Parainfluenza viral infections in children: Correlation of shedding with clinical manifestations

Hall, Caroline Breese; Geiman, Joyce M.; Breese, Burtis B.; Douglas, R. Gordon

doi:10.1016/s0022-3476(77)80811-1

Cited by 41 publications

(19 citation statements)

References 15 publications

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“…Viral survival markely decreases at temperature above 37°C, until at 50°C almost all virus is inactivated within 15 min (401). Room temperature storage of myxoviruses has demonstrated considerable survival variability by decreasing titers by Ͼ50% in as little as 2 h or as long as 1 week, but this rate averages closer to hours than days (16,127,131,354,401). HPIV have their greatest stability at 4°C or if frozen (e.g., Ϫ70°C).…”

Section: Interactions With the Environmentmentioning

confidence: 99%

“…Personto-person spread by direct hand contact appears to be an unlikely means of transmission. However, the amount of virus excreted from an acutely infected child may be more than 10 times greater then that tested (127). HPIV can be efficiently removed from surfaces with most common detergents, disinfectants, or antiseptic agents (29).…”

Section: Mode Of Transmissionmentioning

confidence: 99%

“…Infection in immunocompromised hosts is an exception where giant-cell pneumonia can lead to death. Disease severity has been correlated with HPIV shedding in children (127) but not in adults (352). Species-specific down regulation of mouse smooth muscle receptors have been reported following Sendai virus infection (198).…”

Section: Pathogenesismentioning

confidence: 99%

“…Immunocompromised patients and adults (mostly with chronic lung disease) have persistently shed HPIV-1, HPIV-2, and HPIV-3 for many months (124,257). Throat swabs, nasopharyngeal swabs, nasal washes, and nasal aspiration have all been used successfully to recover HPIV (101,116,127,229,324). The optimal method of collecting clinical samples for HPIV has not been well studied but depends on the method of detection used (e.g., PCR or tissue culture), the age of the patient, and the general health of the patient (i.e)., immunocompromised or with chronic lung disease).…”

Section: Laboratory Diagnosis Collection and Preparation Of Clinical mentioning

confidence: 99%

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Parainfluenza Viruses

2003

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Human parainfluenza viruses (HPIV) were first discovered in the late 1950s. Over the last decade, considerable knowledge about their molecular structure and function has been accumulated. This has led to significant changes in both the nomenclature and taxonomic relationships of these viruses. HPIV is genetically and antigenically divided into types 1 to 4. Further major subtypes of HPIV-4 (A and B) and subgroups/genotypes of HPIV-1 and HPIV-3 have been described. HPIV-1 to HPIV-3 are major causes of lower respiratory infections in infants, young children, the immunocompromised, the chronically ill, and the elderly. Each subtype can cause somewhat unique clinical diseases in different hosts. HPIV are enveloped and of medium size (150 to 250 nm), and their RNA genome is in the negative sense. These viruses belong to the Paramyxoviridae family, one of the largest and most rapidly growing groups of viruses causing significant human and veterinary disease. HPIV are closely related to recently discovered megamyxoviruses (Hendra and Nipah viruses) and metapneumovirus

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Section: Interactions With the Environmentmentioning

confidence: 99%

Section: Mode Of Transmissionmentioning

confidence: 99%

Section: Pathogenesismentioning

confidence: 99%

Section: Laboratory Diagnosis Collection and Preparation Of Clinical mentioning

confidence: 99%

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Parainfluenza Viruses

2003

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“…Respiratory tract infection with influenza-A virus in mice, (Hall et al, 1977) can precipitate and exacerbate asthma has been shown to attenuate significantly the tracheal airway symptoms (Boushey et al, 1980;Empey, 1983). Animal models smooth muscle endothelinB (ETB) receptor-effector system of parainfluenza-1 infection indicate that this virus induces (Henry & Goldie, 1994;Carr et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Influence of parainfluenza‐1 respiratory tract viral infection on endothelin receptor‐effector systems in mouse and rat tracheal smooth muscle

Knott

Henry

McWilliam

et al. 1996

British J Pharmacology

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1 In this study we have compared the effects of parainfluenza-1 respiratory tract viral infection on the density and function of ETA and ETB receptors in rat and mouse tracheal airway smooth muscle. 2 The bronchoconstrictor effect of inhaled methacholine was significantly enhanced in virus-infected rats, at both 4 and 12 days post-inoculation. That is, the concentration of methacholine causing an increase in resistance of 100% (PC,0o methacholine) was significantly lower in virus-infected animals at both 4 and 12 days post-inoculation (n=6-8; P<0.05). 4 and 12 post-inoculation using the ligands BQ-123 (1 gM; ETA receptor-selective) and sarafotoxin S6c (100 nM; ETB receptor-selective). Total specific binding in mice was significantly reduced at day 2 post-inoculation (n =5; P <0.05) but not at days 4 and 12 post-inoculation (n = 5). In control mice, the proportions of ETA and ETB binding sites were 53%:47% at day 2 and 43%:57% at day 4 and these were significantly altered by parainfluenza-1 infection such that, the ratios were 81%:19% at day 2 and 89%:1 % at day 4 (P<0.05). By day 12 post-inoculation, the proportion of ETA and ETB binding sites in tracheal smooth muscle from mice infected with parainfluenza-1 was not significantly different from control. In rat tracheal airway smooth muscle, neither total specific binding nor the ETA and ETB binding site ratio (64%:36%) were significantly altered in virus-inoculated rats at days 2, 4 or 12 post-inoculation (n = 5). 4 Parainfluenza-1 infection in mice had no effect on the sensitivity or maximal contractile effect of endothelin-1 in tracheal smooth muscle at days 2, 4 or 12 post-inoculation (n = 4). In contrast, contraction in response to the ETB receptor-selective agonist sarafotoxin S6c was attenuated by 39% at day 2 and by 93% at day 4 post-inoculation (P<0.05). However, by day 12 post-inoculation, contractions to sarafotoxin S6c were not significantly different between control and virus-infected mice. In parainfluenza-1-infected rats, there were small but significant reductions in the sensitivity to carbachol, endothelin-1 and sarafotoxin S6c whilst the maximal responses to the highest concentrations of these agonists were not significantly altered by virus infection (n = 8).5 BQ-123 (3 giM) had no significant effect on cumulative concentration-effect curves to endothelin-1 in tracheal preparations from control mice (n =4) or parainfluenza-1-infected rats (n = 8). In contrast, in tissues taken from virus-infected mice at day 4 post-inoculation, BQ-123 caused a marked 9.6 fold rightward shift in the concentration-effect curve to endothelin-1 (n=4).6 In summary, we have demonstrated that parainfluenza-1 infection in mice transiently reduced the density of tracheal airway smooth muscle ETB receptors and this was reflected in reduced responsiveness to the ETB receptor-selective agonist sarafotoxin S6c. In contrast, whilst parainfluenza-l infection in rats was associated with the pathological features and bronchial hyperresponsiveness common to respiratory tract ...

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