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PubMed1998

Effect of compounds with antibacterial activities in human milk on respiratory syncytial virus and cytomegalovirus in vitro.

The effect of some antibacterial compounds present in human milk were tested for antiviral activity against respiratory syncytial virus, Semliki Forest virus and cytomegalovirus. These included the gangliosides GM1, GM2 and GM3, sialyl-lactose, lactoferrin and chondroitin sulphate A, B and C, which were all tested for their ability to inhibit the viruses in cell culture. Of the compounds tested, only the ganglioside GM2, chondroitin sulphate B and lactoferrin inhibited the absorption and growth of respiratory syncytial virus in cell culture, and none inhibited the growth of Semliki Forest virus, indicating that lipid antiviral activity was not associated with any of the gangliosides. While the concentrations of these two compounds required to inhibit respiratory syncytial virus were in excess of those present in human milk, sialyl-lactose concentrations similar to those present in human milk increased the growth of cytomegalovirus. Lactoferrin was confirmed as inhibiting both respiratory syncytial virus and cytomegalovirus growth in culture even when used at lower concentrations than those present in human milk. The antiviral activities of GM2, chondroitin sulphate B and lactoferrin were tested when added to an infant formula. Lactoferrin continued to have antiviral activity against cytomegalovirus, but a lower activity against respiratory syncytial virus; ganglioside GM2 and chondroitin sulphate B still maintained antiviral activity against respiratory syncytial virus.

Animals↗
PubMed1991

Handwashing and cohorting in prevention of hospital acquired infections with respiratory syncytial virus.

Hospital acquired infections with respiratory syncytial virus are a major problem. The virus is spread predominantly by infected nasal secretions and we investigated whether we could reduce its incidence by cohorting babies on each ward into designated areas and encouraging staff and parents to wash their hands. We examined the incidence of hospital acquired infection due to respiratory syncytial virus in all children less than 2 years old and in those with congenital heart disease. In 1986-7, before any intervention, 18 (4.2%) of 425 hospitalised children less than 2 years old developed hospital acquired infection due to respiratory syncytial virus. In 1987-8, after intervention, five (0.6%) of 840 children developed hospital acquired infection but there were fewer ward admissions with community acquired infections due to the virus. In 1988-9, when there were more community acquired infections than 1986-7, six (1.1%) of 552 children developed hospital acquired infection. In 1986-7, eight (34.8%) of 23 children less than 2 years old with congenital heart disease developed hospital acquired infection due to respiratory syncytial virus; all eight were among 11 children with congenital heart disease hospitalised for more than 14 days. In 1987-8, one (3.3%) of 30 children with congenital heart disease developed hospital acquired infection due to respiratory syncytial virus and in 1988-9 there was one (2.1%) case out of 47 children with congenital heart disease. Handwashing and cohorting significantly reduce the incidence of nosocomial respiratory syncytial virus infection.

Cohort Studies↗
PubMed1991

Ultrastructural features of alveolar lesions in induced respiratory syncytial virus pneumonia of calves.

Ultrastructural changes occurred in alveolar epithelium in the acute and repair stages of induced respiratory syncytial virus pneumonia induced in eight calves (calf Nos. 1-7, 3 to 6 days old and calf No. 8, 2 weeks old), using a bovine strain of respiratory syncytial virus. Five of the calves were Friesians, three were Hereford x Friesians, and all were male. Tissues from three mock-infected control calves (two Friesian, one Hereford x Friesian) were also examined. Evidence of respiratory syncytial virus infection was observed in both type I and type II pneumocytes from day 4 to day 8 after infection. Infection of type I pneumocytes frequently resulted in necrosis. The response of type II pneumocytes to respiratory syncytial virus infection varied and included hypertrophy, hyperplasia, and syncytial formation. In some infected type II pneumocytes, there were numerous irregular projections of the cell surface, associated with viral budding. Hypertrophy and hyperplasia of type II pneumocytes, epithelial syncytium formation, and irregular cytoplasmic projections from epithelial cells caused considerable thickening of respiratory membrane and occlusion of alveolar lumina. Neutrophils were frequently observed in close association with virus-infected epithelial cells, but evidence of respiratory syncytial virus infection and replication was not observed in alveolar macrophages or neutrophils. Proliferation of type II pneumocytes appeared to play a major role in maintaining the integrity of the alveolar epithelium during the acute stage of the experimental pneumonia. Increased numbers of type II pneumocytes were present on alveolar walls, particularly from 4 to 8 days after infection, and some alveoli were lined entirely by this cell type. In some areas, however, squamous epithelial cells were also involved in covering exposed alveolar basement membrane.

