scholarly journals Differential Mucin Expression by Respiratory Syncytial Virus and Human Metapneumovirus Infection in Human Epithelial Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Ma. Del Rocío Baños-Lara ◽  
Boyang Piao ◽  
Antonieta Guerrero-Plata
Keyword(s):  
Immune Response ◽  
Respiratory Syncytial Virus ◽  
Epithelial Cells ◽  
Viral Infections ◽  
Human Metapneumovirus ◽  
Human Epithelial Cells ◽  
Mucin Expression ◽  
Rsv Infection ◽  
Syncytial Virus ◽  
Tract Disease

Mucins (MUC) constitute an important component of the inflammatory and innate immune response. However, the expression of these molecules by respiratory viral infections is still largely unknown. Respiratory syncytial virus (RSV) and human metapneumovirus (hMPV) are two close-related paramyxoviruses that can cause severe low respiratory tract disease in infants and young children worldwide. Currently, there is not vaccine available for neither virus. In this work, we explored the differential expression of MUC by RSV and hMPV in human epithelial cells. Our data indicate that the MUC expression by RSV and hMPV differs significantly, as we observed a stronger induction of MUC8, MUC15, MUC20, MUC21, and MUC22 by RSV infection while the expression of MUC1, MUC2, and MUC5B was dominated by the infection with hMPV. These results may contribute to the different immune response induced by these two respiratory viruses.

scholarly journals Comparative Analysis of Genes Induced by Respiratory Syncytial Virus and DsRNA in Human Epithelial Cells

2015 ◽  
Vol 18 (2) ◽  
pp. 101
Author(s):  
Gino Valentino Limmon
Keyword(s):  
Gene Expression ◽  
Immune Response ◽  
Respiratory Syncytial Virus ◽  
Epithelial Cells ◽  
High Throughput ◽  
Viral Infections ◽  
Human Epithelial Cells ◽  
Induced Genes ◽  
Syncytial Virus ◽  
Common Signal

Epithelial cells are the primary target of respiratory viral infections and play a pivotal role in virusinducedlung infl ammation and in anti viral immune response. A common signal for the presence of viralinfections and induction of infl ammation is recognition of double stranded RNA (dsRNA). Thus far, therehas not been a high-throughput transcrptome analysis of RSV- or dsRNA-induced genes in primary humanbronchial epithelial cells (PHBE), nor there has been a comparison between dsRNA- and RSV-inducedgenes. To establish the transcriptome profi les and to determine the contribution of dsRNA in the inductionof infl ammation during respiratory virus infection, we compared the gene expression profi les of PHBE cellsthat were infected with Respiratory Syncytial Virus (RSV) or were treated with dsRNA. Our transcriptomeanalysis showed that RSV infection and and dsRNA treatment induced up-regulation of 2024 and 159 genesin PHBE respectively. Comparison of genes revealed that RSV and dsRNA commonly induced 75 genes inPHBE cells. The common up-regulated genes were functionally grouped in multiple response pathwaysinvolved in infl ammation and immune responses. Interestingly, there were several previously unreportedgenes that were up-regulated in primary human epithelial cells that are relevant to a TH2 allergic phenotype.This comparison of a high-throughput gene expression study offers a comprehensive view of transcriptionalchanges induced by dsRNA and RSV, and importantly compares dsRNA-induced genes with RSV-inducedgenes in PHBE cells. Keywords: RSV, dsRNA, transcriptome, immune response, infl ammation

scholarly journals Human Respiratory Syncytial Virus NS 1 Targets TRIM25 to Suppress RIG-I Ubiquitination and Subsequent RIG-I-Mediated Antiviral Signaling

Viruses ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 716 ◽  
Author(s):  
Junsu Ban ◽  
Na-Rae Lee ◽  
Noh-Jin Lee ◽  
Jong Kil Lee ◽  
Fu-Shi Quan ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Viral Infections ◽  
Ectopic Expression ◽  
Suppressive Effect ◽  
Type I ◽  
Antiviral Signaling ◽  
Lower Respiratory Tract Disease ◽  
Rsv Infection ◽  
Syncytial Virus ◽  
Tract Disease

Respiratory syncytial virus (RSV) causes severe acute lower respiratory tract disease. Retinoic acid-inducible gene-I (RIG-I) serves as an innate immune sensor and triggers antiviral responses upon recognizing viral infections including RSV. Since tripartite motif-containing protein 25 (TRIM25)-mediated K63-polyubiquitination is crucial for RIG-I activation, several viruses target initial RIG-I activation through ubiquitination. RSV NS1 and NS2 have been shown to interfere with RIG-I-mediated antiviral signaling. In this study, we explored the possibility that NS1 suppresses RIG-I-mediated antiviral signaling by targeting TRIM25. Ubiquitination of ectopically expressed RIG-I-2Cards domain was decreased by RSV infection, indicating that RSV possesses ability to inhibit TRIM25-mediated RIG-I ubiquitination. Similarly, ectopic expression of NS1 sufficiently suppressed TRIM25-mediated RIG-I ubiquitination. Furthermore, interaction between NS1 and TRIM25 was detected by a co-immunoprecipitation assay. Further biochemical assays showed that the SPRY domain of TRIM25, which is responsible for interaction with RIG-I, interacted sufficiently with NS1. Suppression of RIG-I ubiquitination by NS1 resulted in decreased interaction between RIG-I and its downstream molecule, MAVS. The suppressive effect of NS1 on RIG-I signaling could be abrogated by overexpression of TRIM25. Collectively, this study suggests that RSV NS1 interacts with TRIM25 and interferes with RIG-I ubiquitination to suppress type-I interferon signaling.

