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At least 19 recordsLinked to original sources
PubMed1978

Respiratory syncytial virus infection. Rapid diagnosis in children by use of indirect immunofluorescence.

Specimens of 387 nasopharyngeal suction smears obtained from 354 children hospitalized with acute respiratory infections during an eight-month period were examined for the presence of respiratory syncytial (RS) virus by the indirect immunofluorescence antibody technique (IFAT) and by conventional tissue culture infectivity techniques. Respiratory syncytial virus was identified in nasopharyngeal suction smear specimens from 123 of these specimens (32%) with the use of both techniques. Of the specimens positive on tissue culture 92% were also positive for RS virus by IFAT. However, eight specimens positive for RS virus by tissue culture were negative by IFAT, although three of the specimens were technically unsuitable. Six percent of the specimens negative for RS virus by tissue culture were positive for RS virus antigen when tested by IFAT. Using IFAT, identification of RS virus could be accomplished within four to six hours, whereas isolation by tissue culture took an average period of ten days. These data suggest that IFAT is a reliable means for the rapid diagnosis of RS virus infection in infants and children.

Adolescent↗
PubMed1978

Evaluation of five temperature-sensitive mutants of respiratory syncytial virus in primates: II. Genetic analysis of virus recovered during infection.

Five temperature-sensitive (ts) mutants of respiratory syncytial (RS) virus (ts-1, ts-1 NG-1, ts-1 NG-16, ts-2, and ts-7), previously evaluated forinfectivity and virulence in chimpanzees and owl monkeys, were also assayed for in vivo genetic stability. None of the five mutants tested was completely stable genetically. Thus, virus which had lost some or all of the ts property was recovered from each infected chimpanzee. Significantly, each ts-1 NG-1 isolate retained some degree of temperature sensitivity and hence was not true wild-type virus. Clonal analysis of viruses shed by ts-1, ts-1 NG-1, ts-1 NG-16, or ts-7 infected chimpanzees indicated that in most instances only a minority of the virus shed was altered genetically. Of five chimpanzees infected with the ts-2 mutant, three shed only ts virus, and the remaining two chimpanzees shed only ts+ virus. Such ts+ virus proved to be avirulent when evaluated in chimpanzees or owl monkeys, indicating that loss of the ts property did not restore virulence. Based upon these findings, the ts-2 mutant appears to be a suitable candidate for clinical trials in man.

Animals↗
PubMed1979

Increased resistance to influenza as a possible source of heterozygote advantage in cystic fibrosis.

Cystic fibrosis is the most common lethal or semi-lethal genetic disease in Caucasians of Central European origin, among whom it is inherited as an autosomal recessive trait at a frequency approximately 10 times that expected from recurrent mutation alone. A decreased sialic acid content has been observed in cell surface glycoproteins on cystic fibrosis fibroblasts and in numerous soluble glycoprotein preparations from cystic fibrosis homozygotes. Sialic acid residues on cell surface glycoconjugates play an essential role in the binding and infectivity of myxoviruses and paramyxoviruses, including those causing pandemic influenza. It is suggested that increased resistance to these viruses conferred by similar but quantitatively smaller alterations in sialoglycoconjugate structure in cystic fibrosis heterozygotes may have provided a selective advantage to maintain the high frequency of the cystic fibrosis gene in Caucasian populations.

Cystic Fibrosis↗
PubMed1978

Interferon production in children with respiratory syncytial, influenza, and parainfluenza virus infections.

To better understand the recovery process of infants with lower respiratory tract disease due to respiratory syncytial virus, the production of interferon by 129 children (ages 10 days to 24 months) with RSV infection was compared to that of 20 children with influenza (ages 1 to 36 months), and 37 children with parainfluenza virus infection (ages 4 to 66 months). Interferon assays of 285 nasal washes from children with RSV revealed that interferon production occurred in only 5 (4%) of the children. Significantly more children infected with infleunza virus, 55% (P less than 0.001), and parainfluenza virus, 30% (P less than 0.001), produced interferon. In addition, the quantity of interferon produced by children with RSV (geometric mean titer = 2) was significantly less than that of children with influenza (GMT = 26.8, P less than 0.001) and parainfluenza virus (GMT = 23.5, P less than 0.001). In the children infected with RSV, in constrast to those with influenza, interferon detection was not associated with diminished shedding of virus.

Child, Preschool↗
PubMed1978

Interferon in nasal secretions from infants with viral respiratory tract infections.

