Persistence of Viruses in Upper Respiratory Tract of Children with Asthma

Marin, J; Jeler-Kačar, D; Levstek, V; Macek, V

doi:10.1053/jinf.2000.0688

Cited by 55 publications

(48 citation statements)

References 18 publications

(10 reference statements)

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“…Compared with other studies in asthma (24)(25)(26), our ability to detect HRV in lower airway tissue was greater and may relate to the use of the indirect RT-PCR in situ hybridization method. The sensitivity of the indirect in situ RT-PCR is at least as great as standard PCR methods and an estimated eight times more sensitive than hybridization alone (27), including analysis of biopsy specimens (28).…”

Section: Discussionmentioning

confidence: 56%

The Presence of Rhinovirus in Lower Airways of Patients with Bronchial Asthma

Woś¹,

Sanak²,

Soja³

et al. 2008

Am J Respir Crit Care Med

110

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Rationale: The common cold virus, human rhinovirus (HRV), is the most frequent cause of asthma exacerbations. However, a possible contribution of HRV to the pathogenesis of chronic, persistent asthma has not been defined. Objectives: To determine if patients with stable asthma, who are free of clinical signs of a respiratory infection for at least 3 weeks, harbor HRV in their bronchi more frequently than nonasthmatic control subjects, and whether clinical features of asthma are associated with the presence of HRV. Methods: Immunohistochemistry and the indirect in situ reverse transcription-polymerase chain reaction method were used to detect the presence of HRV in bronchial mucosal biopsies in patients with asthma and nonasthmatic control subjects. Measurements and Main Results: HRV was found by immunohistochemistry in 9 of 14 bronchial biopsies from subjects with asthma (64.3%) and 2 of 6 nonasthmatic control subjects (33.3%) (P 5 0.38). With the more sensitive indirect in situ reverse transcription-polymerase chain reaction method, HRV was found in the mucosal biopsies of 73% of patients with asthma and 22% of nonasthmatic control subjects (P , 0.001). Subjects positive for HRV had lower pulmonary function, higher numbers of blood eosinophils and leukocytes, and eosinophilic infiltration in bronchial mucosa. Conclusions: HRV was detected in the lower airway tissue of patients with asthma significantly more often than in nonasthmatic subjects, and its presence was associated with clinical features of more severe disease.

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Section: Discussionmentioning

confidence: 56%

The Presence of Rhinovirus in Lower Airways of Patients with Bronchial Asthma

Woś¹,

Sanak²,

Soja³

et al. 2008

Am J Respir Crit Care Med

110

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“…Briefly, DNA and RNA extraction was performed on 0.1 mL of cell suspension using the QIAamp blood and viral DNA/RNA kit (QIA-GEN GmbH, Hilden, Germany), according to the manufacturer's instructions. In particular, for the adenovirus an aliquot of DNA was prepared according to the method suggested by Marin et al (16). For rhinovirus, the aliquots of RNA samples were reversed in two cDNA according to the method of Steininger et al (17).…”

Section: Methodsmentioning

confidence: 99%

Soluble Adhesion Molecules and Cytokines in Children Affected by Recurrent Infections of the Upper Respiratory Tract

et al. 2004

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The objective of this study was to compare plasma levels of soluble adhesion molecules and Th1-Th2 type cytokines in 44 children with frequently recurrent respiratory infections (FRRI) of upper airways, defined as having nine or more episodes per year, and in 34 children without recurrence; all subjects were followed-up for 12 mo. The viral etiology was determined by cultures from nasal, pharyngeal, and ear secretions, using PCR and immunofluorescence. Plasma levels of five soluble adhesion molecules (E-selectin, P-selectin, L-selectin, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1) and interferon (IFN)-␥, IL-12, IL-4, and IL-10 were measured in patients and in 15 healthy controls using sandwich ELISA. During acute phase, all patients showed significant increase in plasma levels of soluble adhesion molecules; during the followup, the levels were greater in children with FRRI. A difference of cytokine profile was demonstrated between the patients with and without FRRI: an increased IL-4 and IL-10 release with decreased levels of IFN-␥ and IL-12 suggested a skewing into Th2-type response, in patients with FRRI. This pattern persisted during the follow-up. In patients without recurrence, an increased IFN-␥ and IL-12 release, together with decreased levels of IL-4 and IL-10, showed a skewing into Th1-type responses; in the follow-up these cytokines reached normal values. In conclusion, the abnormal levels of all examined parameters in children with FRRI may reflect the persistence of an inflammatory microenvironment in the airways and an activation of the immune system that may contribute to the frequently recurrence of the respiratory disease. Infections of the URTI are the most common cause of viral morbidity in children. They represent the most frequent managed problem in general pediatric practice (1) and are responsible for more than one third of school absences (2). Many different immunologic problems can concur to the development of respiratory infections (3). Disorders of the aspecific humoral and the specific cellular defense are the principal cause of inflammation in the upper respiratory diseases (4). The recruitment and activation of inflammatory cells at the site of infection involve the expression of leukocyte and vascular adhesion molecules and the generation of pro-inflammatory cytokines, which contribute to the injury of lung epithelial and endothelial barriers (5). An important role in the early transient adhesion phases of leukocytes is mediated by the selectin family, which includes three distinct carbohydrate receptors expressed by either endothelial cells (E-selectin), leukocytes (L-selectin), or platelets and endothelial cells (P-selectin) (6). ICAM-1 and VCAM-1 are membrane glycoproteins, belonging to the immunoglobulin superfamily; ICAM-1 are widely expressed on respiratory epithelial cells, monocytes, macrophages, dendritic cells, and, together with VCAM-1, on vascular endothelial cells (7,8). These adhesion molecules, after a proteolytic cleavage, are found as so...

