scholarly journals A Cross-Study Biomarker Signature of Human Bronchial Epithelial Cells Infected with Respiratory Syncytial Virus

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Luiz Gustavo Gardinassi
Keyword(s):  
Functional Analysis ◽  
Respiratory Syncytial Virus ◽  
Bronchial Epithelial Cell ◽  
Epithelial Cell Line ◽  
Bronchial Epithelial ◽  
Rsv Infection ◽  
Novel Biomarkers ◽  
Syncytial Virus ◽  
Different Strains ◽  
Tract Infections

Respiratory syncytial virus (RSV) is a major cause of lower respiratory tract infections in children, elderly, and immunocompromised individuals. Despite of advances in diagnosis and treatment, biomarkers of RSV infection are still unclear. To understand the host response and propose signatures of RSV infection, previous studies evaluated the transcriptional profile of the human bronchial epithelial cell line—BEAS-2B—infected with different strains of this virus. However, the evolution of statistical methods and functional analysis together with the large amount of expression data provide opportunities to uncover novel biomarkers of inflammation and infections. In view of those facts publicly available microarray datasets from RSV-infected BEAS-2B cells were analyzed with linear model-based statistics and the platform for functional analysis InnateDB. The results from those analyses argue for the reevaluation of previously reported transcription patterns and biological pathways in BEAS-2B cell lines infected with RSV. Importantly, this study revealed a biosignature constituted by genes such asABCC4,ARMC8,BCLAF1,EZH1,FAM118A,FAM208B,FUS,HSPH1,KAZN,MAP3K2,N6AMT1,PRMT2,S100PBP,SERPINA1,TLK2,ZNF322, andZNF337which should be considered in the development of new molecular diagnosis tools.

3-Nitrotyrosine attenuates respiratory syncytial virus infection in human bronchial epithelial cell line

2005 ◽  
Vol 288 (5) ◽  
pp. L988-L996 ◽  
Author(s):  
Yuh-Chin T. Huang ◽  
Zhuowei Li ◽  
Luisa E. Brighton ◽  
Johnny L. Carson ◽  
Susanne Becker ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Epithelial Cell ◽  
Cell Line ◽  
Bronchial Epithelial Cell ◽  
Human Bronchial Epithelial Cell ◽  
Epithelial Cell Line ◽  
Bronchial Epithelial ◽  
Viral Particles ◽  
Rsv Infection ◽  
Syncytial Virus

3-Nitrotyrosine (NO2Tyr), an l-tyrosine derivative during nitrative stress, can substitute the COOH-terminal tyrosine of α-tubulin, posttranslationally altering microtubular functions. Because infection of the cells by respiratory syncytial virus (RSV) may require intact microtubules, we tested the hypothesis that NO2Tyr would inhibit RSV infection and intracellular signaling via nitrotyrosination of α-tubulin. A human bronchial epithelial cell line (BEAS-2B) was incubated with RSV with or without NO2Tyr. The release of chemokines and viral particles and activation of interferon regulatory factor-3 (IRF-3) were measured. Incubation with NO2Tyr increased nitrotyrosinated α-tubulin, and NO2Tyr colocalized with microtubules. RSV-infected cells released viral particles, RANTES, and IL-8 in a time- and dose-dependent manner, and intracellular RSV proteins coprecipitated with α-tubulin. NO2Tyr attenuated the RSV-induced release of RANTES, IL-8, and viral particles by 50–90% and decreased α-tubulin-associated RSV proteins. 3-Chlorotyrosine, another l-tyrosine derivative, had no effects. NO2Tyr also inhibited the RSV-induced shift of the unphosphorylated form I of IRF-3 to the phosphorylated form II. Pre-exposure of the cells to NO2(0.15 ppm, 4 h), which produced diffuse protein tyrosine nitration, did not affect RSV-induced release of RANTES, IL-8, or viral particles. NO2Tyr did not affect the potential of viral spreading to the neighboring cells since the RSV titers were not decreased when the uninfected cells were cocultured with the preinfected cells in NO2Tyr-containing medium. These results indicate that NO2Tyr, by replacing the COOH-terminal tyrosine of α-tubulin, attenuated RSV infection, and the inhibition appeared to occur at the early stages of RSV infection.