Interferon levels in nasal secretions of infants under one year of age, and hospitalized with lower repiratory tract disease, were measured during two respiratory infection seasons. In the first year serial secretions from 50 infants with respiratory syncytial virus infection were examined. Undetectable or low levels of interferon were found in all samples, and mean levels did not fluctuate significantly in relation to disease and recovery. This was in contrast to anti-RSV IgA, which appeared and increased in concentration as virus shedding decreased and stopped. In the second year secretions were obtained from nine infants with influenza A virus infection as well as from 13 with RSV. All those with influenza developed measurable interferon in secretions (geometric mean titer 138 units/ml), which was acid and heat stable, and trypsin sensitive (type I interferon). RSV infection again stimulated very low levels (geometric mean 5 units/ml). The lack of correlation of interferon concentration with cessation of RSV shedding suggests either that it is not involved in recovery or that low levels are adequate. On the other hand, it appears that the young infant is fully capable of a brisk local interferon response, at least to infection by influenza A.

Antibodies, Viral↗
PubMed1979

Cell-mediated immune response to respiratory syncytial virus infection: relationship to the development of reactive airway disease.

The possibility that cell-mediated immunity might play a role in the pathogenesis of infection with respiratory syncytial virus was evaluated in a study of 39 infants. Infection with RSV was confirmed by identification of virus in nasopharyngeal secretions using immunofluorescence, and by tissue culture infectivity. CMI, as determined by a whole blood lymphocyte transformation technique, was evaluated in samples taken 0 to 10 and 20 to 60 days after the onset of illness. Patients diagnosed as having RSV-induced bronchiolitis or recurrence of asthma had evidence of significantly (P less than 0.01) higher degree of CMI in the 0 to 10-day period than patients with RSV pneumonia or upper respiratory illness. Higher CMI activity in the 20 to 60-day period was also seen in patients with more severe illness, with moderate-to-severe degree of hypoxia. A positive correlation was observed between the degree of LTF activity in samples taken 20 to 60 days after the onset of illness ard subsequent episodes of wheezing. Eleven patients had one or more episodes of wheezing in the first six months after RSV infection. LTF activity in samples taken during the 20 to 60-day period from these patients was significantly higher (P less than 0.02) than LTF activity in corresponding samples from six patients who were free of wheezing in the six months after RSV infection. The results suggest that alterations of RSV-specific cell-mediated immune mechanisms may result in an increased tendency toward airway reactivity on primary and subsequent exposure to RSV and possibly to other agents.

Bronchial Spasm↗
PubMed1979

Neonatal respiratory syncytial virus infection.

Respiratory syncytial virus infections are thought to be uncommon in the first month of life. During a community outbreak, we prospectively studied such infection in our neonatal units. Of 82 neonates studied, 66 were hospitalized for six days or longer, and 23 (35 per cent) acquired this virus. Four infants died, two unexpectedly. Infected infants had a significantly shorter gestation and birth weight. Illness was often atypical, with nonspecific signs, especially in infants under three weeks of age, who had significantly less lower-respiratory-tract involvement and lower quantities of virus in their nasal washes. The titer of virus shed correlated with the infants' postnatal, but not gestational, age. Infection was also acquired by 34 per cent of the staff, who appeared to be important in the spread of the virus. These findings suggest that respiratory syncytial virus may readily infect neonates, but the disease may be atypical and may be overlooked.

Adult↗
PubMed1979

Respiratory-syncytial-virus infections, reinfections and immunity. A prospective, longitudinal study in young children.

To better understand acquired immunity to respiratory-syncytial-virus infections, we analyzed data from a 10-year study of respiratory illness in normal children who were followed longitudinally from early infancy. Immunity was measured in terms of failure to become infected or reduction in severity of clinical illness upon reinfection. Outbreaks of infections occurred seven times over the 10-year-period. During epidemics the attack rate for first infection was 98 per cent. The rate for second infections (75 per cent) was modestly reduced (P less than 0.001); that for third infections was 65 per cent. Age and history of infection both influenced illness. Immunity induced by a single infection had no demonstrable effect on illness associated with reinfection one year later; however, a considerable reduction in severity occurred with the third infection. These observations suggest that amelioration of illness--rather than prevention of infection--may be a realistic goal for immunoprophylaxis.

Antibodies, Viral↗
PubMed1979

Respiratory syncytial virus infection in owl monkeys: viral shedding, immunological response, and associated illness caused by wild-type virus and two temperature-sensitive mutants.

