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Serum antibody prevalence of parainfluenza 3 virus in a free-ranging bison (Bison bison) herd from Alaska.

Serum antibody prevalence of parainfluenza 3 virus in the free-ranging Delta bison (Bison bison) herd which is found near Delta Junction, Alaska (USA), increased from 0% to 100% during the period 1977 to 1984. Domestic cattle are hypothesized as the source for the infection. There has been no clinical disease or decrease in productivity in this bison herd since establishment of the infection.

Alaska↗

Clinical manifestations of parainfluenza infection in children.

Parainfluenza viruses are major pathogens causing respiratory illness, manifesting from mild upper respiratory tract infection to bronchiolitis and pneumonia. This retrospective study aimed at providing clinical and epidemiologic data addressing the parainfluenza virus infection in Taiwan. A total of 39 patients were enrolled in this study from March 1999 to December 2000. Infants and young children were the major susceptible population, with 87.2% of them younger than 3 years. No seasonal trend was noted for parainfluenza type 1 and type 2 infections. One clustering of parainfluenza virus type 3 infections occurred in late spring of 2000 based on collected results. Parainfluenza type 1 viral isolates accounted for all of the cases of croup. Most isolates of parainfluenza virus type 3 were associated with upper and/or lower respiratory tract infections. A substantial proportion of the patients had skin involvement; the identification of one case of possible parainfluenza virus-related erythema multiforme is particularly interesting, especially because the chances of a causal relation between viral infection and skin symptoms are formerly thought to be slight. The identification of parainfluenza virus in illnesses classically considered to be due to other viruses is intriguing and may have important implications in the management of childhood illness clinically.

Adolescent↗

Antibody appearance of parainfluenza-3 virus in cattle population in West Azerbaijan Province.

Studies were carried out on antibody appearance to parainfluenza-3 virus in cattle in Iran. The micro-system of HI test has been used for determination of the antibody level. Total percentage of sera with positive titers was 72.67% (336 out of 600). The picture of antibody levels in our results was as follows: 164 sera (27.33%) were negative; 147 (42.50%) had low titers; 168 (28%) showed an average titer and 21 sera (20.17%) were found to possess high antibody titers.

Animals↗

Persistence of viruses in the nasopharynx of apparently healthy children aged 0-5 years. Results of investigations performed in 1982-83.

Virus isolation attempts were made with nasopharyngeal secretions from 400 apparently healthy 0-5-year-old children of a semi-closed community. Repeated virus isolations were achieved in 25 cases subjected to periodic investigations in 1982-83. One-two reisolation(s), 1-5 months apart, of the initially detected viral agents could be obtained in 15 out of the 25 children. The following viruses were reisolated (in decreasing order of frequency): adenoviruses, respiratory syncytial virus, Coxsackie B1 virus, herpes virus type 1, parainfluenza virus type 3. The problems raised by the carriage of respiratory viruses in the nasopharynx of apparently healthy children are discussed.

Adenoviruses, Human↗

Differences in bovine parainfluenza 3 virus variants studied by monoclonal antibodies against viral glycoproteins.

We previously showed that of three bovine parainfluenza 3 virus strains the M strain, which is neurovirulent for young mice, has an extensive syncytium-inducing activity, whereas avirulent SC and 910N strains are weak in this activity. It was also demonstrated that both M and SC strains have very low hemagglutination and neuraminidase activities, while the 910N strain shows these activities to high levels. In the present study, monoclonal antibodies (Mabs) were raised against the glycoproteins of the 910N strain, and utilized to further characterize these three viral strains. Five Mabs against the hemagglutinin-neuraminidase protein, which were classified into four different epitope-recognizing groups, neutralized the M strain much more effectively than the 910N and SC strains, while the Mabs showed lower hemagglutination inhibition (HI) titers against the M and SC strains than the 910N strain. Three Mabs against the fusion protein neutralized the M strain but not the 910N and SC strains, while they showed no HI activity against any of these strains. These findings suggested that the M strain is considerably different from other strains in the structure of the viral envelope proteins.

Animals↗

Neuraminidase activity and syncytial formation in variants of parainfluenza 3 virus.

