Severe Bronchiolitis Research Articles

Independent Predictors of Severity and Hospitalization in Acute Bronchiolitis: Neutrophil/Lymphocyte Ratio and Mean Platelet Volume

Background and Aim Acute bronchiolitis is the most common cause of hospitalization in the first year of life. The neutrophil/lymphocyte ratio (NLR) and mean platelet volume (MPV) are readily calculable laboratory markers used to evaluate systemic inflammation. We aim to evaluate the optimal values of these markers for the prediction of severity and hospitalization in infants with acute bronchiolitis. Materials and Methods A total of 105 patients with acute bronchiolitis and 62 healthy controls aged 1 to 12 months were prospectively enrolled to the study. The patients' group was classified into two groups, namely, outpatient and inpatient, also divided into three groups according to clinical scoring: mild, moderate, and severe. The association of NLR and MPV with clinical severity and hospitalization was investigated. Results The mean age was 7.75 ± 2.98 months in patients and 7.69 ± 2.87 months in controls. The means of NLR were 0.47 and 0.64 in controls and patients, respectively (p = 0.032) and of MPV were 9.64 and 8.9 (p < 0.001), respectively. The means of NLR were 0.73 and 0.50 in inpatient and outpatient groups, respectively (p = 0.014) and of MPV were 8.65 and 9.32 (p = 0.046), respectively. NLR of 0.64 value was calculated as a cutoff for the prediction of hospitalization with 45% sensitivity and 83% specificity (positive predictive value = 81%, negative predictive value = 19%). Conclusion We found that blood neutrophil percentage and blood NLR are increased and also weakly predictive—but insufficient to be clinically useful—for the decision of hospitalization in acute bronchiolitis. When the positive predictive value of an NLR of 0.64 is sufficient to decide hospitalization, the negative predictive value is impractical. MPV value was less in infants with acute bronchiolitis than healthy controls and in inpatients than outpatients with acute bronchiolitis. Low MPV might be marker of inflammation in acute bronchiolitis.

Prenatal and postnatal tobacco smoke exposure and risk of severe bronchiolitis during infancy.

Maternal prenatal smoking has adverse effects on the growing fetus including those of respiratory nature. Although postnatal smoke exposure is a risk factor for respiratory infections, the effects of prenatal smoking independent of postnatal smoke exposure are less established. We hypothesized that both maternal prenatal smoking, and postnatal smoke exposure are risk factors for severe bronchiolitis during infancy. We performed a case-control study of 1353 children born between 1996 and 2011 at a single teaching hospital. Cases were admitted to the same hospital for bronchiolitis during infancy. Maternal prenatal smoking was collected from birth records. Postnatal smoke exposure was collected from review of electronic health records. Multivariable logistic regression was used to evaluate the independent associations of the two smoking variables with severe bronchiolitis. 6% of cases were exposed to maternal prenatal smoking, compared with 4% of controls (P = 0.10). Postnatal smoke exposure was present in the households of 17% of cases compared with 3% of controls (P < 0.001). In a multivariable model with both smoking variables and adjustment for 10 covariates, maternal prenatal smoking was not a significant risk factor for severe bronchiolitis (adjusted OR = 1.02, 95%CI 0.56-1.84). By contrast, postnatal smoke exposure was associated with >300% increased odds (adjusted OR 4.19, 95%CI 2.51-6.98). Although maternal prenatal smoking has many known adverse effects, it was not associated with increased odds of severe bronchiolitis in either unadjusted or multivariable analyses. Postnatal smoke exposure was a consistently strong risk factor. Our findings support ongoing efforts to decrease infant exposure to ambient smoke.

Polymorphisms in the promoter region of IL10 gene are associated with virus etiology of infant bronchiolitis.