Animals↗
PubMed1999

Neural control mechanisms within airways: disruption by respiratory syncytial virus.

UNLABELLED: Among the factors influencing airway function are neural control mechanisms, including adrenergic, cholinergic, nonadrenergic noncholinergic inhibitory, and nonadrenergic noncholinergic excitatory pathways. Respiratory infections affect these pathways in ways that are not entirely clear. OBJECTIVE: To determine acute and chronic effects of respiratory syncytial virus infection on airway neural control mechanisms. STUDY DESIGN: Acute effects were studied in cotton rats, which received human respiratory syncytial virus or uninfected cell culture medium intranasally at 5 weeks of age. Chronic effects were studied in ferrets, which received human respiratory syncytial virus or uninfected cell culture medium intranasally during the first 10 days of life. The responsiveness of tracheal smooth muscle segments was studied in vitro 4 days after infection of cotton rats and when ferrets were 4, 8, and 24 weeks of age. RESULTS: Tracheal smooth muscle segments from cotton rats demonstrated significant increases in contractile responses to nerve stimulation (cholinergic responses). In the presence of neurokinin A, contractile responses increased (enhanced nonadrenergic noncholinergic excitatory response), and relaxation of airways by nerve stimulation (nonadrenergic noncholinergic inhibitory response) was severely impaired. Airway epithelium was also disrupted. These alterations favor airway obstruction and a hyper-responsive state. Contractile responses to nerve stimulation were increased in 4- and 8-week-old ferrets infected with human respiratory syncytial virus compared with ferrets in a control group, a difference that resolved by 24 weeks. Nonadrenergic noncholinergic inhibitory responses were absent in all 4-week-old ferrets and significantly decreased in 8-week-old ferrets infected with human respiratory syncytial virus. A significant difference persisted at 24 weeks of age. CONCLUSION: Human respiratory syncytial virus causes acute and chronic changes in neural control of airways in animal models. When infection occurs early in life, the alterations persist for long periods.

Acute Disease↗
PubMedDate not supplied

Interpretation of syncytial sprouts and bridges in the human placenta.

Human placental villi from normal and pathological material from the eighth to the 40th week of gestation were examined by light, scanning and transmission electron microscopy. Trophoblastic specializations--such as syncytial sprouts of early and late pregnancy, syncytial knots and syncytial bridges--were classified into proliferative and degenerative processes or artefacts caused by tangential sectioning. In early pregnancy and in diabetes mellitus most syncytial sprouts represent the initial phases in the development of villi. In late pregnancy, in particular in pre-eclampsia, most syncytial knots, sprouts and bridges are histological artefacts, caused by tangential sectioning of the trophoblastic surface. The chance of producing such artefacts is increased with increasing section thickness and with increasing branching and tortuosity of the villi. However, a small proportion of the syncytial knots, sprouts and bridges in the last-trimester placenta, those containing coarse pyknotic nuclei, are trophoblastic specializations of a probably degenerative character.

Chorionic Villi↗
PubMed1992

Syncytial giant-cell hepatitis--a specific disease entity?