By a sensitive fluorometric assay method, we could definitely demonstrate neuraminidase activity for two variants of parainfluenza 3 virus, M and SC, which were previously shown to have no detectable neuraminidase activity. The enzyme activities of these viruses were very similar to each other, showing a much lower catalytic rate, a much higher Km value, and a more acidic pH optimum than those of the virus variants of high neuraminidase activity, 910N, LT, and MR. M and SC viruses eluted from guinea pig erythrocytes very poorly, whereas 910N and LT viruses eluted readily. M virus required the aid of a bacterial neuraminidase for effective growth and plaque formation in MDBK cells, but the virus grew well and formed plaques in R66 and Vero cells without the enzyme. SC virus required no exogenous neuraminidase for growth in all of these cell types. Depending on cell type, SC virus induced slight to extensive syncytial formation which was greatly inhibited by exogenous neuraminidase. In contrast, M virus induced extensive syncytial formation in all these cells regardless of the presence or absence of exogenous neuraminidase, although development and disintegration of the syncytia were more or less retarded by the enzyme, especially in MDBK cells. These results indicate that M virus possesses highly potent inducibility of syncytial formation which is further fortified by being low in viral neuraminidase activity.

Adsorption↗

Alveolar macrophage phagocytic kinetics following pulmonary parainfluenza-3 virus infection.

Qualitative and quantitative evaluations of the cellular components of bronchoalveolar washings of calves with experimental parainfluenza-3 virus pneumonitis and control calves were made. Calves were exposed to 10(9) TCID50 of PI-3 by intranasal aerosol exposure and bronchoalveolar cells obtained 7 days after infection by volume-controlled bronchopulmonary lavage. Transient tachypnea and pyrexia occurred in all infected calves, and virus was recoverable at 7 days from nasal swabs and lung tissue. Pulmonary lesions were typical of viral pneumonitis, characterized by patchy alveolitis and bronchiolitis with accumulations of cells and inflammatory debris. The mean total lavage cell yield was elevated in the virus-infected calves, and the percentage of neutrophils was elevated (P less than 0.05). Increased numbers of pulmonary alveolar macrophages (PAM) were also recovered but the difference was not significant. Linear regression equations showed that a decreased proportion of PAM from virus-infected animals were phagocytic. The mean initial phagocytic rates of macrophages from calves with viral pneumonitis were significantly decreased (P less than 0.05) over controls. This difference was concentration dependent and required a phagocytic stimulus in excess of 12.5 X 10(6) beads/ml. Studies of phagocytic kinetics showed that PAM from calves with viral pneumonitis had a lower Vmax than PAM from control calves, but that Km values were comparable. No differences in PAM beta-glucuronidase and acid phosphatase activity were observed. These results indicate depressed phagocytic function in PI-3 virus-inflamed lungs relative to controls. In concert with virus-induced airway lesions, such in vivo depression of PAM phagocytic functions would be expected to depress pulmonary particulate clearance and lung defense mechanisms.

Animals↗

Molecular cloning and sequence analysis of the human parainfluenza 3 virus gene encoding the L protein.

The sequence of the gene encoding the L protein of the human parainfluenza 3 virus was determined by direct dideoxy sequence analysis of the genomic 50 S RNA and confirmed by molecular cloning and sequence analysis of recombinant clones. A series of three overlapping clones was generated by primer extension using genomic 50 S RNA as the template. These clones originate within the 5' end of the hemagglutinin-neuraminidase gene, span the entire L gene, and extend into the extracistronic 5' end of the viral RNA. The L gene extends 6755 nucleotides (inclusive of the putative transcription initiation and polyadenylation signal sequences) and encodes a protein consisting of 2233 amino acids (MW 255,812). There are 44 nucleotides downstream of the putative polyadenylation signal sequence which may represent a negative-strand leader. The complementary sequence of the extracistronic region is nearly identical to the 3' end of the viral RNA. Thirty-three of the first thirty-nine nucleotides of the 3' ends of the plus and minus strands are conserved. Comparison of amino acid sequence homology with other paramyxoviral L proteins indicates a high degree of sequence conservation with Sendai virus (62%) and Newcastle disease virus (28%). In addition, four smaller regions were identified which shared extensive homology with the L protein of vesicular stomatitis virus, a member of the Rhabdoviridae family.

Amino Acid Sequence↗

Chlamydia trachomatis and parainfluenza 2 virus: a shared antigenic determinant?