scholarly journals Comparative Therapeutic Potential of ALX-0171 and Palivizumab against Respiratory Syncytial Virus Clinical Isolate Infection of Well-Differentiated Primary Pediatric Bronchial Epithelial Cell Cultures

2019 ◽  
Vol 64 (2) ◽  
Author(s):  
Lindsay Broadbent ◽  
Hong Guo Parke ◽  
Lyndsey J. Ferguson ◽  
Andrena Millar ◽  
Michael D. Shields ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Epithelial Cell ◽  
Clinical Isolate ◽  
Therapeutic Potential ◽  
Bronchial Epithelial Cell ◽  
Bronchial Epithelial ◽  
Young Infants ◽  
Syncytial Virus ◽  
Well Differentiated ◽  
Tract Infections

ABSTRACT Respiratory syncytial virus (RSV) causes severe lower respiratory tract infections in young infants. There are no RSV-specific treatments available. Ablynx has been developing an anti-RSV F-specific nanobody, ALX-0171. To characterize the therapeutic potential of ALX-0171, we exploited our well-differentiated primary pediatric bronchial epithelial cell (WD-PBEC)/RSV infection model, which replicates several hallmarks of RSV disease in vivo. Using 2 clinical isolates (BT2a and Memphis 37), we compared the therapeutic potential of ALX-0171 with that of palivizumab, which is currently prescribed for RSV prophylaxis in high-risk infants. ALX-0171 treatment (900 nM) at 24 h postinfection reduced apically released RSV titers to near or below the limit of detection within 24 h for both strains. Progressively lower doses resulted in concomitantly diminished RSV neutralization. ALX-0171 was approximately 3-fold more potent in this therapeutic RSV/WD-PBEC model than palivizumab (mean 50% inhibitory concentration [IC50] = 346.9 to 363.6 nM and 1,048 to 1,090 nM for ALX-0171 and palivizumab, respectively), irrespective of the clinical isolate. The number of viral genomic copies (GC) was determined by quantitative reverse transcription-PCR (RT-qPCR), and the therapeutic effect of ALX-0171 treatment at 300 and 900 nM was found to be considerably lower and the number of GCs reduced only moderately (0.62 to 1.28 log10 copies/ml). Similar findings were evident for palivizumab. Therefore, ALX-0171 was very potent at neutralizing RSV released from apical surfaces but had only a limited impact on virus replication. The data indicate a clear disparity between viable virus neutralization and GC viral load, the latter of which does not discriminate between viable and neutralized RSV. This report validates the RSV/WD-PBEC model for the preclinical evaluation of RSV antivirals.

scholarly journals Identification of gene biomarkers for respiratory syncytial virus infection in a bronchial epithelial cell line

2008 ◽  
Vol 2 (3-4) ◽  
pp. 113-125 ◽  
Author(s):  
Yuh-Chin T. Huang ◽  
Zhuowei Li ◽  
Xhevahire Hyseni ◽  
Michael Schmitt ◽  
Robert B. Devlin ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Epithelial Cell ◽  
Virus Infection ◽  
Cell Line ◽  
Respiratory Syncytial Virus Infection ◽  
Bronchial Epithelial Cell ◽  
Epithelial Cell Line ◽  
Bronchial Epithelial ◽  
Syncytial Virus

Respiratory syncytial virus-induced cytokine production by a human bronchial epithelial cell line

1993 ◽  
Vol 265 (5) ◽  
pp. L472-L478 ◽  
Author(s):  
T. L. Noah ◽  
S. Becker
Keyword(s):  
Respiratory Syncytial Virus ◽  
Epithelial Cell ◽  
Cell Line ◽  
Proinflammatory Cytokines ◽  
Bronchial Epithelial Cell ◽  
Human Bronchial Epithelial Cell ◽  
Epithelial Cell Line ◽  
Cytokine Mrna ◽  
Bronchial Epithelial ◽  
Syncytial Virus