Bronchiolitis is the most common infection leading to hospitalization in infancy. Interleukin-10 (IL-10) is an anti-inflammatory cytokine, and in our previous study, IL10 gene rs1800896 (- 1082A/G) polymorphism was associated with viral etiology of infant bronchiolitis. The objective of this study was to evaluate the associations between IL10 single nucleotide polymorphisms (SNPs) at rs1800890 (- 3575A/T), rs1800871 (- 819C/T) or rs1800872 (- 592C/A) either alone or combined with the SNP at rs1800896 (- 1082G/A), and the etiology and severity of infant bronchiolitis. Data on four IL10 SNPs were available from 135 full-term infants, hospitalized for bronchiolitis at age less than 6months, and from 378 to 400 controls. Viral etiology was studied, and oxygen support, feeding support and the length of stay in hospital were recorded during bronchiolitis hospitalization. Infants with rhinovirus bronchiolitis had the IL10 rs1800890 variant AT or TT genotype less often (18.2%) than controls (63.3%, P = 0.03), and likewise, had the IL10 rs1800896 variant AG or GG genotype less often (27.3%) than controls (65.5%, P = 0.009). Twenty-eight infants with bronchiolitis had the variant-variant Grs1800896Trs1800890 haplotype, and none of them had rhinovirus infection. The IL10 rs1800871 or rs1800872 genotypes showed no associations with viruses. No association was found between any genotypes and bronchiolitis severity measures. IL10 rs1800890 and rs1800896 polymorphisms differed between infants with rhinovirus bronchiolitis and controls, but not between infants with respiratory syncytial virus bronchiolitis and controls.

TLR5 rs5744174 gene polymorphism is associated with the virus etiology of infant bronchiolitis but not with post-bronchiolitis asthma.

Background and aimBronchiolitis is a leading cause of hospitalization in infants and is associated with a risk of subsequent asthma. The innate immunity genes, such as those encoding toll‐like receptors (TLRs), are likely to play a role in bronchiolitis and post‐bronchiolitis outcome. Thus far, only one study has considered TLR5 genes in respiratory syncytial virus (RSV) bronchiolitis. The aim of this study was to investigate the association of TLR5 gene polymorphism with virus etiology and severity of bronchiolitis, and with post‐bronchiolitis asthma.MethodsWe recruited 164 infants (age < 6 months) hospitalized for bronchiolitis in this study and determined TLR5 rs5744174 (C > T) single nucleotide polymorphism, virus etiology and severity markers of bronchiolitis, and presence of post‐bronchiolitis asthma until age 11 to 13 years.ResultsRSV was detected in 113 (68.9%), rhinovirus in 19 (11.6%), and some other virus in 20 (12.2%) cases. Non‐RSV etiology was more common among infants with the variant CT or TT genotype in the TLR5 rs5744174 gene than in those with the CC genotype (89.7% vs 71.7%, P = 0.03). TLR5 rs5744174 polymorphism was not associated with the need of supplementary oxygen or feeding support, with the length of hospital stay, or with post‐bronchiolitis asthma at any age.ConclusionThe TLR5 rs5744174 variant genotype may increase the susceptibility to bronchiolitis not caused by RSV.

PGD2/DP2 receptor activation promotes severe viral bronchiolitis by suppressing IFN-λ production.

Prostaglandin D2 (PGD2) signals through PGD2 receptor 2 (DP2, also known as CRTH2) on type 2 effector cells to promote asthma pathogenesis; however, little is known about its role during respiratory syncytial virus (RSV) bronchiolitis, a major risk factor for asthma development. We show that RSV infection up-regulated hematopoietic prostaglandin D synthase expression and increased PGD2 release by cultured human primary airway epithelial cells (AECs). Moreover, PGD2 production was elevated in nasopharyngeal samples from young infants hospitalized with RSV bronchiolitis compared to healthy controls. In a neonatal mouse model of severe viral bronchiolitis, DP2 antagonism decreased viral load, immunopathology, and morbidity and ablated the predisposition for subsequent asthma onset in later life. This protective response was abolished upon dual DP1/DP2 antagonism and replicated with a specific DP1 agonist. Rather than mediating an effect via type 2 inflammation, the beneficial effects of DP2 blockade or DP1 agonism were associated with increased interferon-λ (IFN-λ) [interleukin-28A/B (IL-28A/B)] expression and were lost upon IL-28A neutralization. In RSV-infected AEC cultures, DP1 activation up-regulated IFN-λ production, which, in turn, increased IFN-stimulated gene expression, accelerating viral clearance. Our findings suggest that DP2 antagonists or DP1 agonists may be useful antivirals for the treatment of viral bronchiolitis and possibly as primary preventatives for asthma.