Syncytial giant-cell hepatitis was recently reported to be related to a paramyxovirus and carried a poor prognosis. Twelve patients with syncytial giant-cell hepatitis seen in an 8 1/2-year period in our institute were reviewed. Seven patients had an identifiable aetiological cause: two had autoimmune chronic active hepatitis, one had primary sclerosing cholangitis and autoimmune chronic active hepatitis, two presented with prolonged jaundice after acute hepatitis A and B, one had chronic Epstein-Barr virus infection and the remaining patient was seropositive for antibody to hepatitis C virus. One patient with autoimmune chronic active hepatitis who had frequent syncytial giant cells in the liver responded promptly to corticosteroid treatment and a repeated biopsy 3 years later showed histological improvement with a marked decrease in the number of syncytial giant cells. Of the remaining five patients, three ran a clinical course of fulminant hepatic failure and two had severe chronic active hepatitis. These data indicate that syncytial giant-cell hepatitis is unlikely to be related to only one single aetiological agent and that syncytial giant-cell hepatitis does not always carry an ominous prognosis.

Adolescent↗
PubMedDate not supplied

Preparation and functional characterization of villous cytotrophoblasts free of syncytial fragments.

Recent studies suggest that purified villous cytotrophoblasts are largely contaminated by mononucleated syncytial fragments and therefore unsuitable for studies of trophoblast differentiation. We assessed highly purified (>99.99 per cent) populations of villous trophoblasts for fragment contamination using the syncytial markers placental alkaline phosphatase (PLAP, by immunohistochemistry) and exteriorized phosphatidyl serine (ePS, by flow cytometric analysis). The preparations contained from 4-46 per cent syncytial fragments. However, we find that PLAP negative cells preferentially adhere to tissue culture surfaces and that all preparations were <2 per cent PLAP positive after routine plating and washing procedures. A second purification procedure eliminated dead (propidium iodide permeable) cells and separated viable syncytial fragments (ePS-positive) from viable cytotrophoblasts (ePS-negative) by two colour fluorescence activated cell sorting (FACS). Viable ePS-positive cells were ultrastructurally apoptotic, adhered poorly in culture and those that adhered rapidly underwent apoptosis. Viable ePS-negative cells contained large heterochromic nuclei and cytoplasmic structures, adhered strongly in culture and remained viable. The latter population (putative true villous CT) differentiated into syncytialized cells when cultured with EGF. We conclude that villous CT can be routinely purified, are viable in culture and can undergo syncytial fusion without extensive preformed syncytium.

Adult↗
PubMed2000

Hypoxia and nitric oxide induce a rapid, reversible cell cycle arrest of the Drosophila syncytial divisions.

Cells can respond to reductions in oxygen (hypoxia) by metabolic adaptations, quiescence or cell death. The nuclear division cycles of syncytial stage Drosophila melanogaster embryos reversibly arrest upon hypoxia. We examined this rapid arrest in real time using a fusion of green fluorescent protein and histone 2A. In addition to an interphase arrest, mitosis was specifically blocked in metaphase, much like a checkpoint arrest. Nitric oxide, recently proposed as a hypoxia signal in Drosophila, induced a reversible arrest of the nuclear divisions comparable with that induced by hypoxia. Syncytial stage embryos die during prolonged hypoxia, whereas post-gastrulation embryos (cellularized) survive. We examined ATP levels and morphology of syncytial and cellularized embryos arrested by hypoxia, nitric oxide, or cyanide. Upon oxygen deprivation, the ATP levels declined only slightly in cellularized embryos and more substantially in syncytial embryos. Reversal of hypoxia restored ATP levels and relieved the cell cycle and developmental arrests. However, morphological abnormalities suggested that syncytial embryos suffered irreversible disruption of developmental programs. Our results suggest that nitric oxide plays a role in the response of the syncytial embryo to hypoxia but that it is not the sole mediator of these responses.

Animals↗
PubMed1998

Exit from mitosis in Drosophila syncytial embryos requires proteolysis and cyclin degradation, and is associated with localized dephosphorylation.

