Staphylococcus epidermidis, and to alter intracellular acid phosphatase concentrations. The effect of antiviral serum on phagocytic functions of virus-infected cells was also evaluated. Compared with noninfected controls, alveolar macrophages infected with PI-3 virus were 15.3% less adherent to the glass or plastic surfaces at postinoculation hour (PIH) 72 and were 64.0% less adherent at PIH 168. Significant differences (P less than 0.05) between the numbers of control and infected BAM phagocytizing EAC were observed at PIH 24 through 72, with final values differing by approximately 50%. Similar changes were observed in the phagocytic efficiencies of individual cells. The PI-3 virus-infected BAM that were exposed to antiserum or to immunoglobulins against PI-3 virus had approximately a 2-fold greater inhibition in EAC phagocytosis than did infected BAM exposed to serum without PI-3 activity. Significant differences in latex particle phagocytosis were not observed between infected and control BAM. Compared with control BAM, the PI-3 virus-infected BAM contained significantly lower concentrations of acid phosphatase from PIH 48 through 96; at PIH 96, acid phosphatase concentrations were 4-fold less in infected than in control BAM.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid Phosphatase↗
PubMed2005

Evolution of a T-B- SCID into an Omenn syndrome phenotype following parainfluenza 3 virus infection.

Mutations in both of the recombination activating genes (RAG)1 and RAG2 can lead to either T-B-severe combined immune deficiency (SCID) or Omenn syndrome (OS), two diseases presenting with totally different clinical and laboratory manifestations. The fact that the same mutations can cause either T-B- SCID or OS, even within the same family, lends credibility to the hypothesis that an additional factor (autoantigen or exoantigen) is required in certain circumstances for the development of OS phenotype. We investigated three patients from the same extended family who presented as T-B- SCID due to a homozygous mutation (G1305T) in the RAG2 gene. Our data support the notion that mutated RAG proteins may not always be sufficient to cause OS phenotype, and show evolution from a T-B- SCID into a typical OS phenotype subsequent to parainfluenza 3 virus infection.

B-Lymphocytes↗
PubMed1998

A serologic study of organisms possibly associated with pertussis-like coughing.

OBJECTIVE: To assess the frequency of serologic evidence for an infection with microorganisms other than Bordetella pertussis in children with pertussis-like coughs. METHODS: The study was performed within a protective efficacy trial of an acellular pertussis vaccine. Children who coughed for >7 days and had no laboratory evidence of recent infection with B. pertussis were eligible for the present study. Antibodies to Mycoplasma, Chlamydia, respiratory syncytial virus and influenza viruses A and B were measured by complement fixation, and antibodies to adenovirus and parainfluenza viruses 1, 2 and 3 were measured by enzyme-linked immunosorbent assay (ELISA) in acute and convalescent serum samples. Significant titer rises (4-fold titer rise in complement fixation, 100% increase of units in ELISA) and concentrations of antibodies beyond age-specific reference values were regarded as indicative of recent infection. In some children IgM antibodies to Epstein-Barr virus and to cytomegalovirus were also measured by ELISA. RESULTS: A total of 149 of 1179 (12.6%) children had no laboratory evidence of B. pertussis infection. Serologic evidence for other infections were found in 56% (83 of 149). Adenovirus (33), parainfluenza viruses 1, 2 and 3 (18), Mycoplasma pneumoniae (15) and respiratory syncytial virus (14) were most common. Of this group 48% had been vaccinated against pertussis. CONCLUSION: We present data that a proportion of pertussis-like coughs in children may be caused by adenovirus, parainfluenza viruses, respiratory syncytial virus and Mycoplasma. The differential diagnosis of pertussis-like coughs by laboratory methods should include these infections, especially in vaccinated children.

Adenoviridae Infections↗
PubMed1996

Parainfluenza virus-induced persistence of airway inflammation, fibrosis, and dysfunction associated with TGF-beta 1 expression in brown Norway rats.