Role of mucin 19 in the respiratory tract.

Abstract Human metapneumovirus (HMPV) is a negative sense, single stranded RNA virus that belongs to the Pneumovirdae family, and represents an important pathogen that causes severe bronchiolitis and pneumonia worldwide. There is currently no vaccine against this virus, so it is important to study the aspects of the immune response induced by HMPV in order to understand its mechanism of infection. Because infiltration of mucus is a hallmark of HMPV infection, it is warranted to study the role of mucus in the disease process. Mucin proteins make up the major component of mucus and can be found within the airway and lungs. Using an in vitro model of HMPV infection and human bronchial epithelial cells, we found that HMPV induced predominantly a mucin 19 expression. Those data were confirmed in mice, where HMPV induced predominant levels of muc19 protein. Mucin 19 is a secreted gel-forming mucin, whose function is largely understudied, particularly in the respiratory tract. Our findings led us to hypothesize that mucin 19 plays a role in HMPV infection. To test that, we used a muc19 knockout mouse model. Lung samples were collected at different time points. Sample analysis showed that the absence of muc19 led to an increased pulmonary inflammation and body weight loss. Interestingly, flow cytometry data indicate that the lack of Muc19 resulted in a decreased CD4+ T cell count in the lung, and reduced numbers of CD4+ and CD8+ T cells in the lymph nodes after HMPV infection. These novel findings yield relevant information regarding the contribution of the mucins, specifically Muc19, on the immune response induced by respiratory viral infections in the lung.

74) Viral load and oxygen saturation index patterns in mechanically ventilated infants with RSV

BACKGROUND: Infants with severe RSV bronchiolitis often require mechanical ventilation (MV). Previous studies have shown that viral load (VL) is associated with higher disease severity and infants requiring MV. The effects of viral load on disease severity during MV are unknown. METHODS: This prospective observational study of pediatric patients aged < 2 years, with RSV bronchiolitis, who required …

Type I and III interferon signaling contributes to severe pathogenesis of human metapneumovirus clinical isolates

Abstract Human metapneumovirus (HMPV) is a leading cause of respiratory tract infection in infants and children. The disease outcome of HMPV infection ranges from mild infection to severe bronchiolitis and fatal pneumonia. HMPV was discovered in 2001 and its disease mechanisms are not fully understood. To gain insight into HMPV pathogenesis, we tested nine HMPV clinical isolates in an established C57BL/6 mouse model. HMPV clinical isolates induced variable disease severity ranging from mild to fatal disease. Mice infected by non-virulent strain TN/94-49 did not show significant weight loss, but mice infected with virulent isolate C2-202 showed dramatic weight loss and 40% mortality within 5 days post-infection. These findings were confirmed in other inbred mouse strains. C2-202 infected mice also suffered from impaired pulmonary function post-recovery. Lung virus replication did not correlate with disease severity, suggesting immune-mediated pathogenesis. Further investigation revealed increased type I and III interferons, pro-inflammatory cytokine production, and neutrophil infiltration in C2-202 infected mice. HMPV C2-202 infection also inhibited dendritic cell recruitment and down-regulated MHC-II surface expression on macrophages. Stat1/Stat2 double knockout mice lacking interferon signaling exhibited reduced weight loss, lessened disease severity, and increased dendritic cell recruitment after C2-202 infection. Our results indicate that severe disease caused by HMPV clinical isolates was due to exuberant interferon response leading to immuno-pathological tissue damage. These data suggest interferon signaling plays an important role in HMPV pathogenesis, and thus serves as a potential therapeutic target.

Mid-regional pro-adrenomedullin could be a biomarker of severity in bronchiolitis.

Mid-regional pro-adrenomedullin could be a biomarker of severity in bronchiolitis.