The cyclin proteolysis that accompanies the exit from mitosis in diverse systems appears to be essential for restoration of interphase. The early syncytial divisions of Drosophila embryos, however, occur without detectable oscillations in the total cyclin level or Cdk1 activity. Nonetheless, we found that injection of an established inhibitor of cyclin proteolysis, a cyclin B amino-terminal peptide, prevents exit from mitosis in syncytial embryos. Similarly, injection of a version of Drosophila cyclin B that is refractory to proteolysis results in mitotic arrest. We infer that proteolysis of cyclins is required for exit from syncytial mitoses. This inference can be reconciled with the failure to observe oscillations in total cyclin levels if only a small pool of cyclins is destroyed in each cycle. We find that antibody detection of histone H3 phosphorylation (PH3) acts as a reporter for Cdk1 activity. A gradient of PH3 along anaphase chromosomes suggests local Cdk1 inactivation near the spindle poles in syncytial embryos. This pattern of Cdk1 inactivation would be consistent with local cyclin destruction at centrosomes or kinetochores. The local loss of PH3 during anaphase is specific to the syncytial divisions and is not observed after cellularization. We suggest that exit from mitosis in syncytial cycles is modified to allow nuclear autonomy within a common cytoplasm.

Animals↗
PubMed1984

Syncytial cells in canine parathyroid glands.

Multinucleated syncytial cells consisting of clusters of closely apposed, darkly staining nuclei and densely eosinophilic cytoplasm were present in parathyroid glands from 25 of 36 dogs (69%). They were most often located either peripherally in the parathyroid gland or adjacent to blood vessels. The numbers of nuclei per syncytial cell ranged from two to greater than 30. Syncytial cells had degenerative changes as suggested by vacuolated mitochondria, dilated rough endoplasmic reticulum, irregular nuclear outlines, and condensed nuclear chromatin. These ultrastructural changes contrasted sharply with adjacent chief cells that had well-preserved organelles. The presence of desmosomes and fragments of cell membranes between nuclei suggested that syncytial cells were derived from fusion of adjacent chief cells rather than nuclear division without cytokinesis. Syncytial cells were present in normal, hyperplastic, and inactive parathyroid glands from dogs. There were no significant correlations between the presence of multinucleated cells and age of dog, parathyroid histology, and changes in the concentrations of serum calcium, phosphorus, creatinine, or plasma parathyroid hormone. Syncytial cells occurred frequently in canine parathyroid glands regardless of the state of activity of the gland or the concentration of plasma parathyroid hormone or serum calcium.

Animals↗
PubMedDate not supplied

Vascular endothelial growth factor but not placental growth factor promotes trophoblast syncytialization in vitro.

OBJECTIVE: The object of this study was to determine the effect of epithelial growth factor (EGF), vascular endothelial growth factor (VEGF), and placental growth factor (PlGF) on the differentiation of first-trimester and term cytotrophoblasts. METHODS: The first-trimester trophoblasts were isolated from villous tissue obtained at suction termination (n = 5), and the term trophoblasts were isolated from placentas (n = 6) at elective cesarean. Cultured cells were stimulated with EGF, VEGF, or PlGF at 0.5, 5, and 50 ng/mL, in the presence or absence of N(G)-nitro-L-arginine methyl ester hydrochloride (10(-4) M). Syncytialized trophoblasts were identified by immunostaining with antidesmosomal protein and anti-cytokeratin-7, whereas nuclei were counted in each syncytia using hematoxylin. RESULTS: Without treatment, background levels of syncytialization were significantly higher in term preparations than first-trimester cells. With VEGF and EGF, the number and size of syncytia increased significantly for the first-trimester cytotrophoblasts (P <.05). Neither VEGF nor EGF had any effect on the syncytialization of cultured cells at term. Nitric oxide showed no involvement in syncytial induction, and PlGF had no effect on syncytialization of cytotrophoblasts, from either the first or third trimester. CONCLUSION: Both EGF and VEGF appeared to enhance the in vitro syncytialization of first trimester cytotrophoblasts.