Parainfluenza type 1 (Sendai) virus infection in young rats induces airway growth abnormalities associated with persistent pulmonary dysfunction and hyperresponsiveness. The objectives of this study were to compare virus-susceptible brown Norway (BN) rats and virus-resistant F344 rats and to determine which of several virus-induced structural abnormalities, including bronchiolar hypoplasia, alveolar dysplasia, bronchiolar mural fibrosis, and increases in bronchiolar mast cells, were associated with virus-induced increases in pulmonary resistance and hyperresponsiveness to methacholine. We also determined whether bronchiolar mural thickening and fibrosis may be caused by increased bronchiolar expression of cytokines such as TGF-beta 1 into airways. BN rats infected with virus developed increases in respiratory resistance and hyperresponsiveness that persisted for 28 to 65 d after inoculation. Functional abnormalities were most strongly associated with bronchiolar mural thickening and fibrosis as well as with recruitment of inflammatory cells, including macrophages, mast cells, lymphocytes, and eosinophils, into the bronchiolar wall. F344 rats were resistant to significant virus-induced alterations in bronchiolar airway wall thickness and mast cell increases as well as to pulmonary function abnormalities. BN rats had increase pulmonary mRNA levels of TGF-beta 1 at 10 and 14 d after viral inoculation as compared with F344 rats. BN rats also had greater numbers of bronchiolar macrophages expressing TGF-beta 1 protein that were localized in bronchiolar walls at 10, 14, and 30 d after inoculation. We conclude that recruitment and persistence of airway inflammatory cells and airway wall fibrosis may be important alterations induced by viral lower respiratory disease during early life that can lead to long-term airway dysfunction and hyperresponsiveness. Virus-induced airway fibrosis may be mediated in part by increased TGF-beta 1 gene expression by bronchiolar macrophages in genetically susceptible individuals.

Airway Resistance↗
PubMed1976

Maternal immunoglobulins and parainfluenza 3 virus inhibitors in the nasal and lachrymal secretions and serum of newborn lambs.

Concentrations of IgG, IgM and IgA were measured in the serum, nasal secretions and lachrymal secretions of suckled newborn lambs. The major immunoglobulin constituent of precolostral serum was IgM. Maternal immunoglobulins, of which IgG was predominant, reached peak values on day 1 of life and then declined over the next 3 weeks. Half lives were calculated as: IgG, 13-7 days; IgM, 4-1 days; and IgA 1-8 days. No immunoglobulin was detectable in nasal or lachrymal secretions prior to sucking but IgG was present in all samples of these secretions obtained approximately 24 hr after first sucking. IgG was present in nasal washings from suckled lambs, reared either naturally or on immunoglobulin-free milk substitute and levels declined as the lambs grew older. IgM and IgA did not appear consistently in the secretions until lambs were 2-3 weeks old. It was concluded, therefore, that colostral IgG reaches the nasal and lachrymal secretions of the newborn lamb. However, because the ewes in this experiment had only low serum titres, no maternal antibody to parainfluenza 3 virus (PI3) was detected in the nasal secretions of the lambs, although non-specific inhibitors were present. It is suggested, however, that low levels of maternal antibody in the secretions may play a valuable role in preventing respiratory virus infections of young ruminants before active local production of IgA and IgM begins at 2 to 3 weeks of age.

Animals↗
PubMed1988

Effect of respiratory infections caused by bovine herpesvirus-1 or parainfluenza-3 virus on bovine alveolar macrophage functions.

Calves, 90 to 130 days old, were inoculated with bovine herpesvirus-1 (BHV-1) or parainfluenza-3 (PI-3) virus. Pulmonary lavage specimens obtained from calves before virus inoculation contained 98% alveolar macrophages (AM) and 1% neutrophils. Six days after inoculation, the mean percentage of neutrophils in lavage specimens had significantly increased to 7.9 +/- 6.0% in BHV-1-inoculated calves and to 18.3 +/- 9.9% in PI-3 virus-inoculated calves, reflecting viral-induced pulmonary inflammation that was confirmed histologically. Approximately 75% of AM obtained before virus inoculation had Fc surface receptors, and 60% had C3b receptors. Six days after inoculation, the percentage of AM with Fc and C3b receptors was significantly reduced to 69.7 +/- 8.6% and 27.1 +/- 19.8%, respectively, in BHV-1-inoculated calves and to 67.8 +/- 15.4% and 38.8 +/- 23.2%, respectively, in PI-3 virus-inoculated calves. Alveolar macrophages obtained after virus inoculation were significantly impaired in their ability to phagocytize opsonized Staphylococcus epidermidis, but were able to kill ingested bacteria. Alveolar macrophage dysfunctions caused by BHV-1 or PI-3 respiratory infection did not differ appreciably.