Respiratory syncytial virus (RSV) is the most common cause of lower respiratory infection in infants and young children, but the pathogenesis of RSV-induced inflammation is not well defined. We hypothesized that in vitro infection of a human bronchial epithelial cell line (BEAS) would induce production of proinflammatory cytokines. BEAS cells were infected with RSV, and cells and supernatants were assayed for cytokine mRNA and protein changes at several time points after infection. Cytokine mRNA in BEAS cells was measured by polymerase chain reaction of reverse-transcribed RNA from whole cell lysates; cytokine levels in supernatants were measured by bioassay or immunoassay. Our results indicated that interleukin-5ay or immunoassay. Our results indicated that interleukin-8 (IL-8) was induced at 4 h after infection (during the eclipse phase of RSV infection) with accumulation of IL-8 in supernatants by 24 h after infection. Increased levels of IL-6 and granulocyte macrophage colony-stimulating factor in supernatants were only detected by 96 h after infection, during the RSV replicative phase. Interferon-alpha and -gamma transcripts were not detectable at any time point. We conclude that the effects of RSV on airway inflammation may be at least partly mediated by sequential production of proinflammatory cytokines in infected airway epithelium.

Reappraisal of respiratory syncytial virus as an aetiology of severe acute lower respiratory tract infections in children younger than 5 years in Nigeria

2019 ◽  
Vol 113 (8) ◽  
pp. 446-452
Author(s):  
Damilola M Oladele ◽  
Dimeji P Oladele ◽  
Rasheedat M Ibraheem ◽  
Mohammed B Abdulkadir ◽  
Rasaki Adewole Raheem ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Respiratory Tract ◽  
Lower Respiratory Tract ◽  
Respiratory Tract Infections ◽  
Preventive Strategy ◽  
Lower Respiratory Tract Infections ◽  
Cross Sectional ◽  
Rsv Infection ◽  
Syncytial Virus ◽  
Tract Infections

Abstract Background Acute lower respiratory tract infections (ALRIs) especially severe ALRIs, constitute a global high burden of morbidity and mortality in children <5 y of age and respiratory syncytial virus (RSV) has been documented to a play a major aetiological role. However, Nigerian reports on severe childhood RSV ALRIs are rare and most reports are old. With recent advances in RSV preventive strategy, arises the need for a recent appraisal of RSV infection in children with severe ALRI. The current study thus set out to determine the prevalence of RSV infection among hospitalized children <5 y of age and describe the related social determinants. Methods We performed a descriptive cross-sectional study conducted over 1 y of 120 children, ages 2–59 months, diagnosed with ALRI. Relevant data were obtained and an antigen detection assay was used for viral studies. Results The prevalence of RSV infection was 34.2% and its peak was in the rainy months. The proportion of infants in the RSV-positive group was significantly higher than that in the RSV-negative group (82.9% vs 54.4%; p=0.002). These findings were largely consistent with those of earlier reports. Conclusions RSV has remained a common cause of severe ALRI in infants, especially during the rainy months in Nigeria. It is thus suggested that more effort be focused towards implementing the current global recommendations for the prevention of RSV-associated LRI, particularly in infants.

scholarly journals Chemokine regulation of inflammation during respiratory syncytial virus infection

F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 1837 ◽  
Author(s):  
Rinat Nuriev ◽  
Cecilia Johansson
Keyword(s):  
Respiratory Syncytial Virus ◽  
The Elderly ◽  
Infection Process ◽  
Viral Control ◽  
Small Proteins ◽  
Rsv Infection ◽  
Syncytial Virus ◽  
Tract Infections ◽  
Developed World ◽  
Immune Detection

Respiratory syncytial virus (RSV) can cause severe lower respiratory tract infections especially in infants, immunocompromised individuals and the elderly and is the most common cause of infant hospitalisation in the developed world. The immune responses against RSV are crucial for viral control and clearance but, if dysregulated, can also result in immunopathology and impaired gas exchange. Lung immunity to RSV and other respiratory viruses begins with the recruitment of immune cells from the bloodstream into the lungs. This inflammatory process is controlled largely by chemokines, which are small proteins that are produced in response to innate immune detection of the virus or the infection process. These chemokines serve as chemoattractants for granulocytes, monocytes, lymphocytes and other leukocytes. In this review, we highlight recent advances in the field of RSV infection and disease, focusing on how chemokines regulate virus-induced inflammation.

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