Cell Differentiation↗
PubMed2005

[Stereological study on syncytial cell of human placenta and determinations of total bile acid in cord blood of intrahepatic cholestasis of pregnancy].

OBJECTIVE: To investigate the relation of changes of fetal bile acid and morphologic ultrastructure of human placental syncytial cells in intrahepatic cholestasis of pregnancy (ICP). METHODS: Total bile acid of cord venous blood was measured by cycle enzyme method between intrahepatic cholestasis of pregnancy and control groups after birth. The ultrastructure of human placental syncytial cell was analyzed by morphologic study in two groups. RESULTS: (1) The total bile acid of cord venous blood in ICP group was significantly higher than in control group [(8.6 +/- 3.2) micromol/L vs (4.6 +/- 1.5) micromol/L] (P < 0.05). (2) The amount and number density of syncytial microvilli ultrastructure reduced significantly in ICP group [respectively (21 +/- 12) e/Es, (1.9 +/- 1.3) microm(-3)], compared with control group [respectively (35 +/- 11) e/Es, (4.1 +/- 3.2) microm(-3)] (P < 0.05). The average volume and surface area density of placental syncytial cell in ICP group [respectively (0.1200 +/- 0.0050) microm(3), (2.500 +/- 0.600) microm(2)/microm(3)] were statistically increased compared with that in control group [respectively (0.0500 +/- 0.0010) microm(3), (1.300 +/- 0.400) microm(2)/microm(3)] (P < 0.05). But no significant difference in the volume density of placental syncytial microvilli was observed between two groups (P > 0.05). The average volume, surface area density and volume density of mitochondrion in ICP group [respectively (0.0200 +/- 0.0020) microm(3), (0.600 +/- 0.010) microm(2)/microm(3), (0.0800 +/- 0.0090) microm(3)/microm(3)] were significantly enlarged than in control group [respectively (0.0100 +/- 0.0050) microm(3), (0.500 +/- 0.030) microm(2)/microm(3), (0.0500 +/- 0.0020) microm(3)/microm(3)] (P < 0.05). The average volume, surface area density and volume density of endoplasmic reticulum in ICP group [respectively (0.0200 +/- 0.0010) microm(3), (0.900 +/- 0.010) microm(2)/microm(3), (0.0900 +/- 0.0050) microm(3)/microm(3)] were significantly larger than in control group [respectively (0.0100 +/- 0.0030) microm(3), (0.500 +/- 0.030) microm(2)/microm(3), (0.0500 +/- 0.0010) microm(3)/microm(3)] (P < 0.05). No significant difference in number density of mitochondrion and endoplasmic reticulum between two groups was found (P > 0.05). CONCLUSION: In ICP, high levels of bile acids may impair cellular organelle, resulting in abnormality of physiological function of syncytial cells, and affecting the synthesis and transportation functions of placenta.

Bile Acids and Salts↗
PubMed1998

A number-needed-to-treat analysis of the use of respiratory syncytial virus immune globulin to prevent hospitalization.

OBJECTIVES: To estimate how many infants in selected high-risk subgroups would require treatment with respiratory syncytial virus immune globulin (RSV-IG) to avoid 1 hospital admission and to determine whether this is economically justified. DESIGN: Cost-benefit analysis. Data from 3 randomized controlled trials of RSV-IG are used to estimate the number needed to treat to prevent 1 hospital admission for respiratory syncytial virus infection. The threshold number needed to treat is computed according to a formula incorporating costs and benefits of RSV-IG prophylaxis. Estimates of the willingness to pay were obtained from a sample of 39 health care providers (35 physicians and 4 nurses). MAIN OUTCOME MEASURES: The number needed to treat to prevent 1 hospital admission for respiratory syncytial virus infection. The threshold number needed to treat that would balance costs with benefits. RESULTS: More than 16 (95% confidence interval, 12.5-23.8) infants would need to be treated with RSV-IG to avoid 1 hospital admission for respiratory syncytial virus infection, ranging from 63 for premature infants without chronic lung disease to 12 (confidence interval, 6.3-100.0) for infants with bronchopulmonary dysplasia. A sensitivity analysis of the costs and values of hospital admission for respiratory syncytial virus infection and RSV-IG treatment resulted in a weak recommendation against the treatment of infants with bronchopulmonary dysplasia and strong recommendations that the costs and risks of RSV-IG treatment outweigh the benefits for the combined sample of infants and premature infants without lung disease. CONCLUSIONS: The number-needed-to-treat procedures offer a method to assess evidence of treatment effects and decision rules for whether to accept treatment recommendations. Under plausible assumptions, treatment with RSV-IG is not recommended for infants without lung disease. Institutions can examine cost and benefit assumptions that best fit their own practice setting.