Animals↗
PubMed1975

Clinical and immunologic responses of calves with colostrally acquired maternal antibody against parainfluenza-3 virus to homologous viral infection.

Exposure of colostrum-deprived calves and calves with colostrally acquired maternal antibody to aerosols of parainfluenza-3 (PI-3) virus resulted in signs of infection, leukopenia, and shedding of virus from the nasal passages. However, infection was not as severe in calves with colostrally acquired maternal antibody as it was in colostrum-deprived calves which did not have antibody to PI-3 virus before they were exposed. All calves responded immunologically to PI-3 virus, as indicated by resistance to challenge exposure and subsequent development of virus-neutralizing antibody. However, levels of serum and nasal secretion (NS) antibody at 30 days after viral exposure were lower in calves with colostrally acquired maternal antibody than in colostrum-deprived calves, and a serum antibody response in the former was primarily indicated by an anamnestic response after challenge exposure. After calves were challenge exposed to PI-3 virus, serum and NS antibodies were increased in all calves, but antibody titers were generally lower for calves that had colostrally acquired maternal antibody before their exposure than for those that acquired antibody only after PI-3 viral infection.

Aerosols↗
PubMed2005

Down-regulation of p53 by double-stranded RNA modulates the antiviral response.

p53 has been well characterized as a tumor suppressor gene, but its role in antiviral defense remains unclear. A recent report has demonstrated that p53 can be induced by interferons and is activated after vesicular stomatitis virus (VSV) infection. We observed that different nononcogenic viruses, including encephalomyocarditis virus (EMCV) and human parainfluenza virus type 3 (HPIV3), induced down-regulation of p53 in infected cells. Double-stranded RNA (dsRNA) and a mutant vaccinia virus lacking the dsRNA binding protein E3L can also induce this effect, indicating that dsRNA formed during viral infection is likely the trigger for down-regulation of p53. The mechanism of down-regulation of p53 by dsRNA relies on translation inhibition mediated by the PKR and RNase L pathways. In the absence of p53, the replication of both EMCV and HPIV3 was retarded, whereas, conversely, VSV replication was enhanced. Cell cycle analysis indicated that wild-type (WT) but not p53 knockout (KO) fibroblasts undergo an early-G(1) arrest following dsRNA treatment. Moreover, in WT cells the onset of dsRNA-induced apoptosis begins after p53 levels are down-regulated, whereas p53 KO cells, which lack the early-G(1) arrest, rapidly undergo apoptosis. Hence, our data suggest that the down-regulation of p53 facilitates apoptosis, thereby limiting viral replication.

Animals↗
PubMed1990

Effect of bovine herpesvirus-1 or parainfluenza-3 virus on immune receptor-mediated functions of bovine alveolar macrophages in the presence or absence of virus-specific serum or pulmonary lavage fluids collected after virus infection.

The immune receptor-mediated functions of bovine alveolar macrophages (AM) inoculated in vitro with bovine herpesvirus-1 (BHV-1) or parainfluenza-3 (PI-3) virus were tested in the presence or absence of virus-specific antiserum or pulmonary lavage fluids collected from calves 6 days after inoculation with BHV-1 or PI-3 virus. The Fc and C3b phagocytic indices of noninoculated AM, collected from 6- to 16-week-old calves, ranged from 75 to 87 and 59 to 64, respectively, and the binding indices ranged from 5 to 8 and 22 to 28, respectively. Infection of AM with either BHV-1 or PI-3 virus had no significant effect on receptor-mediated phagocytosis or binding, with the exception of a significant (P less than 0.05) decrease, from 64 to 46, of the C3b phagocytic index of PI-3 virus-infected AM. The addition of lavage fluids, collected after BHV-1 or PI-3 virus infection, to AM infected with the respective virus caused a significant (P less than 0.05) decrease in phagocytic indices with values for the Fc and C3b indices in BHV-1-infected AM decreasing from 81 to 49 and from 47 to 8, respectively, and those for the PI-3 virus-infected AM from 79 to 51 and from 46 to 15, respectively. The binding indices of virus-infected AM increased with the addition of viral lavage fluids, but the only significant (P less than 0.05) increase was for C3b binding in PI-3 virus-infected cells, which increased from 33 to 56.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

In vitro antiviral activities of sulfated polysaccharides from a marine microalga (Cochlodinium polykrikoides) against human immunodeficiency virus and other enveloped viruses.