Glucagon-like peptide 1 receptor signaling attenuates respiratory syncytial virus–induced type 2 responses and immunopathology

GLP-1R signaling, an emerging anti-inflammatory therapeutic 59 target, 60 attenuated type 2-associated immunopathology in mice infected with a strain of RSV that was 61 isolated from a hospitalized infant with severe lower respiratory tract infection and bronchiolitis.

Interleukin-13 associates with life-threatening rhinovirus infections in infants and young children.

Delineate risk factors associated with severe hypoxemia (O2 sat ≤87%) in infants and children younger than 2 years hospitalized with single pathogen HRV infection. Prospective study in a yearly catchment population of 56 560 children <2 years old between 2011 and 2013 in Argentina. All children with respiratory signs and O2 sat <93% on admission were included. HRV infections were identified by reverse transcriptase-polymerase chain reaction. Epidemiologic, clinical, viral, and immunological risk factors were assessed. Among 5012 hospitalized patients, HRV was detected as a single pathogen in 347 (6.92%) subjects. Thirty-two (9.2%) had life-threatening disease. Traditional risk factors for severe bronchiolitis did not affect severity of illness. HRV viral load, HRV groups, and type II and III interferons did not associate with severe hypoxemia. Interleukin-13 Levels in respiratory secretions at the time of admission (OR = 7.43 (3-18.4); P < 0.001 for IL-13 >10 pg/mL) predisposed to life-threatening disease. Targeted interventions against IL-13 should be evaluated to decrease severity of HRV illness in infancy and early childhood.

Modified Tal Score: Validated score for prediction of bronchiolitis severity.

To further validate the use of the Modified Tal Score (MTS), a clinical tool for assessing bronchiolitis severity, by physicians with varying experience and training levels, and to determine the ability of the MTS to predict bronchiolitis severity. This prospective cohort study included infants of <12 months of age who were diagnosed with bronchiolitis and assessed via MTS. We calculated the intra-class correlation coefficient (ICC) among four groups of raters: group 1, board-certified pediatric pulmonologists; group 2, board-certified pediatricians; group 3, senior pediatric residents; and group 4, junior pediatric residents. Clinical outcomes were determined as length of oxygen support and length of stay (LOS). We assessed MTS's prediction of these outcomes. Relative risk (RR) for clinical severity was calculated via a Generalized Linear Model. Twenty-four physicians recorded a total of 600 scores for 50 infants (average age 5 ± 3 months; 56% male). The ICC values with group 1 as a reference were 0.92, 0.87, and 0.83, for groups 2, 3, and 4, respectively (P < 0.001). RR for oxygen support required was; 1.33 (CI 1.12-1.57), 1.26 (1.1-1.46), 1.26 (1.06-1.5), and 1.21 (0.93-1.58) for groups 1, 2, 3, and 4, respectively. RR for LOS was; 1.15 (CI 0.97-1.37), 1.19 (1.03-1.38), 1.18 (1.0-1.39), and 1.18 (0.93-1.51) for groups 1, 2, 3, and 4, respectively. The MTS is a simple and valid scoring system for evaluating infants with acute bronchiolitis, among different physician groups. The first score upon admission is a fair predictor of oxygen requirement at 48 h, and LOS at 72 h.

Characteristics of children admitted to intensive care with acute bronchiolitis

To assess factors associated with outcome in children admitted to paediatric intensive care (PIC) with bronchiolitis. A retrospective study of children admitted to the PICU at St Mary’s Hospital, London with bronchiolitis over a 6-year period (2011–2016). All bronchiolitis admissions < 2 years were included. Data collected particularly noted risk factors for severity, demographics, microbiology and outcome. We compared respiratory syncytial virus (RSV) with non-RSV status. Multivariate analysis was performed. Two hundred seventy-four patients were identified. Median age was 60 days (IQR 28–150 days), 63% were male, 90% were invasively ventilated and 42% were previously healthy. Pre-existing co-morbidities were present in 38%. The most frequently isolated pathogens were RSV (60%) and rhinovirus (26%). Co-infection was present in 45%, most commonly with RSV, rhinovirus and bacterial pathogens. Median length of stay (LOS) was 6 days (IQR 4.75–10). Younger age, prematurity, RSV, co-infection and co-morbidity were identified as significant risk factors for prolonged LOS. Six children died. Five of these had documented co-morbidities.Conclusion: RSV causes more severe bronchiolitis than other viruses. Nearly half of children admitted to PICU with RSV were previously healthy. Current guidelines for immunoprophylaxis of RSV bronchiolitis should be re-considered.What is Known:• Bronchiolitis is one of the most common reasons for unplanned PICU admission. The most common virus causing bronchiolitis is RSV• Bronchiolitis severe enough to require admission to PICU is associated with frequent morbidity but has low mortality.What is New:• RSV causes more severe bronchiolitis than other viruses.• Nearly half of all children admitted to PICU with RSV were previously healthy.