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“…Although early epidemiologic studies concluded that persistent adenovirus infections were benign, recent evidence employing PCR to identify pathogens at sites of disease suggest a role for the species C viruses in a variety of chronic diseases in immunocompetent individuals. A remarkable 80% of children with asthma have adenovirus DNA in their nasopharynx (compared with only 5% of age-matched controls) when tested at a time of disease quiescence (23). An equally high percentage of asthmatic children yield viral capsid protein on bronchoalveolar lavage (22).…”

Section: Vol 76 2002 Human Adenovirus Dna In Mucosal Lymphocytes 10613mentioning

confidence: 99%

Prevalence and Quantitation of Species C Adenovirus DNA in Human Mucosal Lymphocytes

Garnett

Erdman

et al. 2002

J Virol

283

280

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The common species C adenoviruses (serotypes Ad1, Ad2, Ad5, and Ad6) infect more than 80% of the human population early in life. Following primary infection, the virus can establish an asymptomatic persistent infection in which infectious virions are shed in feces for several years. The probable source of persistent virus is mucosa-associated lymphoid tissue, although the molecular details of persistence or latency of adenovirus are currently unknown. In this study, a sensitive real-time PCR assay was developed to quantitate species C adenovirus DNA in human tissues removed for routine tonsillectomy or adenoidectomy. Using this assay, species C DNA was detected in Ficoll-purified lymphocytes from 33 of 42 tissue specimens tested (79%). The levels varied from fewer than 10 to greater than 2 ؋ 10 6 copies of the adenovirus genome/10 7 cells, depending on the donor. DNA from serotypes Ad1, Ad2, and Ad5 was detected, while the rarer serotype Ad6 was not. When analyzed as a function of donor age, the highest levels of adenovirus genomes were found among the youngest donors. Antibody-coated magnetic beads were used to purify lymphocytes into subpopulations and determine whether viral DNA could be enriched within any purified subpopulations. Separation of T cells (CD4/8-expressing and/or CD3-expressing cells) enriched viral DNA in each of nine donors tested. In contrast, B-cell purification (CD19-expressing cells) invariably depleted or eliminated viral DNA. Despite the frequent finding of significant quantities of adenovirus DNA in tonsil and adenoid tissues, infectious virus was rarely present, as measured by coculture with permissive cells. These findings suggest that human mucosal T lymphocytes may harbor species C adenoviruses in a quiescent, perhaps latent form.The common adenovirus serotypes of species C (Ad1, Ad2, Ad5, and Ad6) cause roughly 5% of symptomatic upper respiratory tract (5) and 15% of lower respiratory tract (3) infections in children younger than 5 years.

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Persistence of Viruses in Upper Respiratory Tract of Children with Asthma

Abstract: The persistent presence of viruses in the upper respiratory tract of asthmatic children shows a possible connection between viral infections and asthma.

Cited by 55 publications

References 18 publications

The Presence of Rhinovirus in Lower Airways of Patients with Bronchial Asthma

The Presence of Rhinovirus in Lower Airways of Patients with Bronchial Asthma

Soluble Adhesion Molecules and Cytokines in Children Affected by Recurrent Infections of the Upper Respiratory Tract

Prevalence and Quantitation of Species C Adenovirus DNA in Human Mucosal Lymphocytes

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