A marine microalga, Cochlodinium polykrikoides, produces extracellular sulfated polysaccharides. Isolation and purification of the polysaccharides were accomplished by precipitation with ethanol and Cetavlon, followed by DEAE-cellulose column chromatography (polysaccharides A1 and A2). These polysaccharides, which were homogeneous when analysed by both ultracentrifugal and electrophoretic methods, were composed of mannose, galactose, glucose and uronic acid, together with sulfate groups (S = 7-8% w/w). Both A1 and A2 inhibited the cytopathic effect of influenza virus types A and B in MDCK cells, that of respiratory syncytial virus types A and B in HEp-2 cells, that of human immunodeficiency virus type 1 in MT-4 cells; and, except A1 for herpes simplex virus type 1 and A2 for parainfluenza virus type 2 in HMV-2 cells, the cochlodinium polysaccharides showed no antiviral activity against parainfluenza virus types 2 and 3, measles virus, mumps virus or herpes simplex virus type 1 in HMV-2 cells. No cytotoxicity for host cells was observed with these polysaccharides at a concentration of 100 micrograms ml-1. Inhibitory effects on various viruses were achieved at concentrations that were not markedly inhibitory to the blood coagulation process.

Animals↗
PubMed1984

Association of parainfluenza-3 virus with bovine macrophages and blood cells: an in vitro study.

Bovine blood cells and peritoneal and lung macrophages were exposed in vitro to parainfluenza-3 (PI-3) virus. Residual nonadsorbed PI-3 virus (expressed in percentage of input virus) in the supernate of the various cell fractions 1 hour after incubation at 37 C was as follows: lung macrophages, 11%; peritoneal macrophages, 59%; monocytes, 26%; RBC, 14%; lymphocytes, 28%; and polymorphonuclear cells (PMN), 63%. Lung macrophages, monocytes, lymphocytes, and PMN were monitored over a 72-hour period for hemadsorption of chicken RBC. Hemadsorption increased for lung macrophages and monocytes, whereas it decreased for lymphocytes and PMN. Infective virus could not be recovered from PMN, RBC, lymphocytes, or monocytes for more than 24 hours after PI-3 infection. Recovery of infective PI-3 virus from infected peritoneal and lung macrophages extended over 4 to 8 days, respectively.

Animals↗
PubMed2000

Viral pneumonias. Epidemic respiratory viruses.

Influenza, respiratory syncytial, and parainfluenza viruses usually cause mild, self-limited illness in adults. However, elderly and immunocompromised persons are at increased risk for development of severe pneumonia. Clinical and radiographic features of epidemic viral pneumonias are often nonspecific. Newer and faster methods of viral culture and viral antigen detection have improved the capability for definitive diagnosis in recent years. Preventive measures for influenza virus pneumonia center on limiting exposure of high-risk patients to active cases of influenza, administering annual vaccinations, and providing chemoprophylaxis. Prophylaxis against RSV is effective in preventing complications. No effective vaccines have been developed against RSV or parainfluenza. Therapy for viral pneumonia is primarily supportive. Amantadine may be beneficial for influenza virus pneumonia, and ribavirin may be useful for RSV and parainfluenza virus disease. However, further definitive studies are necessary to determine their roles in these viral pneumonias.

Adult↗
PubMed1975

Multiple sclerosis and parainfluenza 1 virus. History of the isolation of the virus and expression of phenotypic differences between the isolated virus and Sendai virus.

54 cultures were established from brain tissue obtained 2-3 hrs after death from 1 case of multiple sclerosis and 30 cultures from another case. Following fusion with indicator cells in the presence of lysolecithin, a parainfluenza type 1 virus (6/94 virus) was isolated from cultures representing one plaque area in the first case and one plaque area in the second case. A cell line chronically infected with the 6/94 virus has been maintained for more than 100 passages in vitro. A close relationship to the Sendai Hemagglutinating Virus of Japan (HVJ) is indicated from RNA-RNA hybridization and the patterns of electrophoretic mobilities of viral polypeptides. Conversely, differences in optima for growth-requirement temperatures, hemolytic activity and the capability to fuse mammalian cells, distinguishes 6/94 virus and HVJ as distinct phenotypic entities of a closely related genotype.

Adult↗