The CD8 T Cell Response to Respiratory Virus Infections.

Humans are highly susceptible to infection with respiratory viruses including respiratory syncytial virus (RSV), influenza virus, human metapneumovirus, rhinovirus, coronavirus, and parainfluenza virus. While some viruses simply cause symptoms of the common cold, many respiratory viruses induce severe bronchiolitis, pneumonia, and even death following infection. Despite the immense clinical burden, the majority of the most common pulmonary viruses lack long-lasting efficacious vaccines. Nearly all current vaccination strategies are designed to elicit broadly neutralizing antibodies, which prevent severe disease following a subsequent infection. However, the mucosal antibody response to many respiratory viruses is not long-lasting and declines with age. CD8 T cells are critical for mediating clearance following many acute viral infections in the lung. In addition, memory CD8 T cells are capable of providing protection against secondary infections. Therefore, the combined induction of virus-specific CD8 T cells and antibodies may provide optimal protective immunity. Herein, we review the current literature on CD8 T cell responses induced by respiratory virus infections. Additionally, we explore how this knowledge could be utilized in the development of future vaccines against respiratory viruses, with a special emphasis on RSV vaccination.

Atteintes bronchiolaires de la polyarthrite rhumatoïde et du syndrome de Gougerot-Sjögren

Rheumatoid arthritis and Sjogren's syndrome are the two main connective tissue diseases associated with bronchiolar disorders, including constrictive bronchiolitis and cellular bronchiolitis. The prevalence of bronchiolitis is difficult to assess. Most patients have little or no symptoms. More severe and life-threatening bronchiolitis is possible, although rare. The diagnosis of bronchiolar involvement is based on lung imaging and lung function tests; histological proof is usually not required. Treatment includes non-specific measures (bronchodilators, vaccination, rehabilitation), long-term macrolides and a corticosteroid and/or immunosuppressive trial.

The epidemiology of respiratory syncytial virus: A retrospective review from Steve Biko Academic Hospital 2013 - 2016.

Background Respiratory syncytial virus (RSV) bronchiolitis is a seasonal disease that has an enormous burden on health systems across the world. RSV disease manifestations in children range from mild upper respiratory tract infections to severe lower respiratory tract infections, including pneumonia and bronchiolitis. In South Africa, the seasonality of RSV disease causing both upper and lower respiratory tract illness is well documented. Objectives To describe the incidence of RSV bronchiolitis among patients ≤24 months of age who presented to a tertiary institution with a diagnosed viral bronchiolitis over a 4-year period. Secondary aims included determining: (i) the risk factors for the development of RSV bronchiolitis; (ii) the fatality rates and risk factors associated with mortality; (iii) the correlation with c-reactive protein values and risk of comorbid bacterial infection; and (iv) the impact of seasonality on RSV incidence. Methods A retrospective chart-based analysis of laboratory-confirmed RSV cases in children ≤24 months, presenting to Steve Biko Academic Hospital from January 2013 to December 2016, was undertaken. Epidemiology, risk factors and local weather data were collected as part of the analysis. Results During the 4-year period, a total of 1 127 nasopharyngeal aspirates (NPAs) was collected. RSV was isolated from 162 NPAs by either immunofluorescence (84%) or polymerase chain reaction (16%). Of the 162 patients with RSV bronchiolitis, 131 (80.9%) had a known HIV status. Only 2 (1.5%) of the patients whose status was known were HIV-infected; 26 (19.8%) were HIV-exposed and confirmed negative; and 103 (78.6%) HIV-unexposed. Forty-nine patients (30.2%) with RSV required intensive care unit (ICU, either paediatric or neonatal) admission. Thirty-four (69.4%) of these were <6 months old. Prematurity (27.8%) and cardiac lesions (13%) were the most common risk factors for acquiring the disease identified in patients with RSV bronchiolitis. Conclusion RSV is still a commonly detected virus among infants who are admitted for bronchiolitis. Significant risk factors associated with admission due to RSV bronchiolitis were prematurity, being <6 months of age and congenital cardiac disease. Male gender and HIV status did not appear to increase the risk of RSV bronchiolitis. In fact, HIV seems to have a protective effect against specifically RSV bronchiolitis in children <2 years of age. Young babies, especially premature infants with RSV bronchiolitis, are at considerable risk of requiring ICU admission, which leads to a significant increase in admission costs.

