Rhinovirus

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Sebastian L Johnston - One of the best experts on this subject based on the ideXlab platform.

  • Recent advances in understanding Rhinovirus immunity.
    F1000Research, 2018
    Co-Authors: Spyridon Makris, Sebastian L Johnston
    Abstract:

    Rhinoviruses are the most common cause of upper respiratory tract infections. However, they can induce exacerbations of chronic obstructive pulmonary disease and asthma, bronchiolitis in infants, and significant lower respiratory tract infections in children, the immunosuppressed, and the elderly. The large number of Rhinovirus strains (currently about 160) and their antigenic diversity are significant obstacles in vaccine development. The phenotype of immune responses induced during Rhinovirus infection can affect disease severity. Recognition of Rhinovirus and a balance of innate responses are important factors in Rhinovirus-induced morbidity. Immune responses to Rhinovirus infections in healthy individuals are typically of the T helper type 1 (Th1) phenotype. However, Rhinovirus-driven asthma exacerbations are additionally characterised by an amplified Th2 immune response and airway neutrophilia. This commentary focuses on recent advances in understanding immunity toward Rhinovirus infection and how innate and adaptive immune responses drive Rhinovirus-induced asthma exacerbations.

  • Rhinovirus 16 induced ifn α and ifn β are deficient in bronchoalveolar lavage cells in asthmatic patients
    The Journal of Allergy and Clinical Immunology, 2012
    Co-Authors: Annemarie Sykes, Onn Min Kon, Jonathan Macintyre, Ajerico Del Rosario, Mark Mchale, Mariabelen Trujillotorralbo, Eteri Bakhsoliani, Patrick Mallia, Michael R. Edwards, Sebastian L Johnston
    Abstract:

    Background Asthmatic patients have defective Rhinovirus-induced IFN-β and IFN-λ production from bronchial epithelial cells and IFN-λ from bronchoalveolar lavage (BAL) cells. Whether bronchoalveolar lavage cells have defective type I interferon responses to Rhinovirus is unknown, as are mechanisms explaining defective Rhinovirus interferon induction in asthmatic patients. Objective We sought to investigate Rhinovirus induction of type I interferons in BAL and blood mononuclear cells from asthmatic patients and healthy subjects and to investigate mechanisms of any deficiency observed. Methods BAL and blood mononuclear cells from atopic asthmatic patients and healthy subjects were infected with Rhinovirus ex vivo . Interferon proteins were analyzed by using ELISA. mRNA expression of key components of interferon induction pathways were analyzed by using quantitative PCR. Results Rhinovirus induction of type I interferon protein was delayed and deficient in BAL cells from asthmatic patients, and lower interferon levels were associated with greater airway hyperresponsiveness and skin prick test response positivity. Expression of Toll-like receptor (TLR) 3, TLR7, TLR8, retinoic acid–inducible gene I (RIG-I), melanoma differentiation–associated gene 5 (MDA-5), TIR domain–containing adapter-inducing IFN-β (TRIF), myeloid differentiation primary response gene 88 (MyD88), caspase recruitment domain adaptor inducing IFN-β (CARDIF), IL-1 receptor–associated kinase 4 (IRAK4), IκB kinase β (IKKB), IκB kinase ι (IKKI), interferon regulatory factors 3 and 7, and Rhinovirus induction of expression of the virus-inducible molecules TLR3, TLR7, RIG-I, and MDA-5 were not impaired in these interferon-deficient BAL cells in asthmatic patients. Defective Rhinovirus interferon induction was not observed in blood mononuclear cells. Conclusions Rhinovirus induction of type I interferons in BAL cells is delayed and deficient and might be a marker of more severe asthma. Defective Rhinovirus interferon induction in asthmatic patients was not accompanied by differences in the expression or induction of key molecules implicated in viral induction of interferons.

  • Protein kinase R, IκB kinase-β and NF-κB are required for human Rhinovirus induced pro-inflammatory cytokine production in bronchial epithelial cells
    Molecular Immunology, 2007
    Co-Authors: Michael R. Edwards, Marc B Hershenson, Christopher A. Hewson, Vasile Laza-stanca, Hoy-tsun H. Lau, Naofumi Mukaida, Sebastian L Johnston
    Abstract:

    Abstract Rhinovirus infections cause the majority of acute exacerbations of airway diseases such as asthma and chronic obstructive pulmonary disease, with increased pro-inflammatory cytokine production by infected bronchial epithelial cells contributing to disease pathogenesis. Theses diseases are a huge cause of morbidity worldwide, and contribute a major economic burden to healthcare costs. Current steroid based treatments are only partially efficient at controlling virus induced inflammation, which remains an unmet therapeutic goal. Although NF-κB has been implicated, the precise mechanisms of Rhinovirus induction of pro-inflammatory gene expression in bronchial epithelial cells are unclear. We hypothesised that Rhinovirus replication and generation of dsRNA was an important process of pro-inflammatory cytokine induction. Using pharmalogical (2-aminopurine and a new small molecule inhibitor) and genetic inhibition of the dsRNA binding kinase protein kinase R, striking inhibition of dsRNA (polyrIC) and Rhinovirus induced CCL5, CXCL8 and IL-6 protein was observed. Using confocal microscopy, Rhinovirus induced protein kinase R phosphorylation co-located with NF-κB p65 nuclear translocation. Focusing on CXCL8, both Rhinovirus infection and dsRNA treatment required IκB kinase-β for induction of CXCL8. Analysis of cis-acting sites in the CXCL8 promoter revealed that both Rhinovirus infection and dsRNA treatment upregulated CXCL8 promoter activation via NF-κB and NF-IL6 binding sites. Together, the results demonstrate the importance of dsRNA in induction of pro-inflammatory cytokines by Rhinoviruses, and suggest that protein kinase R is involved in NF-κB mediated gene transcription of pro-inflammatory cytokines via IκB kinase-β. These molecules regulating Rhinovirus induction of inflammation represent therapeutic targets.

  • Airborne Rhinovirus detection and effect of ultraviolet irradiation on detection by a semi-nested RT-PCR assay
    BMC Public Health, 2003
    Co-Authors: Theodore A Myatt, Sebastian L Johnston, Stephen Rudnick, Donald K Milton
    Abstract:

    Background Rhinovirus, the most common cause of upper respiratory tract infections, has been implicated in asthma exacerbations and possibly asthma deaths. Although the method of transmission of Rhinoviruses is disputed, several studies have demonstrated that aerosol transmission is a likely method of transmission among adults. As a first step in studies of possible airborne Rhinovirus transmission, we developed methods to detect aerosolized Rhinovirus by extending existing technology for detecting infectious agents in nasal specimens. Methods We aerosolized Rhinovirus in a small aerosol chamber. Experiments were conducted with decreasing concentrations of Rhinovirus. To determine the effect of UV irradiation on detection of rhinoviral aerosols, we also conducted experiments in which we exposed aerosols to a UV dose of 684 mJ/m^2. Aerosols were collected on Teflon filters and Rhinovirus recovered in Qiagen AVL buffer using the Qiagen QIAamp Viral RNA Kit (Qiagen Corp., Valencia, California) followed by semi-nested RT-PCR and detection by gel electrophoresis. Results We obtained positive results from filter samples that had collected at least 1.3 TCID_50 of aerosolized Rhinovirus. Ultraviolet irradiation of airborne virus at doses much greater than those used in upper-room UV germicidal irradiation applications did not inhibit subsequent detection with the RT-PCR assay. Conclusion The air sampling and extraction methodology developed in this study should be applicable to the detection of Rhinovirus and other airborne viruses in the indoor air of offices and schools. This method, however, cannot distinguish UV inactivated virus from infectious viral particles.

  • Reducing agents inhibit Rhinovirus-induced up-regulation of the Rhinovirus receptor intercellular adhesion molecule-1 (ICAM-1) in respiratory epithelial cells
    The FASEB Journal, 2002
    Co-Authors: Alberto Papi, Cinzia Maria Bellettato, Luminita A Stanciu, Nikolaos G. Papadopoulos, Silvano Pinamonti, Stephen Townley Holgate, Klaus Degitz, Sebastian L Johnston
    Abstract:

    Rhinoviruses are the major cause of common colds and of asthma exacerbations. Intercellular adhesion molecule-1 (ICAM-1) has a central role in airway inflammation and is the receptor for 90% of Rhinoviruses. Rhinovirus infection of airway epithelium induces ICAM-1. Because redox state is directly implicated in inflammatory responses via molecular signaling mechanisms, here we studied the effects of reducing agents on Rhinovirus-induced ICAM-1 expression, mRNA up-regulation, promoter activation, and nuclear factor activation. To investigate the effects of Rhinovirus infection on the intracellular redox balance, we also studied whether Rhinovirus infection triggers the production of reactive oxygen species. We found that reduced (GSH) but not oxidized (GSSG) glutathione (1-100 mM) inhibited in a dose-dependent manner Rhinovirus-induced ICAM-1 up-regulation and mRNA induction in primary bronchial and A549 respiratory epithelial cells. GSH but not GSSG also inhibited Rhinovirus-induced ICAM-1 promoter activation and Rhinovirus-induced NF-kB activation. In parallel, we found that Rhinovirus infection induced a rapid increase of intracellular superoxide anion that was maximal at the time of NF-kB activation. This oxidant generation was completely inhibited by GSH. We conclude that redox-mediated intracellular pathways represent an important target for the therapeutic control of Rhinovirus-induced diseases.

