The pathogenesis of sendai virus infection in the mouse lung (Plates V-VII)

Robinson, T. W. E.; Cureton, R. J. R.; Heath, R. B.

doi:10.1099/00222615-1-1-89

Cited by 73 publications

(49 citation statements)

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“…The failure to detect increased amounts of antibodies in either serum or bronchial secretions until the 2nd wk of the infection confirms results obtained in previous studies (Robinson et al, 1968;Robinson, Cureton and Heath, 1969), and these findings seem to exclude the role of immune processes in the termination of primary virus infections. It was, therefore, of interest to find an increased number of immunoglobulin-containing cells in the infected tissues as early as the 2nd day, and a further increase by the 5th day.…”

Section: Discussionsupporting

confidence: 79%

“…There was an early transitory polymorphonuclear leucocyte response followed by a more prolonged and intense mononuclear cell response. The changes found were similar to those described in detail by Robinson et al (1968).…”

Section: Histological Changessupporting

confidence: 78%

“…IN a previous paper it was shown that Sendai virus infection of mice could be used for the study of the pathogenesis of viral infections of respiratory mucous membranes (Robinson, Cureton and Heath, 1968). In particular, it was possible to use this model system to correlate growth and eradication of virus with certain defence factors such as the inflammatory changes, interferon and antibody production.…”

Section: S T U D I E S O F T H E I M M U N E R E S P O N S E Imentioning

confidence: 99%

“…The procedures used for obtaining specimens from these mice, for the assay of virus in monkey-kidney tissue cultures and for haemagglutination inhibition (HI) tests for antibody have been described previously (Robinson et al, 1968). Virus assays were carried out on pooled lung suspensions obtained from groups of three mice, and antibody titrations were done on individual specimens of serum and bronchial washings or on pools as indicated in the text.…”

Section: Infection Of Micementioning

confidence: 99%

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Studies Of The Immune Response In Sendai Virus Infection Of Mice

Blandford

Cureton

Heath

1971

Journal of Medical Microbiology

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Section: Discussionsupporting

confidence: 79%

Section: Histological Changessupporting

confidence: 78%

Section: S T U D I E S O F T H E I M M U N E R E S P O N S E Imentioning

confidence: 99%

Section: Infection Of Micementioning

confidence: 99%

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Studies Of The Immune Response In Sendai Virus Infection Of Mice

Blandford

Cureton

Heath

1971

Journal of Medical Microbiology

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“…Changes in the histological appearance of tracheal tissue associated with parainfluenza-1 virus infection in rats and mice seen in this study were similar to those described previously (Robinson et al, 1968;Massion et al, 1993) and were similar to changes observed in other animal models of respiratory tract viral infections (Buckner et al, 1985;Henry et al, 1991). These included marked alterations in the structure of the epithelial cell layer and cellular infiltration into the submucosal layer of the trachea that were apparent at day 4 post-inoculation in both species.…”

Section: Discussionsupporting

confidence: 74%

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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A comparison in germ‐free mice of the pathogenesis of Sendai virus and mouse pneumonia virus infections

Carthew

Sparrow

1980

The Journal of Pathology

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The poathogenesis of Sendai virus and pneumonia virus of mice (PVM) was studied using the immunoperoxidase technique on paraffin lung sections. The pathology of Sendai virus corresponds to that of a bronchopneumonia, with virus demonstrated by immunoperoxidase in the bronchial epithelium, and sometimes in macrophages, for a period of 2--9 days post-infection. Pneumonia virus of mice produces an interstitial pneumonia with virus demonstrated in the bronchial epithelium but also in the alveolar walls and alveolar macrophages. This virus can be demonstrated between 2 and 7 days post-infection. This technique was used to demonstrate PVM in the case of a natural outbreak of this disease and may eventually become a routine technique for the screening of lung tissue for respiratory viruses.

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The pathogenesis of sendai virus infection in the mouse lung (Plates V-VII)

Cited by 73 publications

References 1 publication

Studies Of The Immune Response In Sendai Virus Infection Of Mice

Studies Of The Immune Response In Sendai Virus Infection Of Mice

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

A comparison in germ‐free mice of the pathogenesis of Sendai virus and mouse pneumonia virus infections

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