Rhinovirus identification by BglI digestion of picornavirus RT-PCR amplicons

Papadopoulos, Nikolaos G.; Hunter, Jenny; Sanderson, G.; Meyer, J.; Johnston, Sebastian L.

doi:10.1016/s0166-0934(99)00045-2

Cited by 53 publications

(41 citation statements)

References 12 publications

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“…A nasal wash was obtained and reverse transcription-PCR (RT-PCR) was used for detection of viral RNA in nasal washing samples as previously described [13,14]. PCR reactions were performed for rhinoviruses, adenoviruses, respiratory syncytial virus, metapneumonovirus, coronaviruses, influenza viruses A and B, parainfluenza viruses 1, 2 and 3, and bocavirus [15].…”

Section: Methodsmentioning

confidence: 99%

Exhaled Breath Temperature Increases during Mild Exacerbations in Children with Virus-Induced Asthma

Xepapadaki

Xatziioannou²,

Chatzicharalambous³

et al. 2010

Int Arch Allergy Immunol

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Background: Exhaled breath temperature (EBT) has been suggested as a non-invasive surrogate marker of airway inflammation in asthma. The aim of the study was to evaluate differences in EBT between periods of controlled disease and during exacerbations in children with virus-induced asthma. Methods: Twenty-nine children (aged 6–14 years) with a history of intermittent, virus-induced asthma were included in this case-control study. Cases presented with a common cold and/or mild exacerbation of asthma, while controls were free of asthmatic or common cold symptoms during the previous 6 weeks. A baseline questionnaire was obtained. Atopy assessment, central temperature and a spirometric measurement were recorded. EBT was measured with a new device (Delmedica, Singapore). A nasal wash (for identification of common respiratory viruses) was obtained. Results: Twenty-four children (12 from each group) completed the study. Groups were homogeneous with respect to baseline characteristics. PCR revealed the presence of a virus in 3 out of 17 controls and 10 out of 12 cases (17.6 and 83.3%, respectively, p = 0.002). The most commonly identified virus was rhinovirus (3/3 controls and 7/10 cases, p = 0.02). EBT values were significantly higher for cases (34.91 ± 0.62°C) compared to controls (34.18 ± 1.1°C, p = 0.032). No important differences were observed in the increase rate of EBT (Δe°T) between groups. Conclusions: Changes in airway inflammation during virus-induced asthma exacerbations are reflected in EBT changes. These preliminary data suggest a possible role of EBT measurements in the assessment of airway inflammation in children with virus-induced asthma.

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Section: Methodsmentioning

confidence: 99%

Exhaled Breath Temperature Increases during Mild Exacerbations in Children with Virus-Induced Asthma

Xepapadaki

Xatziioannou²,

Chatzicharalambous³

et al. 2010

Int Arch Allergy Immunol

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“…The presence of cytopathic effect (CPE) in the wells was used to calculate the TCID 50 using the Karber formula (12)(13)(14). Furthermore, cell infectivity was confirmed by detecting the presence of HRV RNA within the cell using RT-PCR (23).…”

Section: Methodsmentioning

confidence: 99%

Human Rhinovirus Selectively Modulates Membranous and Soluble Forms of Its Intercellular Adhesion Molecule–1 (ICAM-1) Receptor to Promote Epithelial Cell Infectivity

Whiteman

Bianco

Knight

et al. 2003

Journal of Biological Chemistry

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Human rhinoviruses are responsible for many upper respiratory tract infections. 90% of rhinoviruses utilize intercellular adhesion molecule-1 (ICAM-1) as their cellular receptor, which also plays a critical role in recruitment of immune effector cells. Two forms of this receptor exist; membrane-bound (mICAM-1) and soluble ICAM-1 (sICAM-1). The soluble receptor may be produced independently from the membrane-bound form or it may be the product of proteolytic cleavage of mICAM-1. The ratio of airway epithelial cell expression of mICAM-1 to the sICAM-1 form may influence cell infectivity and outcome of rhinovirus infection. We therefore investigated the effect of rhinovirus on expression of both ICAM-1 receptors in normal human bronchial epithelial cells. We observed separate distinct messenger RNA transcripts coding for mICAM-1 and sICAM-1 in these cells, which were modulated by virus. Rhinovirus induced mICAM-1 expression on epithelial cells while simultaneously down-regulating sICAM-1 release, with consequent increase in target cell infectivity. The role of protein tyrosine kinases was investigated as a potential mechanistic pathway. Rhinovirus infection induced rapid phosphorylation of intracellular tyrosine kinase, which may be critical in up-regulation of mICAM-1. Elucidation of the underlying molecular mechanisms involved in differential modulation of both ICAM-1 receptors may lead to novel therapeutic strategies. Human rhinoviruses (HRV)1 are the most frequent cause of upper respiratory tract infections known as the "common cold." Although these infections are generally mild and self-limiting, they inflict a heavy economical burden due to high loss of productivity and medical costs (1). Currently, there is no effective treatment for HRV infections; over the counter cold remedies only alleviate the symptoms but do not eradicate the virus.Primarily, HRV target epithelial cells for attachment and entry. These cells express intercellular adhesion molecule 1 (ICAM-1), the receptor for 90% of HRV serotypes (2). Both this major group of HRV and the 10% of HRV that use alternative receptors for cell attachment enhance cell surface ICAM-1 expression (3). This glycoprotein, belonging to the immunoglobulin supergene family, consists of five Ig-like domains (4); domains 1 and 2 have been shown to fit snugly in a key-lock relationship into reciprocal canyons on the HRV shell (5). In addition, to this critical role as a docking molecule during HRV infection, ICAM-1 through separate domains with its cognate ligand LFA-1 (CD18/CD11a) drives the migration of immuneeffector cells to sites of inflammation (6). While most studies refer to the membranous form of ICAM-1, a soluble form (sICAM-1) has also been described (7). The molecular mass of sICAM-1 is similar to the molecular mass of the extracellular domain of ICAM-1 (80 -114 kDa) depending on the level of glycosylation, suggesting that this soluble circulating form of ICAM-1 consists of most of the extracellular domain of membranous ICAM-1 (7). Several circulating isoform...

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“…Differentiation of rhinoviruses from other picornaviruses was achieved by restriction enzyme digestion of the PCR product [26].…”

Section: Detection Of Virus Rnamentioning

confidence: 99%

Raised interferon‐β, type 3 interferon and interferon‐stimulated genes – evidence of innate immune activation in neutrophilic asthma

Silva

Hilzendeger

Moermans

et al. 2016

Clin Experimental Allergy

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Rhinovirus identification by BglI digestion of picornavirus RT-PCR amplicons

Cited by 53 publications

References 12 publications

Exhaled Breath Temperature Increases during Mild Exacerbations in Children with Virus-Induced Asthma

Exhaled Breath Temperature Increases during Mild Exacerbations in Children with Virus-Induced Asthma

Human Rhinovirus Selectively Modulates Membranous and Soluble Forms of Its Intercellular Adhesion Molecule–1 (ICAM-1) Receptor to Promote Epithelial Cell Infectivity

Raised interferon‐β, type 3 interferon and interferon‐stimulated genes – evidence of innate immune activation in neutrophilic asthma

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