The human immune response to RSV includes a loop between the tumor suppressor p53 and expression of APOBEC3 genes

BackgroundRespiratory syncytial virus (RSV) infects nearly all children by theirsecond year of life with re‐infections occurring throughout adolescence andadulthood. RSV infection typicallyresults in mild host symptoms. However, susceptible individuals can develop severe lower respiratory tract infectionsand bronchiolitis, sometimes leading to hospitalization or death. Recently we established that in addition toits protective role against cancer development, the tumor suppressor p53 alsocontributes to host immune responses regulating the expression of several genesincluding the APOBEC3 family of DNA cytidine deaminases (A3), consideredsentinels in innate immune response against viral infections.ObjectiveUsinghuman lung cancer cells, we tested the role of p53 in response to RSV infectionand its replication through the regulation of the A3 gene family as well asother components of the immune response.MethodsA549 and H1299 cells were infected with RSV (Strain A2). Cells were thenharvested 72–120 hours post‐infection and qPCR and Nanostring arrays? were usedto evaluate mRNA expression of RSV‐g, P53, A3s and other immune targets. Expression of RSV was assessed? by ConfocalMicroscopy and cytofluorometry while Annexin V/PI assay was used to evaluateapoptosis.ResultsIn response to acute and chronic RSV infection in human lung cancer cells, p53 was activated and had an impact on RSV replication, which involves theexpression in a p53 dependent manner of several members of the A3 gene familyas well as other innate immune genes. APOBEC3G (A3G) was highly induced in a dose‐ and time‐dependent mannerafter RSV only in lung cancer cells harboring WT p53. Accordingly, overexpression of A3G in lungcancer cells reduced RSV replication. Furthermore, a Nanotstring transcriptome analysis (immune code set) after RSV infectionrevealed a strong p53 dependent regulation of immune response genes, includingseveral components of the innate immune antiviral response. In addition, RSV infection induced p53phosphorylation at serine 15 and triggered p53‐dependent apoptosis in p53 functional cells while p53 deficiency correlated with increased viralreplication and increased syncytia phenotype.ConclusionsOverall, our findings establish that the “guardian of the genome” role ascribed to p53 also extends to a unique component of the immune system – the A3 genes – revealing novel components in the antiviralimmune response against RSV infection.Support or Funding InformationSupported by NIEHS Division of Intramural Research Program.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

First-line treatment using high-flow nasal cannula for children with severe bronchiolitis: Applicability and risk factors for failure