Intranasal inoculation of owl monkeys with wild-type respiratory syncytial virus induced upper respiratory tract disease in each of seven animals. The response of owl monkeys to two highly defective, temperature-sensitive, multiple-lesion mutants was then compared to the pattern seen with wild-type respiratory syncytial virus. These mutants, ts-1 NG-1 and ts-1 NG-16, were derived from the ts-1 mutant that had been remutagenized with nitrosoguanidine (NG). Previously the ts-1 NG-1 and ts-1 NG-16 mutants had been shown to be more temperature sensitive and more stable genetically than their ts-1 parent. Both ts-1 NG-1 and ts-1 NG-16 produced infection that was delayed in onsent compared to wild-type virus infection. However, the mutants were shed from the upper respiratory tract for the same period of time and at the same titer as wild-type virus. The serum neutralizing antibody response to infection with the mutants was nearly equivalent to that elicited by wild-type virus. However, the extent of disease induced by the mutants was significantly less than that seen with wild-type virus. These observations suggest that the mutants are potential vaccine condidates and should be subjected to additional in vivo testing in primates and, ultimately, humans.

Animals↗
PubMed1979

Reye's syndrome associated with respiratory syncytial virus infection.

An upper respiratory tract infection in a 22-month-old boy was followed by rapid loss of consciousness, hypoglycaemia, uraemia, and death. Necropsy examination showed fatty change of liver and kidneys, severe cerebral oedema, bronchiolitis, and endocardial fibroelastosis affecting the left ventricle. Immunofluorescence staining showed infection with respiratory syncytial virus (RSV). The clinical and pathological findings were those of Reye's syndrome, not previously reported accompanying RSV infection.

Humans↗
PubMed1979

Observations on outbreaks of respiratory disease in calves associated with parainfluenza type 3 virus and respiratory syncytial virus infection.

In four outbreaks of indoor calf pneumonia, dyspnoea was a prominent clinical finding. At necropsy it was associated with pneumonia involving the cranial lobes of the lung and severe pulmonary emphysema. Histological examination of lung tissue revealed bronchiolitis and alveolitis with alveolar epithelial cell hyperplasia and multinucleate syncytium formation. Intraalveolar haemorrhage, intra-alveolar oedema and hyaline membrane formation were also noted. In all cases parainfluenza type 3 (PI3) virus was isolated from the lungs. In each of the four outbreaks there was evidence of PI3 virus and respiratory syncitial virus (RSV) infection.

Animals↗
PubMed1979

Clinical significance of pulmonary function tests. Alterations in pulmonary function following respiratory viral infection.

Respiratory viral illness is a major cause of morbidity in both adults and children. This report focuses on both the acute and chronic effects on respiratory function of these ubiquitous infections. Infant airways are particularly vulnerable due to the relatively low conductance in immature peripheral airways. Bronchiolitis, caused predominantly by respiratory syncytial virus, is the most important of these viral illnesses and is emerging as a major risk factor for the subsequent development of obstructive airway diseases in adults, possibly by interference with normal alveolar proliferation. The basic pathogenic mechanism involved in adult respiratory viral infection is bronchial hyperreactivity, presumably secondary to epithelial damage and resultant sensitization of rapidly adapting airway receptors. In addition, there may be virus-related alterations in the autonomic and humoral regulation of airway tone. Viral infections may alter the effects of common air pollutants on respiratory function.

Adult↗
PubMed1978

Respiratory syncytial virus infection in adults: clinical, virologic, and serial pulmonary function studies.

We prospectively studied 10 previously healthy adults who developed an acute respiratory illness while working in an infants' ward during a community outbreak of respiratory syncytial virus infection. In addition to clinical and viral evaluation, total respiratory resistance before and after carbachol aerosol inhalation was measured. All 10 subjects had respiratory syncytial virus infection documented by viral isolation, and all developed pronounced cough, nasal congestion, and fever. Eight subjects missed work for an average of 6 days. In all 10 patients, the total respiratory resistance was significantly elevated through 8 weeks. Altered airway reactivity, characterized by exaggerated responses of pulmonary resistance to carbachol challenge, was also observed through the first 8 weeks of evaluation. In this group, respiratory syncytial virus produced a protracted illness associated with appreciable morbidity. The pathophysiologic mechanism of this illness in part appeared to arise from altered airway reactivity.

Acute Disease↗