Improved detection of rhinoviruses in nasal and throat swabs by seminested RT‐PCR

Ireland, Deborah C.; Kent, Julie; Nicholson, Karl G.

doi:10.1002/jmv.1890400204

Cited by 91 publications

(92 citation statements)

References 21 publications

(13 reference statements)

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“…Although other studies have shown that respiratory virus infections may lead to exacerbations in patients with chronic chest disease [1][2][3][4][5][6][7][8][9][10] recently been described and evaluated in our laboratory [26]. RT The results of this study illustrate the morbidity and undoubted economic importance of respiratory virus infections.…”

Section: Discussionmentioning

confidence: 75%

Impact of respiratory virus infection in patients with chronic chest disease

et al. 1993

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SUMMARYThis study investigated the morbidity associated with respiratory virus infections in patients with well-documented chest disease, and the risk of transmission between close contacts. Patients informed the study team if they were exposed to a family member or colleague with a cold. Patients and symptomatic index cases recorded respiratory symptoms during the study period. Acute nasopharyngeal swabs and paired sera were obtained for viral diagnosis.Twenty-five (43 %) of 58 recorded exposures resulted in a symptomatic illness and 16 (28%) patients developed lower respiratory tract symptoms. Sixteen (64%) of the 25 symptomatic patients contacted their general practitioner, 14 (56 %) received antibiotics and 4 (16 %) were hospitalized. Mean duration of illness was 106 days in symptomatic patients and 5-7 days in their corresponding index cases (P < 0005). Mean symptom scores were 100X6 in symptomatic patients and 62-2 in index cases (P < 0 01). Respiratory viruses were identified in 19 (33%) episodes. Rhinovirus, coronavirus and respiratory syncytial virus infections were all associated with lower respiratory tract exacerbations.

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Section: Discussionmentioning

confidence: 75%

Impact of respiratory virus infection in patients with chronic chest disease

et al. 1993

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“…Serological diagnosis of rhinovirus is hampered by the large number of serotypes (>100) and limited cross-reactivity [22]. Recently, it has been found that detection of rhinovirus could be improved by up to five times using PCR [14,23]. Thus, using PCR, rhinovirus has been shown to be the predominant virus, associated with 50% of asthmatic exacerbations in children and 33% in adults and 19% of exacerbations of cystic fibrosis, with smaller proportions of exacerbations attributed to other viruses [6,18,24].…”

Section: Discussionmentioning

confidence: 99%

Detection of rhinovirus in induced sputum at exacerbation of chronic obstructive pulmonary disease

Seemungal

Harper-Owen²,

Bhowmik³

et al. 2000

Eur Respir J

309

208

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Common colds are associated with exacerbations of chronic obstructive pulmonary disease (COPD). However, the role of the common cold virus (human rhinovirus) in the production of symptoms and lower airway inflammation at COPD exacerbation is unknown.Thirty three patients with moderate-to-severe COPD were seen at baseline, when the number of chest infections in the previous year was noted, and acutely at COPD exacerbation. Within 48 h after the onset of the exacerbation and at baseline, nasal aspirates and induced sputum were taken for rhinovirus reverse transcriptase polymerase chain reaction (RT-PCR) analysis and determination of cytokine levels. Symptoms, recorded on diary cards, were noted and forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) measured.At exacerbation, mean FEV1 and FVC fell significantly from baseline (p<0.001). Ten of 43 exacerbations were associated with rhinovirus infection, detected in induced sputum. In four of these, nasophageal samples contained no detectable rhinovirus. All baseline samples were negative for rhinovirus. The simultaneous presence of increased nasal discharge/nasal congestion (in 26 of the 43 exacerbations) and increased sputum (29 exacerbations) was strongly associated with the presence of rhinovirus (odds ratio 6.15; p=0.036). Total symptom scores were greater for rhinovirus as compared to nonrhinovirus exacerbations (p=0.039). Median baseline sputum interleukin-6 levels rose from 90.2 to 140.3 pg . mL -1 at exacerbation (p=0.005); the change was greater in the presence of rhinovirus infection (p=0.008).Rhinovirus infection can be detected at chronic obstructive pulmonary disease exacerbation. This is associated with elevation of lower airway interleukin-6 levels, which may mediate lower airway symptom expression during chronic obstructive pulmonary disease exacerbations. Eur Respir J 2000; 16: 677±683.

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“…Respiratory syncytial virus, adenovirus, influenza A and B, and parainfluenza types 1, 2, or 3 were either detected by 1) direct fluorescent Ab testing with virus-specific mAbs (Meridian Bioscience and Dako) or 2) isolation in cell culture (cell lines include LLC-MK, A549, Hep-2, Vero, and MRC-5) and identification with the virus-specific monoclonal antisera, 48 h after inoculation. Human rhinovirus (19,20) and coronavirus 229E and OC43 (21) were detected by previously described RT-PCRs, and human metapneumovirus detection utilized in-house primers designed to target nuc and matrix genes. For aspirates with sufficient sample remaining for retesting (the majority), respiratory viruses were detected by Respiratory MultiCode-PLx assay (22) and human rhinovirus was identified with a molecular typing assay (23).…”

Section: Subjects and Clinical Assessmentsmentioning

confidence: 99%

Interactions between Innate Antiviral and Atopic Immunoinflammatory Pathways Precipitate and Sustain Asthma Exacerbations in Children

Subrata

Bizzintino

Mamessier

et al. 2009

The Journal of Immunology

188

172

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Severe asthma exacerbations in children requiring hospitalization are typically associated with viral infection and occur almost exclusively among atopics, but the significance of these comorbidities is unknown. We hypothesized that underlying interactions between immunoinflammatory pathways related to responses to aeroallergen and virus are involved, and that evidence of these interactions is detectable in circulating cells during exacerbations. To address this hypothesis we used a genomics-based approach involving profiling of PBMC subpopulations collected during exacerbation vs convalescence by microarray and flow cytometry. We demonstrate that circulating T cells manifest the postactivated “exhausted” phenotype during exacerbations, whereas monocyte/dendritic cell populations display up-regulated CCR2 expression accompanied by phenotypic changes that have strong potential for enhancing local inflammation after their recruitment to the atopic lung. Notably, up-regulation of FcεR1, which is known to markedly amplify capacity for allergen uptake/presentation to Th2 effector cells via IgE-mediated allergen capture, and secondarily programming of IL-4/IL-13-dependent IL-13R+ alternatively activated macrophages that have been demonstrated in experimental settings to be a potent source of autocrine IL-13 production. We additionally show that this disease-associated activation profile can be reproduced in vitro by cytokine exposure of atopic monocytes, and furthermore that IFN-α can exert both positive and negative roles in the process. Our findings suggest that respiratory viral infection in atopic children may initiate an atopy-dependent cascade that amplifies and sustains airway inflammation initiated by innate antiviral immunity via harnessing underlying atopy-associated mechanisms. These interactions may account for the unique susceptibility of atopics to severe viral-induced asthma exacerbations.

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Improved detection of rhinoviruses in nasal and throat swabs by seminested RT‐PCR

Cited by 91 publications

References 21 publications

Impact of respiratory virus infection in patients with chronic chest disease

Impact of respiratory virus infection in patients with chronic chest disease

Detection of rhinovirus in induced sputum at exacerbation of chronic obstructive pulmonary disease

Interactions between Innate Antiviral and Atopic Immunoinflammatory Pathways Precipitate and Sustain Asthma Exacerbations in Children

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