BackgroundViral bronchiolitis is the leading cause of hospitalization in children during the first 12 months of life. There is evidence to support the use of noninvasive ventilation in bronchiolitis. A recent respiratory management of bronchiolitis is the use of high-flow nasal cannula (HFNC) therapy. The primary objective of this study was to evaluate the use of HFNC as the first-line treatment for children with severe bronchiolitis and the secondary objective was to identify factors for HFNC therapy failure. MethodsObservational prospective study in a pediatric intensive care unit (PICU), during two consecutive seasons (2013–2014 without recommendation and 2014–2015 with a study design suggesting HFNC as first-line treatment). The percentages of children treated with HFNC, nasal continuous or biphasic positive airway pressure (nCPAP/BiPAP) and invasive ventilation were compared. Associations between parameters recorded and HFCN therapy failure were established. ResultsThe percentage of patients treated with HFNC at admission was higher during the second season (90%, n=55/61) than the first season (34%, n=14/41) (p<0.0001). In bivariate analysis, heart rate, pH, and pCO2 were significantly associated with the occurrence of HFNC therapy failure in time-varying Cox regression models using all available values (i.e., admission and repeated measures during the first 5 days of hospitalization). Only pCO2 remained independently associated as a factor of HFNC failure in the multivariate Cox model with a hazard ratio per 5mmHg of 1.37 (95%CI: 1.01–1.87; P=0.046). ConclusionIn our PICU, HFNC therapy for children with bronchiolitis can potentially decrease the use of nCPAP. In this study, the factor of failure was higher pCO2. Studies to evaluate PCO2 level to discriminate HFNC versus CPAP indication could be useful.

The Effect of Respiratory Syncytial Virus on the Severity of Acute Bronchiolitis in Hospitalized Infants: A Prospective Study from Turkey

Objectives: Respiratory syncytial virus (RSV) is a major cause of respiratory infections in infants and children. The aim of this study was to evaluate clinical significance of respiratory infections as single pathogen RSV, respiratory viruses with RSV and those with bronchiolitis caused by other respiratory viruses. Methods: A total of 316 throat swabs were collected from children diagnosed with acute bronchiolitis. Real-time polymerase chain reaction was used to identify the viruses in the samples. The subjects were divided into three groups: single pathogen RSV, agents with RSV and agents without RSV. Binary logistic regression analysis was used to evaluate the corelation between single and multiple RSV infection group and infections without RSV group for parameters including age, wheezing, supplemental oxygen therapy. Results: The overall positivity for viruses in the study was found to be 75% with a co-infection rate of 34.2%. Compared to children with RSV alone, children with any other agents accompanying RSV, were not very likely to have fever, wheezing or supplemental oxygen therapy. Conclusions: The findings of our study suggest that RSV still represents a large burden of bronchiolitis since it is associated with the hospitalization of children, particularly those less than six months old. We can not foresee the clinical presentation of specific agent or agents in connection to being with or without RSV in infants with any level of bronchiolitis. The study agrees with the concept that co infections with or without RSV do not increase the severity of the disease.

Interferon lambda receptor 1 (IFNL1R) transcript is highly expressed in rhinovirus bronchiolitis and correlates with disease severity

BackgroundAs the expression of type III IFN receptor is restricted to the mucosal surfaces, its evaluation could be crucial to characterize the role of IFNλs during bronchiolitis. ObjectivesThis study was designed to investigate airway type III IFN receptor (IFNLR1/IL10RB) expression during respiratory syncytial virus (RSV) or human rhinovirus (HRV) bronchiolitis. Study designSeventy-one 1–6 month old infants hospitalized with their first episode of acute RSV or HRV bronchiolitis were selected for this study. Expression of IFNLR1, IL10RB and IFN-stimulated genes (ISGs) MxA and ISG56 in cells of nasopharyngeal washings taken within the first 48 h of admission were determined by a real-time hydrolysis probe RT-PCR assay. The ability of types I and III IFNs to induce the expression of both IFNLR1 and IL10RB in vitro was also evaluated. ResultsAirway IFNLR1 transcript levels were significantly higher in HRV bronchiolitis infants compared to those with RSV bronchiolitis. No differences were recorded for IL10RB-mRNA between RSV or HRV infection. IFNLR1 mRNA levels increased significantly in infants infected with the C species of HRV and in those with a higher clinical score index and with an eosinophil count >3%. There were no correlations in vivo between type III IFN receptors and those of ISGs and neither IFNLR1 nor IL10RB were induced in vitro by IFNs. ConclusionsThese results suggest that IFNLR1 are increased in HRV-infected infants with more severe bronchiolitis and blood eosinophilia and in those infected with the HRVC species.