A tracheal aspirate from which parainfluenza 2 (PI-2) virus but not chlamydiae was isolated demonstrated positive immunofluorescence of elementary body- and reticulate body-like particles on direct examination with anti-chlamydia monoclonal antibodies (Syva Co.). In subsequent studies, we found this reagent to show specific staining of this strain of PI-2 as well as of 3 of 18 additional PI-2 strains that were evaluated.

Antigens, Viral↗

Inhibition of multiplication of parainfluenza 3 virus in prostaglandin-treated WISH cells.

Influence of prostaglandins E2 (PGE2) and F2alpha (PGF 2alpha) on multiplication of myxovirus parainfluenza 3 was investigated. At concentrations of 0.01--1 mug/ml prostaglandins had no direct cytotoxic effects. PGE2 and PGF2alpha inhibited multiplication of parainfluenza 3 virus at concentrations 0.1--10 mug/ml. The inhibitory effect was most pronounced when the prostaglandins were added to medium for the whole period of virus multiplication (48 hours) while little or no effect was found when prostaglandins were added before virus inoculation or for 2 hours after infection. It is suggested that prostaglandins exert an inhibitory effect on the replication phase of the virus by influencing the growth of the WISH cells.

Amnion↗

[Substances with antiviral activity. XIII. Synthesis and in vitro activity of thiosemicarbazones of 1-benzoyl- and 1-benzyl-2-chloro-3-formylindoles].

A series of 1-benzoyl- and 1-benzyl-2-chloro-3-formylindole thiosemicarbazones was synthesized and investigated for antiviral activity against vaccinia virus IHD strain and parainfluenza virus type 3, HA-I/CR-8 strain. The results confirmed the previously observed high activity against vaccinia virus of m-substituted benzoyl derivatives. On the contrary, the analogous benzyl derivatives showed marginal activity; the compound (V c), however, was the most active against the parainfluenza virus.

Antiviral Agents↗

Analysis of bovine parainfluenza-3 virus replication in bovine embryonic lung cells by indirect fluorescent antibody and hemadsorption assays.

The temporal manifestation of bovine parainfluenza-3 virus (BPI3V) proteins in the cytoplasm and on the surface of bovine embryonic lung (BEL) cells was characterized by indirect fluorescent antibody (IFA) and hemadsorption (HAd) assays. Intracellular proteins appeared earliest at 0.5 h post inoculation (p.i.) and the infection spread to virtually all cells by 48 h p.i. Viral proteins on the surface of cells were seen first at 16 h p.i., and by 48 h p.i. the entire cell monolayer was IFA positive. Hundred-fold less virus in the inoculum delayed appearance of the intracellular as well as cell-surface viral proteins by 24 h and allowed the infection of only about 1/3 of the cells by 48 h p.i. Kinetics of the development in the proportion of HAd-positive cells correlated with those of the surface fluorescence-positive cells. Morphology of the manifestation of BPI3V proteins is characterized by microphotography.

Animals↗

[Effect of various infections on the development, course and outcome of glomerulonephritis in children].

Bacteriological and virological tests were made at the disease onset and repeatedly in 100 children (66 boys and 34 girls) aged 2 to 15 years suffering from acute glomerulonephritis. The throat mucus was found to contain streptococci and staphylococci; direct immunofluorescence demonstrated antigens of influenza A1, A3, B virus, of parainfluenza virus, serotypes 1 and 3, of adenovirus and respiratory and syncytial virus; HBs-antigens, specific viral and bacterial antibodies were detected in the blood serum. At the onset of acute glomerulonephritis, 52.5% of the patients were diagnosed to have bacterial infection, 12.5% respiratory viral infection, and 27.5% mixed infection (respiratory viral and bacterial). Besides, 25.5% of the patients showed HBs-antigenemia. HBs-antigenemia and mixed (respiratory viral and bacterial) infection were found to produce an adverse effect on the course and outcome of acute glomerulonephritis. Long-term circulation of some viral antibodies (mostly to parainfluenza-3 antigen) was revealed on repeated studies as was their untoward effect on the outcome of acute glomerulonephritis.

Adenoviruses, Human↗

Bovine viral diarrhoea, bovine herpesvirus and parainfluenza-3 virus infection in three cattle herds in Egypt in 2000.

