Severe Illnesses Due to Adenovirus Type 7 in Children

Steen-Johnsen, J; Ørstavik, I; Attramadal, Arne

doi:10.1111/j.1651-2227.1969.tb04700.x

Cited by 38 publications

(13 citation statements)

References 11 publications

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“…In this paper references were given to descriptions of a similar pathology found in more than 60 infants in whom d,eath was attributed to infections by adenovirus of serotypes 7 or 3, while later reports have added more cases and expanded the age range affected and the number of serotypes concerned (Levin, Dietrich, and Guillory, 1967;Angella and Connor, 1968;Steen-Johnsen, Orstavik, and Attramadal, 1969). The characteristic features have been a combination of necrotizing bronchitis, bronchiolitis, and pneumonia, necrosis of bronchial mucous glands, and the presence of intranuclear inclusions in many surviving cells.…”

Section: Discussionmentioning

confidence: 97%

“…A few cases with persisting pulmonary lesions have been described (Lamy, Frezal, and Cohen-Solal, 1963;Clarke et al, 1964;Steen-Johnsen et al, 1969), but sequelae were not mentioned in reports of other adenovirus epidemics (Sterner, 1962). The consistent finding of bronchiolar and bronchial obliteration in the pathological material from the Auckland epidemic suggests that this was of major importance in the pathogenesis of other pulmonary sequelae.…”

Section: Discussionmentioning

confidence: 99%

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Bronchiolitis obliterans, bronchiectasis, and other sequelae of adenovirus type 21 infection in young children

Becroft¹

1971

J Clin Pathol

239

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SYNOPSIS A remarkably high incidence of bronchiectasis and other pulmonary sequelae was observed in young children affected during an epidemic of severe lower respiratory tract infections apparently caused by adenovirus type 21. The histopathological findings are described in four cases in which one or both lungs were obtained for examination at intervals ranging from two months to three years after the acute infections. Widespread bronchiolar obliteration (bronchiolitis obliterans) was a striking finding in all four. The severity of bronchial inflammation and of bronchiectasis was proportional to the time elapsed since the acute infections. Bronchiolar obliteration is a likely sequel of the necrotizing bronchiolitis which may occur during acute adenovirus infections. The role of bronchiolar obliteration in the pathogenesis of bronchiectasis and other chronic lung disease is discussed. Adenoviruses may be a major cause of post-infectious bronchiectasis in childhood.The symptoms of bronchiectasis in childhood frequently date from an acute respiratory infection, and in four large series these infections were considered the likely initiating factor in 48 % to 77 % of cases (

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Bronchiolitis obliterans, bronchiectasis, and other sequelae of adenovirus type 21 infection in young children

Becroft¹

1971

J Clin Pathol

239

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“…3,[21][22][23] Although it may be difficult to differentiate adenovirus bronchiolitis from bronchiolitis caused by other respiratory virus (RSV, influenza, and parainfluenza) solely on clinical and radiological data, various studies demonstrate that adenovirus infections have a higher prevalence of consolidation and atelectasis on chest radiography. 24,25 The presence of patchy consolidation in two thirds, and atelectasis in half of our patients at the time of the initial episode of bronchiolitis is in striking contrast to the known relative scarcity of roentgenographic abnormalities in classical RSV bronchiolitis.…”

Section: Discussionmentioning

confidence: 99%

Clinical course of postinfectious bronchiolitis obliterans

et al. 2000

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We performed a prospective observational study to define the clinical course and the prognostic factors of 31 patients with postinfectious bronchiolitis obliterans. All patients presented with an episode of acute bronchiolitis in the first 2 years of life, and respiratory symptoms and signs persisted since then. Other diseases which may cause chronic airflow obstruction were excluded. The patients were followed after their inclusion in the study and the clinical findings were recorded in a standardized questionnaire and form. Repeated chest radiographs and lung perfusion scans were obtained in all 31 patients and semiannual spirometry was performed in 8 older patients. Eight patients had lung biospies. The clinical course varied in the 31 patients during a mean of 3.5 years of follow‐up. The outcome of the patients included clinical remission (22.6%), persistence of respiratory symptoms and signs (67.7%), and death (9.7%). An older age at onset of illness and presence of atopy as suggested by an elevated serum IgE appeared to predispose to a poor prognosis. Pediatr Pulmonol. 2000; 29:341–350. © 2000 Wiley‐Liss, Inc.

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“…ADENOVIRAL INFECTION CAUSES pneumonia and disseminated disease in immunocompromised and nonimmunocompromised hosts (1,7,33). Chronic sequelae of inflammation also occur, including bronchiectasis, bronchiolitis obliterans, and hyperlucent lung syndrome (12,17,(30)(31)(32).…”

mentioning

confidence: 99%

Tumor necrosis factor-α activation by adenovirus E1A 13S CR3 occurs in a cell-dependent and cell-independent manner

Sanchez

Booth²,

Metcalf³

2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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The adenovirus (Ad) early gene product 13S transactivates the tumor necrosis factor (TNF)-α promoter in inflammatory cells. We examined both the subdomains of E1A and the upstream TNF promoter elements involved. In both Jurkat and U-937 cells, zinc finger or carboxyl region mutation of Ad E1A 13S conserved region 3 resulted in a significant loss of transactivation of the TNF promoter (≥69%). For both cell types there was a TNF-negative regulatory element in the −242 to −199 region and a positive regulatory element between −199 and −118. In contrast, an upstream positive regulatory element was detected in different regions in both cell types. In U-937 cells the positive regulatory unit was between −600 and −576, whereas in Jurkat cells it was between −576 and −242. The U-937 upstream element was dependent on a site previously designated epsilon in cooperation with an adjacent nuclear factor-κB-2a site. Therefore, transactivation of the TNF promoter by Ad 13S in lymphocyte and monocyte cell types involves similar subdomains of the E1A protein, but cell-specific TNF promoter elements.

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Severe Illnesses Due to Adenovirus Type 7 in Children

Cited by 38 publications

References 11 publications

Bronchiolitis obliterans, bronchiectasis, and other sequelae of adenovirus type 21 infection in young children

Bronchiolitis obliterans, bronchiectasis, and other sequelae of adenovirus type 21 infection in young children

Clinical course of postinfectious bronchiolitis obliterans

Tumor necrosis factor-α activation by adenovirus E1A 13S CR3 occurs in a cell-dependent and cell-independent manner

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