Cost Savings↗
PubMed1995

Testing models predicting severity of respiratory syncytial virus infection on the PICNIC RSV database. Pediatric Investigators Collaborative Network on Infections in Canada.

OBJECTIVES: To determine the sensitivity and specificity of published prognostic models to predict morbidity resulting from lower respiratory tract disease caused by respiratory syncytial virus in an independent pediatric population and to assess the accuracy of single risk factors in predicting adverse outcome. DESIGN: All articles obtained from a MEDLINE search that used the terms prognosis or sequelae and respiratory syncytial virus, and from the references of these articles, were reviewed. Studies were included if risk factors and outcomes were defined and if information was available in a database of prospectively enrolled patients with respiratory syncytial virus infections. A probability of adverse outcome was assigned to each patient in the cohort using prognostic models described in the articles. A test was considered positive if the probability of the adverse outcome was 5% or more. PATIENTS: Six hundred eighty-nine patients hospitalized with respiratory syncytial virus in seven tertiary care centers across Canada were prospectively enrolled in the Pediatric Investigators Collaborative Network on Infections in Canada database. MAIN OUTCOME MEASURES: The sensitivity and specificity of single predictors and of models in predicting severe disease were determined. RESULTS: The sensitivity of single predictors varied from 17% to 46%. A model that used age and oxygen saturation at admission in previously well infants had a sensitivity of 98% and a specificity of 47% when predicting intensive care unit admission. Another model that included age at hospitalization, gestational age, presence of an underlying condition, and respiratory syncytial virus subtype used to predict the outcome of a high severity index had a sensitivity of 77% and a specificity of 76%. When the above model was modified by exclusion of viral subgroup, sensitivity increased to 94%, but specificity decreased to 46%. CONCLUSION: Previously described prognostic models were generalizable to an independent study population.

Canada↗
PubMed1995

Incidence of adenovirus and respiratory syncytial virus in chronic otitis media with effusion using the polymerase chain reaction.

The aim of this study is to investigate the role of adenovirus and respiratory syncytial virus in the cause of chronic otitis media with effusion by use of the polymerase chain reaction for detection. The polymerase chain reaction has proved to be more sensitive and specific than viral cultures and immunoassays in the detection of viruses in other specimens. Adenovirus and respiratory syncytial virus were chosen because these viruses have been the most commonly isolated viruses in middle ear effusions in studies using other techniques. The effusions (132 total) were sterilely collected from 88 children undergoing myringotomy and ventilation tube placement for chronic otitis media with effusion. Nine (6.8%) specimens were positive for adenovirus by the polymerase chain reaction, and 13 (9.9%) were positive for respiratory syncytial virus by the polymerase chain reaction. Only one specimen was positive for adenovirus and respiratory syncytial virus by viral culture and immunofluorescence, respectively. Our results show that the polymerase chain reaction can be used to detect adenovirus and respiratory syncytial virus in chronic middle ear effusions and that PCR is more sensitive than viral culture and immunofluorescence techniques.