This study reported field outbreaks of bovine viral diarrhoea virus (BVDV) infection, either alone or mixed with bovine herpesvirus-1 (BHV-1) and/or parainfluenza-3 virus (PI-3V) in Egypt during 2000. In Lower Egypt, young calves in three cattle herds in El-Minufiya Province, El-Fayoum Province and in governmental quarantine in El-Behira Province, showed symptoms of enteritis, either alone or accompanied by respiratory manifestations. The affected herds were visited and the diseased animals were clinically examined. Many epidemiological aspects, such as morbidities, mortalities and case fatalities, as well as the abortive rate, were calculated. Ethylenediamine tetra-acetic acid-blood samples, sterile nasal swabs and serum samples were obtained for virological and serological diagnosis. The laboratory investigations revealed that the main cause of calf mortalities in the three herds was infection with BVDV, either alone, as on the El-Minufiya farm, or mixed with PI-3V, as on the El-Fayoum farm, or mixed with both BHV-1 and PI-3V, as in the herd in governmental quarantine in El-Behira Province. A total of nine dead calves from the three herds were submitted for thorough post-mortem examination. Tissue samples from recently dead calves were obtained for immunohistochemical and histopathological studies. The most prominent histopathological findings were massive degeneration, necrosis and erosions of the lining epithelium of the alimentary tract. Most of the lymphoreticular organs were depleted of lymphocytes. In pneumonic cases, bronchopneumonia and atypical interstitial pneumonia were evident. The present study suggested that the immunosuppressive effect of BVDV had predisposed the animals to secondary infection with BHV-1 and PI-3V. This study concluded that concurrent infection with BVDV, BHV-1 and PI-3V should be considered as one of the infectious causes of pneumoenteritis and, subsequently, the high morbidities and mortalities among young calves in Egypt. Preventive and control measures against these infectious agents should therefore be adopted. All animals imported into Egypt should be free from BVDV infection. Control programmes for the detection and removal of BVDV-persistent cattle should be applied in cattle herds all over the country.

Animals↗

Bovine parainfluenza-3 virus proteins recognized by antibodies of aerosol-exposed calves.

Bovine parainfluenza-3 (BPI-3) virus proteins were radiolabeled with [35S]methionine. Control serum containing antibodies to BPI-3 virus obtained from calves that had been immunized by aerosol exposure and by IM inoculation and sera of cattle that were exposed to BPI-3 virus by aerosol only were used to immunoprecipitate BPI-3 virus proteins. The immunoprecipitates were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Viral proteins with estimated molecular weights of 72,000, 70,000, and 58,000 were recognized by the control serum and the sera from calves exposed to BPI-3 virus only by aerosol. These proteins were the hemagglutinin/neuraminidase, nucleoprotein, and fusion protein. The results indicated that a single aerosol exposure to BPI-3 virus induces antibodies to the same BPI-3 virus proteins as do combined aerosol and parenteral inoculations with the virus.

Aerosols↗

Molecular cloning and sequence analysis of the human parainfluenza 3 virus gene encoding the matrix protein.

The sequence of the matrix (M) protein gene and contiguous intergenic regions of the human parainfluenza 3 virus (PF3) was determined by molecular cloning. The encoded M protein contains 354 amino acids and has a predicted mol wt of 39,506. The M protein amino acid sequence was compared to the homologous proteins from other members of the Paramyxoviridae family. The PF3 protein shared 61% homology with the Sendai virus protein and approximately 35% homology with measles and canine distemper virus proteins. Little homology was observed with respiratory syncytial virus. The M protein appears to be the most highly conserved among the Paramyxoviridae proteins.

Amino Acid Sequence↗

Bovine herpesvirus-1 and parainfluenza-3 virus interactions: clinical and immunological response in calves.

Calves infected with bovine herpesvirus-1 (BHV-1) or both BHV-1 and parainfluenza-3 virus (PIV-3) developed clinical signs including fever, cough, and nasal and ocular discharges. Animals infected with both viruses appeared more depressed and showed higher rectal temperature, while calves inoculated with PIV-3 alone had a very mild clinical disease. Both BHV-1 and PIV-3 were recovered from nasal secretions up to six to eight days postinoculation. However, the virus titers were lower in calves with mixed infection. An increase in serum antibodies to both BHV-1 and PIV-3 was detected by serum neutralization and enzyme-linked immunosorbent assay. Antibody responses were delayed and significantly lower in calves given mixed infection than in calves infected with a single virus. Interleukin-2 activity in cultures of lymphocytes from BHV-1 and BHV-1 plus PIV-3 infected calves was higher compared to control calves.

Animals↗