Carlos A Camargo - One of the best experts on this subject based on the ideXlab platform.

  • association of Rhinovirus c bronchiolitis and immunoglobulin e sensitization during infancy with development of recurrent wheeze
    JAMA Pediatrics, 2019
    Co-Authors: Kohei Hasegawa, Jonathan M Mansbach, Cindy S Bauer, Ashley F Sullivan, Stephen J. Teach, Susan Wu, Pedro A Piedra, James E Gern, Yury A Bochkov, Carlos A Camargo
    Abstract:

    Importance Rhinovirus infection in early life, particularly with allergic sensitization, is associated with higher risks of developing recurrent wheeze and asthma. While emerging evidence links different Rhinovirus species (eg, Rhinovirus C) to a higher severity of infection and asthma exacerbation, to our knowledge, little is known about longitudinal associations of Rhinovirus C infection during infancy with subsequent morbidities. Objective To examine the association of different viruses (respiratory syncytial virus [RSV], Rhinovirus species) in bronchiolitis with risks of developing recurrent wheeze. Design, Setting, and Participants This multicenter prospective cohort study of infants younger than 1 year who were hospitalized for bronchiolitis was conducted at 17 hospitals across 14 US states during 3 consecutive fall to winter seasons (2011-2014). Exposures Major causative viruses of bronchiolitis, including RSV (reference group) and 3 Rhinovirus species (Rhinovirus A, B, and C). Main Outcomes and Measures Development of recurrent wheeze (as defined in national asthma guidelines) by age 3 years. Results This analytic cohort comprised 716 infants who were hospitalized for RSV-only or Rhinovirus bronchiolitis. The median age was 2.9 months (interquartile range, 1.6-3.8 months), 541 (76%) had bronchiolitis with RSV only, 85 (12%) had Rhinovirus A, 12 (2%) had Rhinovirus B, and 78 (11%) had Rhinovirus C infection. Overall, 231 (32%) developed recurrent wheeze by age 3 years. In the multivariable Cox model, compared with infants with RSV-only infection, the risk of recurrent wheeze was not significantly different in those with Rhinovirus A or B (Rhinovirus A: hazard ratio [HR], 1.27; 95% CI, 0.86-1.88; Rhinovirus B: HR, 1.39; 95% CI, 0.51-3.77; bothP > .10). By contrast, infants with Rhinovirus C had a significantly higher risk (HR, 1.58; 95% CI, 1.08-2.32). There was a significant interaction between virus groups andIgEsensitization on the risk of recurrent wheeze (Pfor interaction  Conclusions and Relevance This multicenter cohort study of infants hospitalized for bronchiolitis demonstrated between-virus differences in the risk of developing recurrent wheeze. Infants with Rhinovirus C infection, along with IgE sensitization, had the highest risk. This finding was driven by the association with a subtype of recurrent wheeze: children with subsequent development of asthma.

  • Rhinovirus species in children with severe bronchiolitis multicenter cohort studies in the united states and finland
    Pediatric Infectious Disease Journal, 2019
    Co-Authors: Kohei Hasegawa, Jonathan M Mansbach, Laura Toivonen, Tuomas Jartti, Pedro A Piedra, James E Gern, Yury A Bochkov, Carlos A Camargo
    Abstract:

    In this analysis of 2 prospective multicenter, multi-year cohorts of children hospitalized for bronchiolitis in the United States and Finland, 306 Rhinovirus infections were genotyped. Rhinovirus-A and -C species were predominant in the US study, while Rhinovirus-C species was predominant in the Finland study. In both cohorts, there were no significant between-species differences in clinical characteristics, including acute severity measures.

  • prednisolone for the first Rhinovirus induced wheezing and 4 year asthma risk a randomized trial
    Pediatric Allergy and Immunology, 2017
    Co-Authors: Annamari Koistinen, Riitta Turunen, Minna Lukkarinen, Tytti Vuorinen, Olli Ruuskanen, Tero Vahlberg, Carlos A Camargo, James E Gern, Tuomas Jartti
    Abstract:

    Background Previous findings show that corticosteroid treatment during the first acute wheezing episode may reduce recurrent wheezing in children with high Rhinovirus genome load at 12-month follow-up. Longer-term effects have not been investigated prospectively. Methods After PCR-confirmation of Rhinovirus from nasopharyngeal aspirate, 79 children with the first acute wheezing episode were randomized to receive orally prednisolone or placebo for three days. The initiation of asthma control medication before the age of 5 years was confirmed from medical record and/or from parental interview. The outcome was the time to initiation of regular asthma control medication. Interaction analysis examined Rhinovirus genome load. Results Fifty-nine (75%) children completed the follow-up. Asthma control medication was initiated in 40 (68%) children at the median age of 20 months. Overall, prednisolone did not affect the time to initiation of asthma control medication when compared to placebo (p=0.99). Rhinovirus load modified the effect of prednisolone regarding the time to initiation of asthma control medication (p-value for interaction=0.04). In children with high Rhinovirus load (>7000 copies/mL)(n=23), the risk for initiation of medication was lower in the prednisolone group compared to the placebo group (p=0.05). In the placebo group asthma medication was initiated to all children with high Rhinovirus load (n=9) during the 14 months after the first wheezing episode. Conclusions Overall, prednisolone did not affect the time to initiation of asthma control medication when compared to placebo. However, prednisolone may be beneficial in first-time wheezing children whose episode was severe and associated with high Rhinovirus load. (ClinicalTrials. gov, NCT00731575). This article is protected by copyright. All rights reserved.

  • detection of respiratory syncytial virus and Rhinovirus in healthy infants
    BMC Research Notes, 2015
    Co-Authors: Kohei Hasegawa, Vasanthi Avadhanula, Jonathan M Mansbach, Rachel W Linnemann, Pedro A Piedra, James E Gern, Carlos A Camargo
    Abstract:

    Despite the research importance of Rhinovirus detection in asymptomatic healthy infants, the literature remains sparse. To investigate the prevalence of respiratory syncytial virus (RSV) and Rhinovirus (and its species). We conducted a cross-sectional study of 110 healthy, non-hospitalized infants without acute illness at an academic medical center from November 2013 through May 2014. We tested nasal swab specimens by using polymerase chain reaction and genetic sequencing. Overall, the median age was 3.8 months (IQR 2.0–5.1 months), 56 % were male, and 90 % were born >37 weeks. RSV was detected in nasal swabs from infants (1.8 %). By contrast, Rhinovirus was detected in nasal swabs from 16 infants (14.5 %). Molecular typing assay revealed Rhinovirus species: six Rhinovirus-A (5.5 %), one Rhinovirus-B (0.9 %), eight Rhinovirus-C (7.3 %), and one untypeable (0.9 %). In this cross-sectional study of healthy, community-based infants, RSV was rare (<2 %) in nasal swabs, while Rhinovirus was detected in 14.5 % with a predominance of Rhinovirus-A and -C. These finding are important for understanding the clinical significance of Rhinovirus detection among infants hospitalized for bronchiolitis.

  • Detection of respiratory syncytial virus and Rhinovirus in healthy infants.
    BMC research notes, 2015
    Co-Authors: Kohei Hasegawa, Vasanthi Avadhanula, Jonathan M Mansbach, Rachel W Linnemann, Pedro A Piedra, James E Gern, Carlos A Camargo
    Abstract:

    Despite the research importance of Rhinovirus detection in asymptomatic healthy infants, the literature remains sparse. To investigate the prevalence of respiratory syncytial virus (RSV) and Rhinovirus (and its species). We conducted a cross-sectional study of 110 healthy, non-hospitalized infants without acute illness at an academic medical center from November 2013 through May 2014. We tested nasal swab specimens by using polymerase chain reaction and genetic sequencing. Overall, the median age was 3.8 months (IQR 2.0–5.1 months), 56 % were male, and 90 % were born >37 weeks. RSV was detected in nasal swabs from infants (1.8 %). By contrast, Rhinovirus was detected in nasal swabs from 16 infants (14.5 %). Molecular typing assay revealed Rhinovirus species: six Rhinovirus-A (5.5 %), one Rhinovirus-B (0.9 %), eight Rhinovirus-C (7.3 %), and one untypeable (0.9 %). In this cross-sectional study of healthy, community-based infants, RSV was rare (

James E Gern - One of the best experts on this subject based on the ideXlab platform.

  • Rhinovirus C Is Associated With Severe Wheezing and Febrile Respiratory Illness in Young Children.
    The Pediatric infectious disease journal, 2020
    Co-Authors: Riku Erkkola, Riitta Turunen, Tytti Vuorinen, Matti Waris, James E Gern, Yury A Bochkov, Kati Räisänen, Miia K. Laine, Paula A. Tähtinen, Aino Ruohola
    Abstract:

    BACKGROUND Rhinovirus is the most common virus causing respiratory tract illnesses in children. Rhinoviruses are classified into species A, B and C. We examined the associations between different Rhinovirus species and respiratory illness severity. METHODS This is a retrospective observational cohort study on confirmed Rhinovirus infections in 134 children 3-23 months of age, who were enrolled in 2 prospective studies on bronchiolitis and acute otitis media, respectively, conducted simultaneously in Turku University Hospital, Turku, Finland, between September 2007 and December 2008. RESULTS Rhinovirus C is the most prevalent species in our study, and it was associated with severe wheezing and febrile illness. We also noted that history of atopic eczema was associated with wheezing. CONCLUSIONS Our understanding of Rhinovirus C as the most pathogenic Rhinovirus species was fortified. Existing research supports the idea that atopic characteristics are associated with the severity of the Rhinovirus C-induced illness.

  • association of Rhinovirus c bronchiolitis and immunoglobulin e sensitization during infancy with development of recurrent wheeze
    JAMA Pediatrics, 2019
    Co-Authors: Kohei Hasegawa, Jonathan M Mansbach, Cindy S Bauer, Ashley F Sullivan, Stephen J. Teach, Susan Wu, Pedro A Piedra, James E Gern, Yury A Bochkov, Carlos A Camargo
    Abstract:

    Importance Rhinovirus infection in early life, particularly with allergic sensitization, is associated with higher risks of developing recurrent wheeze and asthma. While emerging evidence links different Rhinovirus species (eg, Rhinovirus C) to a higher severity of infection and asthma exacerbation, to our knowledge, little is known about longitudinal associations of Rhinovirus C infection during infancy with subsequent morbidities. Objective To examine the association of different viruses (respiratory syncytial virus [RSV], Rhinovirus species) in bronchiolitis with risks of developing recurrent wheeze. Design, Setting, and Participants This multicenter prospective cohort study of infants younger than 1 year who were hospitalized for bronchiolitis was conducted at 17 hospitals across 14 US states during 3 consecutive fall to winter seasons (2011-2014). Exposures Major causative viruses of bronchiolitis, including RSV (reference group) and 3 Rhinovirus species (Rhinovirus A, B, and C). Main Outcomes and Measures Development of recurrent wheeze (as defined in national asthma guidelines) by age 3 years. Results This analytic cohort comprised 716 infants who were hospitalized for RSV-only or Rhinovirus bronchiolitis. The median age was 2.9 months (interquartile range, 1.6-3.8 months), 541 (76%) had bronchiolitis with RSV only, 85 (12%) had Rhinovirus A, 12 (2%) had Rhinovirus B, and 78 (11%) had Rhinovirus C infection. Overall, 231 (32%) developed recurrent wheeze by age 3 years. In the multivariable Cox model, compared with infants with RSV-only infection, the risk of recurrent wheeze was not significantly different in those with Rhinovirus A or B (Rhinovirus A: hazard ratio [HR], 1.27; 95% CI, 0.86-1.88; Rhinovirus B: HR, 1.39; 95% CI, 0.51-3.77; bothP > .10). By contrast, infants with Rhinovirus C had a significantly higher risk (HR, 1.58; 95% CI, 1.08-2.32). There was a significant interaction between virus groups andIgEsensitization on the risk of recurrent wheeze (Pfor interaction  Conclusions and Relevance This multicenter cohort study of infants hospitalized for bronchiolitis demonstrated between-virus differences in the risk of developing recurrent wheeze. Infants with Rhinovirus C infection, along with IgE sensitization, had the highest risk. This finding was driven by the association with a subtype of recurrent wheeze: children with subsequent development of asthma.

  • Rhinovirus species in children with severe bronchiolitis multicenter cohort studies in the united states and finland
    Pediatric Infectious Disease Journal, 2019
    Co-Authors: Kohei Hasegawa, Jonathan M Mansbach, Laura Toivonen, Tuomas Jartti, Pedro A Piedra, James E Gern, Yury A Bochkov, Carlos A Camargo
    Abstract:

    In this analysis of 2 prospective multicenter, multi-year cohorts of children hospitalized for bronchiolitis in the United States and Finland, 306 Rhinovirus infections were genotyped. Rhinovirus-A and -C species were predominant in the US study, while Rhinovirus-C species was predominant in the Finland study. In both cohorts, there were no significant between-species differences in clinical characteristics, including acute severity measures.

  • prednisolone for the first Rhinovirus induced wheezing and 4 year asthma risk a randomized trial
    Pediatric Allergy and Immunology, 2017
    Co-Authors: Annamari Koistinen, Riitta Turunen, Minna Lukkarinen, Tytti Vuorinen, Olli Ruuskanen, Tero Vahlberg, Carlos A Camargo, James E Gern, Tuomas Jartti
    Abstract:

    Background Previous findings show that corticosteroid treatment during the first acute wheezing episode may reduce recurrent wheezing in children with high Rhinovirus genome load at 12-month follow-up. Longer-term effects have not been investigated prospectively. Methods After PCR-confirmation of Rhinovirus from nasopharyngeal aspirate, 79 children with the first acute wheezing episode were randomized to receive orally prednisolone or placebo for three days. The initiation of asthma control medication before the age of 5 years was confirmed from medical record and/or from parental interview. The outcome was the time to initiation of regular asthma control medication. Interaction analysis examined Rhinovirus genome load. Results Fifty-nine (75%) children completed the follow-up. Asthma control medication was initiated in 40 (68%) children at the median age of 20 months. Overall, prednisolone did not affect the time to initiation of asthma control medication when compared to placebo (p=0.99). Rhinovirus load modified the effect of prednisolone regarding the time to initiation of asthma control medication (p-value for interaction=0.04). In children with high Rhinovirus load (>7000 copies/mL)(n=23), the risk for initiation of medication was lower in the prednisolone group compared to the placebo group (p=0.05). In the placebo group asthma medication was initiated to all children with high Rhinovirus load (n=9) during the 14 months after the first wheezing episode. Conclusions Overall, prednisolone did not affect the time to initiation of asthma control medication when compared to placebo. However, prednisolone may be beneficial in first-time wheezing children whose episode was severe and associated with high Rhinovirus load. (ClinicalTrials. gov, NCT00731575). This article is protected by copyright. All rights reserved.

  • detection of respiratory syncytial virus and Rhinovirus in healthy infants
    BMC Research Notes, 2015
    Co-Authors: Kohei Hasegawa, Vasanthi Avadhanula, Jonathan M Mansbach, Rachel W Linnemann, Pedro A Piedra, James E Gern, Carlos A Camargo
    Abstract:

    Despite the research importance of Rhinovirus detection in asymptomatic healthy infants, the literature remains sparse. To investigate the prevalence of respiratory syncytial virus (RSV) and Rhinovirus (and its species). We conducted a cross-sectional study of 110 healthy, non-hospitalized infants without acute illness at an academic medical center from November 2013 through May 2014. We tested nasal swab specimens by using polymerase chain reaction and genetic sequencing. Overall, the median age was 3.8 months (IQR 2.0–5.1 months), 56 % were male, and 90 % were born >37 weeks. RSV was detected in nasal swabs from infants (1.8 %). By contrast, Rhinovirus was detected in nasal swabs from 16 infants (14.5 %). Molecular typing assay revealed Rhinovirus species: six Rhinovirus-A (5.5 %), one Rhinovirus-B (0.9 %), eight Rhinovirus-C (7.3 %), and one untypeable (0.9 %). In this cross-sectional study of healthy, community-based infants, RSV was rare (<2 %) in nasal swabs, while Rhinovirus was detected in 14.5 % with a predominance of Rhinovirus-A and -C. These finding are important for understanding the clinical significance of Rhinovirus detection among infants hospitalized for bronchiolitis.

Robert J Sherertz - One of the best experts on this subject based on the ideXlab platform.

  • DISPERSAL OF STAPHYLOCOCCUS AUREUS INTO THE AIR ASSOCIATED WITH A Rhinovirus INFECTION
    Infection Control and Hospital Epidemiology, 2005
    Co-Authors: Stefano Bassetti, Barbara A. Bassetti-wyss, Lori Mason, Werner E. Bischoff, Beth A Reboussin, Mark Walter, Ralph B. D'agostino, Jack M Gwaltney, Michael A. Pfaller, Robert J Sherertz
    Abstract:

    OBJECTIVE: To determine whether healthy adult nasal carriers of Staphylococcus aureus can disperse S. aureus into the air after Rhinovirus infection. DESIGN: We investigated the cloud phenomenon among adult nasal carriers of S. aureus experimentally infected with a Rhinovirus. Eleven volunteers were studied for 16 days in an airtight chamber wearing street clothes, sterile garb, or sterile garb plus surgical mask; Rhinovirus inoculation occurred on day 2. Daily quantitative air, nasal, and skin cultures for S. aureus; cold symptom assessment; and nasal Rhinovirus cultures were performed. SETTING: Wake Forest University School of Medicine, Winston-Salem, North Carolina. PARTICIPANTS: Wake Forest University undergraduate or graduate students who had persistent nasal carriage of S. aureus for 4 or 8 weeks. RESULTS: After Rhinovirus inoculation, dispersal of S. aureus into the air increased 2-fold with peak increases up to 34-fold. Independent predictors of S. aureus dispersal included the time period after Rhinovirus infection and wearing street clothes (P

  • DISPERSAL OF STAPHYLOCOCCUS AUREUS INTO THE AIR ASSOCIATED WITH A Rhinovirus INFECTION
    Infection control and hospital epidemiology, 2005
    Co-Authors: Stefano Bassetti, Barbara A. Bassetti-wyss, Lori Mason, Werner E. Bischoff, Beth A Reboussin, Mark Walter, Ralph B. D'agostino, Jack M Gwaltney, Michael A. Pfaller, Robert J Sherertz
    Abstract:

    Objective: To determine whether healthy adult nasal carriers of Staphylococcus aureus can disperse S. aureus into the air after Rhinovirus infection. Design: We investigated the “cloud” phenomenon among adult nasal carriers of S. aureus experimentally infected with a Rhinovirus. Eleven volunteers were studied for 16 days in an airtight chamber wearing street clothes, sterile garb, or sterile garb plus surgical mask; Rhinovirus inoculation occurred on day 2. Daily quantitative air, nasal, and skin cultures for S. aureus ; cold symptom assessment; and nasal Rhinovirus cultures were performed. Setting: Wake Forest University School of Medicine, Winston-Salem, North Carolina. Participants: Wake Forest University undergraduate or graduate students who had persistent nasal carriage of S. aureus for 4 or 8 weeks. Results: After Rhinovirus inoculation, dispersal of S. aureus into the air increased 2-fold with peak increases up to 34-fold. Independent predictors of S. aureus dispersal included the time period after Rhinovirus infection and wearing street clothes ( P S. aureus into the air ( P Conclusion: Virus-induced dispersal of S. aureus into the air may have an important role in the transmission of S. aureus and other bacteria.

  • airborne dispersal as a novel transmission route of coagulase negative staphylococci interaction between coagulase negative staphylococci and Rhinovirus infection
    Infection Control and Hospital Epidemiology, 2004
    Co-Authors: Werner E. Bischoff, Beth A Reboussin, Stefano Bassetti, Jack M Gwaltney, Michael A. Pfaller, Barbara A Bassettiwyss, Michelle L Wallis, Brian K Tucker, Ralph B Dagostino, Robert J Sherertz
    Abstract:

    Objective: To investigate whether Rhinovirus infection leads to increased airborne dispersal of coagulase-negative staphylococci (CoNS). Design: Prospective nonrandomized intervention trial. Setting: Wake Forest University School of Medicine, Winston-Salem, North Carolina. Participants: Twelve nasal Staphylococcus aureus- CoNS carriers among 685 students screened for S. aureus nasal carriage. Interventions: Participants were studied for airborne dispersal of CoNS in a chamber under three conditions (street clothes, sterile gown with a mask, and sterile gown without a mask). After 2 days of pre-exposure measurements, volunteers were inoculated with a Rhinovirus and observed for 14 days. Daily quantitative nasal and skin cultures for CoNS and nasal cultures for Rhinovirus were performed. In addition, assessment of cold symptoms was performed daily, mucous samples were collected, and serum titers before and after Rhinovirus inoculation were obtained. Sneezing, coughing, and talking events were recorded during chamber sessions. Results: All participants had at least one nasal wash positive for Rhinovirus and 10 developed a symptomatic cold. Postexposure, there was a twofold increase in airborne CoNS ( P = .0004), peaking at day 12. CoNS dispersal was reduced by wearing a gown (57% reduction, P P = .7). Nasal and skin CoNS colonization increased after Rhinovirus infection ( P Conclusions: We believe this is the first demonstration that a viral pathogen in the upper airways can increase airborne dispersal of CoNS in nasal S. aureus carriers. Gowns, gloves, and caps had a protective effect, whereas wearing a mask did not further reduce airborne spread.

Phillip G. Bardin - One of the best experts on this subject based on the ideXlab platform.

  • Vascular endothelial growth factor induction by Rhinovirus infection
    Journal of Medical Virology, 2006
    Co-Authors: Dinesha De Silva, Reena Ghildyal, Hayat Dagher, Nicholas Freezer, John W. Wilson, Mandy Lindsay, Xun Li, Phillip G. Bardin
    Abstract:

    Vascular participation manifested by a runny nose (rhinorrhea) is a prominent feature of the acute consequences of Rhinovirus infection. Vascular endothelial growth factor (VEGF) is an angiogenic factor that also induces potent increases in vascular permeability; it is a candidate mediator of rhinorrhea in response to Rhinovirus infection as well as contributing to enhanced vascular leakage in Rhinovirus-linked asthma exacerbations. It has been shown that Rhinovirus induces significant increases in both VEGF protein and mRNA in primary airway fibroblasts [Ghildyal et al. (2005): J Med Virol 75:608–615]. The current studies assessed VEGF responses to Rhinovirus in primary culture airway epithelium, in epithelial and fibroblast cell lines and in Rhinovirus-infected nasal secretions. Epithelial and fibroblast cells were infected with Rhinovirus serotype 16 and VEGF protein and isoforms assessed by ELISA and RT-PCR, respectively. VEGF protein was released by both epithelial and fibroblast cell lines and primary airway epithelial cells in culture but was not increased following Rhinovirus infection. PCR products coding for four or five of the six known VEGF isoforms were produced (121, 145, 165 and 183, and/or 189 amino acids) in cell lines and primary culture cells, but no specific isoform was linked to Rhinovirus infection. Nasal VEGF was also measured in a cohort of asthmatics with verified Rhinovirus and respiratory syncytial virus (RSV) infection. VEGF was not raised following Rhinovirus infection alone, but was increased significantly if concomitant RSV infection was present. The data suggest that fibroblasts rather than the epithelium may play a key role in VEGF mediated vascular responses after Rhinovirus infection. This may aid recruitment of inflammatory cells and contribute to airway inflammation and bronchial obstruction. J. Med. Virol. 78:666–672, 2006. © 2006 Wiley-Liss, Inc.

  • Vascular endothelial growth factor induction by Rhinovirus infection.
    Journal of medical virology, 2006
    Co-Authors: Dinesha De Silva, Reena Ghildyal, Hayat Dagher, Mandy Lee Lindsay, Nicholas Freezer, John W. Wilson, Phillip G. Bardin
    Abstract:

    Vascular participation manifested by a runny nose (rhinorrhea) is a prominent feature of the acute consequences of Rhinovirus infection. Vascular endothelial growth factor (VEGF) is an angiogenic factor that also induces potent increases in vascular permeability; it is a candidate mediator of rhinorrhea in response to Rhinovirus infection as well as contributing to enhanced vascular leakage in Rhinovirus-linked asthma exacerbations. It has been shown that Rhinovirus induces significant increases in both VEGF protein and mRNA in primary airway fibroblasts [Ghildyal et al. (2005): J Med Virol 75:608-615]. The current studies assessed VEGF responses to Rhinovirus in primary culture airway epithelium, in epithelial and fibroblast cell lines and in Rhinovirus-infected nasal secretions. Epithelial and fibroblast cells were infected with Rhinovirus serotype 16 and VEGF protein and isoforms assessed by ELISA and RT-PCR, respectively. VEGF protein was released by both epithelial and fibroblast cell lines and primary airway epithelial cells in culture but was not increased following Rhinovirus infection. PCR products coding for four or five of the six known VEGF isoforms were produced (121, 145, 165 and 183, and/or 189 amino acids) in cell lines and primary culture cells, but no specific isoform was linked to Rhinovirus infection. Nasal VEGF was also measured in a cohort of asthmatics with verified Rhinovirus and respiratory syncytial virus (RSV) infection. VEGF was not raised following Rhinovirus infection alone, but was increased significantly if concomitant RSV infection was present. The data suggest that fibroblasts rather than the epithelium may play a key role in VEGF mediated vascular responses after Rhinovirus infection. This may aid recruitment of inflammatory cells and contribute to airway inflammation and bronchial obstruction.

  • Rhinovirus detection: comparison of real-time and conventional PCR.
    Journal of virological methods, 2004
    Co-Authors: Hayat Dagher, Reena Ghildyal, Paul Hutchinson, Howard Donninger, Phillip G. Bardin
    Abstract:

    Rhinoviruses are important human respiratory viruses and the major causative agents of the common cold. Historically, detection of Rhinovirus has been by virus culture and this was significantly improved by the use of PCR assays. Recently real-time PCR was developed but to date there have been no reported comparisons of conventional and real-time PCR assays for detection of Rhinovirus. In this study, we first compared real-time PCR (SYBR Green I) to conventional PCR for the detection of Rhinovirus in serially diluted standard DNA and Rhinovirus stock to determine the limits of detection. Next, assays were compared for sensitivity to detect Rhinovirus in cell culture with a known number of infected cells. Finally, the assays were compared using clinical samples known to contain Rhinovirus. Real-time PCR was 10-fold more sensitive than conventional PCR to detect Rhinovirus in standard DNA and in virus stock and >10-fold more sensitive to detect Rhinovirus in cultured cells. Real-time PCR was significantly superior for detection of Rhinovirus in patients' nasal aspirates (sensitivity 72% versus 39%, P < 0.05). In summary, we found that real-time PCR was more sensitive than conventional PCR and reduced post-PCR processing. Hence, real-time PCR is suitable for both research and clinical purposes.