Adenoviridae Infections↗
PubMed2005

Respiratory syncytial virus pneumonia: mechanisms of inflammation and prolonged airway hyperresponsiveness.

PURPOSE OF REVIEW: Respiratory syncytial virus is the leading viral pathogen associated with lower respiratory tract infection in young children worldwide. The pathogenesis of acute bronchiolitis and the mechanisms by which the virus induces long-term airway disease remain to be elucidated. This review highlights new findings reported in the English-language medical literature from January 2004 to January 2005. RECENT FINDINGS: Several studies have confirmed a strong association between respiratory syncytial virus infection in infancy and an increased risk for recurrent wheezing. Evidence indicates that the exaggerated immune response and abnormal neurogenic mechanisms induced by the virus play a significant role in the pathogenesis of the disease. Different genetic and immune markers have been correlated with acute disease severity and with increased risk of long-term pulmonary abnormalities. Recently, the application of real time polymerase chain reaction has demonstrated the persistence of respiratory syncytial virus RNA in the lungs of infected mice for months after inoculation. This unexpected observation has stimulated discussions as to whether the long-term presence of the virus could contribute to the long-term airway disease observed in children after respiratory syncytial virus lower respiratory tract infection. SUMMARY: Despite almost half a century of active research into the pathogenesis of respiratory syncytial virus-induced acute and chronic airway disease, many questions remain unresolved. Studies in animal models demonstrate that interventions reducing viral replication resulted in improvement of acute disease severity and long-term pulmonary abnormalities. The stage is ready for clinical studies to determine whether preventing or delaying the primary infection could reduce the incidence of recurrent wheezing in children.

Animals↗
PubMed2001

Encephalopathy associated with respiratory syncytial virus bronchiolitis.

Respiratory syncytial virus is an extremely common cause of childhood respiratory infections resulting in significant morbidity and mortality. Although apnea is a well-known complication in young infants with respiratory syncytial virus bronchiolitis, the encephalopathy associated with this infection is not well recognized. Our study reveals an incidence of encephalopathy of 1.8% in a total of 487 patients with respiratory syncytial virus bronchiolitis studied over a period of almost 4 years. Seizures were the presenting complication. Based on our study of a cohort of children with respiratory syncytial virus bronchiolitis, we believe that neurologic complications, although relatively uncommon, represent a significant component of this common childhood illness. Furthermore, respiratory syncytial virus has been shown to release several mediators that could directly or indirectly be neurotoxic and induce an encephalopathy associated with the respiratory illness.

Bronchiolitis, Viral↗
PubMed1994

[Virological diagnosis and treatment of respiratory syncytial virus infections].

Respiratory syncytial virus infections occur frequently in children, often localized in the upper respiratory tract. Outcome is usually quite satisfactory, but in nearly one half of the infants lower tract involvement may cause severe respiratory insufficiency leading to hospitalization in about 1% of the cases. Its frequency has been estimated at 20 to 30% of the viral infections in hospitalized infants, 10 times the frequency of the other respiratory virus. Respiratory syncytial epidemias last about 4 to 5 months with a seasonal peak in december and january. The direct detection of respiratory syncytial antigens in nasal specimens by immunofluorescence or enzymatic immunoassay is the key to rapid diagnosis. They appear as performant and more convenient than specific IgM antibodies or nucleic acid detections, and than virus isolation on cell culture, which is justified to evaluate strain sensitivity to ribavirin. Immunofluorescence has also been used to identify the subgroups A and B from 1981 to 1993, and respiratory syncytial subgroup A seems to signify more severe disease. Symptomatic assistance may require hydratation, oxygenotherapy and respiratory physical therapy. Antibiotics should not be given as a routine treatment since bacterial superinfection is infrequent, but may be indicated in cases with associated signs of complications. Indications for bronchodilators and corticosteroids are still under debate. Significant results have been obtained with ribavirin and specific anti respiratory syncytial immunoglobulins but further evaluations are still required to precise their use in clinical practice.

Antibodies, Viral↗