scholarly journals Crawling with Virus: Translational Insights from a Neonatal Mouse Model on the Pathogenesis of Respiratory Syncytial Virus in Infants

2015 ◽  
Vol 90 (1) ◽  
pp. 2-4 ◽  
Author(s):  
Dahui You ◽  
Jordy Saravia ◽  
David Siefker ◽  
Bishwas Shrestha ◽  
Stephania A. Cormier
Keyword(s):  
Immune Response ◽  
Respiratory Syncytial Virus ◽  
Mouse Model ◽  
Severe Infection ◽  
Neonatal Mouse ◽  
Cell Type ◽  
Human Infants ◽  
Rsv Infection ◽  
Syncytial Virus ◽  
Infant Immune Response

The infant immune response to respiratory syncytial virus (RSV) remains incompletely understood. Here we review the use of a neonatal mouse model of RSV infection to mimic severe infection in human infants. We describe numerous age-specific responses, organized by cell type, observed in RSV-infected neonatal mice and draw comparisons (when possible) to human infants.

RESPIRATORY SYNCYTIAL VIRUS LUNG INFECTION IN INFANTS: IMMUNOREGULATORY ROLE OF INFECTED ALVEOLAR MACROPHAGES

PEDIATRICS ◽  
1995 ◽  
Vol 96 (2) ◽  
pp. 391-391
Author(s):  
Leon S. Greos
Keyword(s):  
Immune Response ◽  
Respiratory Syncytial Virus ◽  
Lung Injury ◽  
Alveolar Macrophages ◽  
Lung Infection ◽  
Local Immune Response ◽  
Rsv Infection ◽  
Syncytial Virus

Alveolar macrophages are infected by RSV in vivo and coexpress potent immunomodulatory molecules that potentially regulate local immune response or lung injury caused by RSV infection.

scholarly journals Metabolic Reprogramming of Nasal Airway Epithelial Cells Following Infant Respiratory Syncytial Virus Infection

Viruses ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 2055
Author(s):  
Andrew R. Connelly ◽  
Brian M. Jeong ◽  
Mackenzie E. Coden ◽  
Jacob Y. Cao ◽  
Tatiana Chirkova ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Epithelial Cells ◽  
Early Life ◽  
Airway Epithelial Cells ◽  
Metabolic Reprogramming ◽  
Flux Analysis ◽  
Nasal Airway ◽  
Airway Epithelial ◽  
Rsv Infection ◽  
Syncytial Virus

Respiratory syncytial virus (RSV) is a seasonal mucosal pathogen that infects the ciliated respiratory epithelium and results in the most severe morbidity in the first six months of life. RSV is a common cause of acute respiratory infection during infancy and is an important early-life risk factor strongly associated with asthma development. While this association has been repeatedly demonstrated, limited progress has been made on the mechanistic understanding in humans of the contribution of infant RSV infection to airway epithelial dysfunction. An active infection of epithelial cells with RSV in vitro results in heightened central metabolism and overall hypermetabolic state; however, little is known about whether natural infection with RSV in vivo results in lasting metabolic reprogramming of the airway epithelium in infancy. To address this gap, we performed functional metabolomics, 13C glucose metabolic flux analysis, and RNA-seq gene expression analysis of nasal airway epithelial cells (NAECs) sampled from infants between 2–3 years of age, with RSV infection or not during the first year of life. We found that RSV infection in infancy was associated with lasting epithelial metabolic reprogramming, which was characterized by (1) significant increase in glucose uptake and differential utilization of glucose by epithelium; (2) altered preferences for metabolism of several carbon and energy sources; and (3) significant sexual dimorphism in metabolic parameters, with RSV-induced metabolic changes most pronounced in male epithelium. In summary, our study supports the proposed phenomenon of metabolic reprogramming of epithelial cells associated with RSV infection in infancy and opens exciting new venues for pursuing mechanisms of RSV-induced epithelial barrier dysfunction in early life.

Control of Nosocomial Respiratory Syncytial Viral Infections

PEDIATRICS ◽  
1978 ◽  
Vol 62 (5) ◽  
pp. 728-732
Author(s):  
Caroline Breese Hall ◽  
Joyce M. Geiman ◽  
R. Gordon Douglas ