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PubMed1996

Laboratory diagnosis of acute lower respiratory tract viral infections in children.

This report summarizes and compares the results of complement fixation test (CFT), virus isolation (VI), and direct immunofluorescence test (DIF) for the antigen detection of respiratory syncytial virus (RSV), influenza A virus (Flu A), and adenovirus in 62 children with acute lower respiratory tract infections (ALRI) in Kuwait. It includes, as well, CFT results for parainfluenza virus and Mycoplasma pneumoniae. Combining the three methods, a potential causative agent was identified in 56 (90 per cent) children, of whom 14 (22 per cent) had evidence of infection with more than one pathogen. RSV was most frequently identified followed by Flu A, parainfluenza, Mycoplasma pneumoniae and adenovirus. Virus isolation proved the best method for identification of RSV, Flu A, and adenovirus [identified 52 (84 per cent) cases]. DIF was sensitive for RSV detection (sensitivity 84 per cent, specificity 94 per cent), and less sensitive for Flu A (sensitivity 62 per cent, specificity 98 per cent). However, DIF was completely insensitive to adenovirus (no positives). CFT was positive for the five pathogens in 44 (71 per cent) of the population studied; therefore, almost 20 per cent of positive identifications would have been missed if VI and DIF were not done. The sensitivity and specificity of CFT for RSV, adenovirus and Flu A were 71, 75, and 31 per cent, and 94, 96, and 94 per cent, respectively. Based on the results of this pilot study, it appears that a combination of the three tests yields the best rate of virus detection. Cell culture cannot be discarded for the identification of some respiratory viruses, especially adenovirus, until better techniques, or more sensitive reagents are applied. However, since RSV is the virus most commonly involved in children with ALRI, we recommend using DIF on routine basis for diagnosis. Its results compare well with virus isolation; it is simple, rapid, and inexpensive.

Acute Disease↗
PubMedDate not supplied

[Varying nature of the cell receptors for influenza and para-influenza viruses].

A comparative study of receptors for influenza virus, fowl plague virus, and human parainfluenza type 3 virus was carried out. Natural receptors of guinea pig erythrocytes were destroyed with neuraminidase, and individual gangliosides GM1, GD1a, and GT1b were inserted into their membranes. The labeled virus was adsorbed on the erythrocytes modified in this manner, and the degree of restoration of the receptor activity of erythrocytes lost after neuraminidase treatment was determined. Two gangliosides, GD1a and GT1b, were found to be capable of functioning as specific receptors for influenza virus. Both gangliosides restored completely the virus adsorption on erythrocytes. In contrast, none of the three gangliosides used did not restore parainfluenza virus adsorption. It is concluded that the nature of influenza and parainfluenza virus receptors is different.

Adsorption↗
PubMed1983

Disseminated parainfluenza infection in a child with severe combined immunodeficiency.

An 8-month-old male infant with severe combined immunodeficiency syndrome was admitted to the hospital with pneumonitis and, subsequently, died at 21 months of age. During his lengthy hospitalization, parainfluenza virus type 3 (PIV-3) was isolated from respiratory secretions and unusual sites, such as pericardial fluid, CSF, and WBCs. A postmortem examination showed apparent viral pancreatitis, and PIV-3 was isolated from the lung, brain, and pericardial fluid. To our knowledge, this is the first reported case of disseminated parainfluenza infection identified during life. We speculated that a mutant fusion protein may have been elaborated by the virus, allowing dissemination beyond the respiratory tract.

Brain↗
PubMed1996

Acute bronchiolitis in tropical Africa: a hospital-based perspective in Ibadan, Nigeria.

In a 30-month prospective study of severe acute lower respiratory infections in hospitalized pre-school Nigerian children, acute bronchiolitis was diagnosed in 67 cases; 19 (28.4%) and 2 (3.0%) of these had concomitant pneumonia or croup, respectively. The peak prevalence was in the wet (rainy) season (May-October). The male/female (M:F) ratio in infants < or = 6 months was 2.9:1, differing significantly from the 1.1:1 in older subjects (P = 0.04). None of the subjects had severe malnutrition. Neither a high fever (> or = 39 degrees C), nor tachypnea on admission was significantly correlated with co-existing pneumonia. Of the 29 subjects in whom it was possible to explore viral immunofluorescence studies and/or serodiagnosis, we identified 26 viral identifications in 18 (62.1%) cases; 6 (20.7%) had > or = 2 viruses. Respiratory syncytial virus was identified in 11 (38.0%) of the 29 cases, and parainfluenza virus (PIV) types 1, 2, and 3 in 10 (34.5%). PIV type 3 accounted for 7 cases, including 3 with bacteremia. Bacterial isolates were made in 9 (21.4%) of 42 blood cultures and in the only lung aspirate; Staphylococcus epidermidis and Staphylococcus aureus accounted for 4 and 3 cases, respectively. Although bacteremia was 2.9 times more common in cases with co-existing pneumonia or croup, the respective frequency of virus-positive cases and that of bacteremia was not significantly different between cases with bronchiolitis alone and those with associated pneumonia or croup. No deaths were recorded, but subjects aged > 6 months had a significantly shorter hospital stay than those < 6 months old (P = 0.02). Despite the limited sample size, our findings reflect the etiological importance of the paramyxoviruses and the seasonal pattern of bronchiolitis in tropical Africa.

Acute Disease↗
PubMed1981

Nosocomial viral respiratory infections: perennial weeds on pediatric wards.

The frequency and importance of nosocomial infections of the respiratory tract in pediatrics have generally been underestimated. In part this has resulted from the emphasis on bacterial infections which occur primarily in select at-risk populations. Most respiratory infections in pediatric patients, hospital- and community-acquired, are viral and all patients are potentially susceptible The epidemiologic patterns of these viral respiratory agents on the ward mirror those seen in the community in terms of frequency, season, age affected and severity of illness. Hence, the most frequent nosocomial agents are the viruses that occur in outbreaks or epidemics and cause respiratory illness, epidemic respiratory viruses--respiratory syncytial virus, which causes the greatest morbidity and mortality; influenza, and the parainfluenza viruses. Their import, as exemplified by respiratory syncytial virus, results from (1) the severity of disease produced in young children, which is magnified in those hospitalized with certain underlying conditions; (2) the abundant and prolonged viral shedding, allowing easy spread; (3) the potential susceptibility of all patients and staff, since infections recur throughout life; and (4) the difficulty in controlling nosocomial spread.

Child, Preschool↗
PubMed1995

Antiviral screening of British Columbian medicinal plants.

One hundred methanolic plant extracts were screened for antiviral activity against seven viruses. Twelve extracts were found to have antiviral activity at the non-cytotoxic concentrations tested. The extracts of Rosa nutkana and Amelanchier alnifolia, both members of the Rosaceae, were very active against an enteric coronavirus. A root extract of another member of the Rosaceae, Potentilla arguta, completely inhibited respiratory syncytial virus. A Sambucus racemosa branch tip extract was also very active against respiratory syncytial virus while the inner bark extract of Oplopanax horridus partially inhibited this virus. An extract of Ipomopsis aggregata demonstrated very good activity against parainfluenza virus type 3. A Lomatium dissectum root extract completely inhibited the cytopathic effects of rotavirus. In addition to these, extracts prepared from the following plants exhibited antiviral activity against herpesvirus type 1: Cardamine angulata, Conocephalum conicum, Lysichiton americanum, Polypodium glycyrrhiza and Verbascum thapsus.

Animals↗
PubMed1990

Host cell-dependent lateral mobility of viral glycoproteins.

The lateral mobility of viral envelope proteins on the plasma membranes of infected cells is an important factor in both virus assembly and pathogenesis. The envelope glycoproteins of measles and human parainfluenza virus are mobile on the surfaces of infected HeLa cells and undergo lateral redistribution in the presence of specific antibody, forming unipolar caps. In contrast, no such redistribution was observed with influenza virus hemagglutinin (HA) or vesicular stomatitis virus (VSV) G glycoproteins on infected HeLa cell surfaces. However, the HA and G glycoproteins were both found to be mobile in the plasma membrane of CV-1 cells, or human or murine peritoneal macrophages. These results indicate that host cell-dependent as well as virus-specific factors are involved in determining viral glycoprotein mobility. No significant differences in the patterns of synthesis of influenza or VSV viral proteins were found in the various cell types examined. The HA and G proteins, when expressed from vaccinia virus recombinants, were each found to be immobile in HeLa cells and mobile in CV-1 cells, thus indicating that the host cell-dependent differences in mobility are an intrinsic property of each viral glycoprotein molecule and not the result of interaction with other viral components. It is suggested that the association of viral glycoproteins with either the cytoskeleton or membrane-associated cellular proteins may be related to the observed differences in lateral mobility.

Animals↗
PubMed2006

The cell biology of acute childhood respiratory disease: therapeutic implications.

Respiratory syncytial virus (RSV), the recently identified human metapneumovirus (HMPV), and the human parainfluenza viruses (HPIVs), cause most cases of childhood croup, bronchiolitis, and pneumonia. Influenza virus also causes a significant burden of disease in young children, although its significance in children was not fully recognized until recently. This article discusses pathogens that have been studied for several decades, including RSV and HPIVs, and also explores the newly identified viral pathogens HMPV and human coronavirus NL63. The escalating rate of emergence of new infectious agents, fortunately meeting with equally rapid advancements in molecular methods of surveillance and pathogen discovery, means that new organisms will soon be added to the list. A section on therapies for bronchiolitis addresses the final common pathways that can result from infection with diverse pathogens, highlighting the mechanisms that may be amenable to therapeutic approaches. The article concludes with a discussion of the overarching impact of new diagnostic strategies.

Acute Disease↗
PubMed2005

Cooperativity of actin and microtubule elements during replication of respiratory syncytial virus.

Many paramyxoviruses appear to require cytoskeletal elements for particular steps in the virus life cycle. Measles virus and Sendai virus exhibit a requirement for microtubules in replication in vitro, whereas parainfluenza virus type 3 and RSV require actin for replication. To further elucidate the role of cytoskeletal function and rearrangement in the viral life cycle of RSV, we investigated the efficiency of virus entry, transcription, replication, and budding in the presence of a variety of pharmacological agents that stabilize or depolymerize actin or microtubules. We found that alteration of microtubule or actin function resulted in blocks at entry, formation of cell-associated virus, virus release, local cell-to-cell spread, and syncytium formation. Actin and microtubules act in cooperation to facilitate replication of RSV, although microtubules play a dominant role in the formation of cell-associated virus while actin plays a more prominent role in virus release.

Actins↗
PubMed1998

Pseudotype formation of Moloney murine leukemia virus with Sendai virus glycoprotein F.

Mixed infection of cells with both Moloney murine leukemia virus (MoMLV) and related or heterologous viruses produces progeny pseudotype virions bearing the MoMLV genome encapsulated by the envelope of the other virus. In this study, pseudotype formation between MoMLV and the prototype parainfluenza virus Sendai virus (SV) was investigated. We report for the first time that SV infection of MoMLV producer cells results in the formation of MoMLV(SV) pseudotypes, which display a largely extended host range compared to that of MoMLV particles. This could be associated with SV hemagglutinin-neuraminidase (SV-HN) glycoprotein incorporation into MoMLV envelopes. In contrast, solitary incorporation of the other SV glycoprotein, SV fusion protein (SV-F), resulted in a distinct and narrow extension of the MoMLV host range to asialoglycoprotein receptor (ASGP-R)-positive cells (e.g., cultured human hepatoma cells). Since stably ASGP-R cDNA-transfected MDCK cells, but not parental ASGP-R-negative MDCK cells, were found to be transduced by MoMLV(SV-F) pseudotypes and transduction of ASGP-R-expressing cells was found to be inhibited by ASGP-R antiserum, a direct proof for the ASGP-R-restricted tropism of MoMLV(SV-F) pseudotypes was provided. Cultivation of ASGP-R-positive HepG2 hepatoma cells on Transwell-COL membranes led to a significant enhancement of MoMLV(SV-F) titers in subsequent flowthrough transduction experiments, thereby suggesting the importance of ASGP-R accessibility at the basolateral domain for MoMLV(SV-F) pseudotype transduction. The availability of such ASGP-R-restricted MoMLV(SV-F)-pseudotyped vectors opens up new perspectives for future liver-restricted therapeutic gene transfer applications.

Animals↗
PubMed2005

Inflammatory and bronchospastic factors in asthma exacerbations caused by upper respiratory tract infections.

It is still uncertain how viral respiratory infections cause acute exacerbations of bronchial asthma, although several mechanisms have been proposed. We studied the relationship between the airway narrowing and the inflammatory and bronchospastic factors in peripheral venous blood and urine, in 30 patients with asthma at the exacerbations caused by upper respiratory tract infections (URTIs). Acute exacerbations caused decreases in peak expiratory flow rate (PEFR) in all 30 patients with asthma. Asthma exacerbations caused the rises in serum levels of interleukin-6, soluble intercellular adhesion molecule-1 and eosinophil cationic protein, concentrations of urinary leukotriene E4 and plasma histamine, compared with those in patients with asthma at a stable condition and those in 30 control subjects (p < 0.05). The values of PEFR at the exacerbations correlated with the levels of these factors. Treatment with oral glucocorticoids reversed the decreases in PEFR and the increases in these factors. At the onset of URTIs, rhinovirus and influenza type A virus were identified in 13 and 7 patients, respectively. Each of parainfluenza virus, adenovirus, and enterovirus was identified in one patient. These findings suggest that respiratory viral infections may cause acute asthma exacerbations via the production of mediators that induce inflammation and bronchospasm.

Acute Disease↗
PubMed1992

Monoclonal and polyclonal antibodies for immunohistochemical detection of bovine parainfluenza type 3 virus in frozen and formalin-fixed paraffin-embedded tissues.

Accurate identification of bovine parainfluenza type 3 virus in bovine respiratory disease requires dependable, sensitive, and specific techniques for detection in affected animals. Immunohistochemical testing can be a rapid and reliable means of demonstration of virus in tissues from suspect cases; however, this procedure is dependent upon the quality of the antisera directed against the viral antigens. The production of rabbit polyclonal and murine monoclonal antibodies directed against bovine parainfluenza type 3 virus and techniques for their use in fresh-frozen and formalin-fixed paraffin-embedded tissues in immunofluorescence and immunoperoxidase-based immunohistochemical tests are described.

Animals↗
PubMed1984

Antibody and complement-mediated cytotoxicity for bovine parainfluenza-3 virus-infected cells.

An antibody-complement-mediated cytotoxicity assay was employed to determine whether susceptible host cells infected with bovine parainfluenza-3 virus could be destroyed by the humoral immune mechanism. The cytotoxicity assay yielded 21.5% to 76.9% specific release of 51Cr with sera collected from calves 28 days after inoculation with the virus. A multiplicity of infection of 5, a postinfection period of 2 days, an antibody dilution of 1:10, and an incubation period of 12 hours with antibody and complement were found to be optimal for this assay.

Animals↗
PubMed2003

[Parainfluenza type 3 virus infection in neonates with cardiac arrhythmia].

The aim of the study was to assess the frequency of the occurrence of parainfluenza type 3 virus infection in neonates with cardiac arrhythmia. In 12 (17%) out of 70 of neonates parainfluenza type 3 virus infection was recognized basing on serologic hemagglutinin inhibition test. Ten of them were diagnosed with mild course of myocarditis. Among 12 neonates infected with parainfluenza type 3 virus supraventricular and ventricular arrhythmia was observed in 5 and mild periodical bradycardia was diagnosed. None of the neonates were treated with antiarrhythmic medications. The authors would like to point out that interpretation of the serologic tests in neonates are difficult.

Antibodies, Viral↗
PubMed2001

Epithelial cells infected with respiratory syncytial virus are resistant to the anti-inflammatory effects of hydrocortisone.

In this work we continue our study of the biochemical responses of respiratory epithelial cells to infection with human paramyxovirus pathogens. In our earlier studies, we detected elevated concentrations of the proinflammatory chemokines MIP-1alpha and IL-8 in upper and lower respiratory tract secretions from patients infected with respiratory syncytial virus (RSV). Here we demonstrate the same trend for individuals infected with parainfluenza virus (PIV), with elevated concentrations of MIP-1alpha and IL-8 (means of 309 +/- 51 and 2280 +/- 440 pg/ml/mg protein, respectively) detected in nasal wash samples from 17 patients with culture-positive PIV. Similar to our findings with RSV, cells of the HEp-2 epithelial line and primary cultures of human bronchial epithelial cells respond to PIV infection with production and release of both MIP-1alpha and IL-8. Addition of the glucocorticoid anti-inflammatory agent hydrocortisone (200-1000 ng/ml) attenuated the production of MIP-1alpha and IL-8 in PIV-infected cells while having minimal to no effect on the production of these mediators from cells infected with RSV. Neither virus infection resulted in a change in the total cellular concentration of glucocorticoid receptors, nor did hydrocortisone exert any differential effect on viral replication. As repression of chemokine production by epithelial cells is likely to result in diminished recruitment of proinflammatory leukocytes, these results may explain in part why glucocorticoid therapy reduces the symptoms associated with acute PIV infection, but have little to no effect in the overall outcome in the case of RSV.

Anti-Inflammatory Agents↗
PubMed1998

Etiology of respiratory tract infection in adults in a general practice setting.

A prospective study was conducted over a 3-month winter period in three general practice clinics in an urban population in southern Israel to identify the etiological agents of respiratory tract infections (RTI) in adults. RTI was defined as an acute febrile illness with cough, coryza, sore throat or hoarseness. Serum samples were taken from all patients in both the acute and convalescent phases of their illness. Tests were conducted for detection of 17 microorganisms known to cause RTI, including serological tests for 16 known pathogens. An etiological diagnosis was established in 80 (66%) of the 122 patients who participated in the study. The distribution of the etiological agents was as follows: influenza B virus in 27 (22%) patients. Chlamydia pneumoniae in 22 (18%), Legionella spp. in 15 (12%), Mycoplasma pneumoniae in 13 (11%), influenza A virus in 11 (9%), Bordetella pertussis in 9 (7%), adenovirus in 4, Epstein Barr virus in 4, Haemophilus influenzae in 3, beta-hemolytic streptococci in 3, Streptococcus pneumoniae in 2, respiratory syncytial virus in 2, parainfluenza 1 virus in 2 and parainfluenza 2 virus in 1. No patients were found to be infected with Coxiella burnetii, Moraxella catarrhalis or parainfluenza 3 virus. More than one pathogen was identified in 27 (34%) patients in whom an etiological diagnosis was established. It is concluded that RTI is caused by a broad spectrum of etiological agents, a considerable number of patients having evidence of infection with more than one pathogen. The therapeutic significance of these findings should be elucidated in further studies.

Adult↗
PubMed2001

Role of matrix and fusion proteins in budding of Sendai virus.

Paramyxoviruses are assembled at the surface of infected cells, where virions are formed by the process of budding. We investigated the roles of three Sendai virus (SV) membrane proteins in the production of virus-like particles. Expression of matrix (M) proteins from cDNA induced the budding and release of virus-like particles that contained M, as was previously observed with human parainfluenza virus type 1 (hPIV1). Expression of SV fusion (F) glycoprotein from cDNA caused the release of virus-like particles bearing surface F, although their release was less efficient than that of particles bearing M protein. Cells that expressed only hemagglutinin-neuraminidase (HN) released no HN-containing vesicles. Coexpression of M and F proteins enhanced the release of F protein by a factor greater than 4. The virus-like particles containing F and M were found in different density gradient fractions of the media of cells that coexpressed M and F, a finding that suggests that the two proteins formed separate vesicles and did not interact directly. Vesicles released by M or F proteins also contained cellular actin; therefore, actin may be involved in the budding process induced by viral M or F proteins. Deletion of C-terminal residues of M protein, which has a sequence similar to that of an actin-binding domain, significantly reduced release of the particles into medium. Site-directed mutagenesis of the cytoplasmic tail of F revealed two regions that affect the efficiency of budding: one domain comprising five consecutive amino acids conserved in SV and hPIV1 and one domain that is similar to the actin-binding domain required for budding induced by M protein. Our results indicate that both M and F proteins are able to drive the budding of SV and propose the possible role of actin in the budding process.

Actins↗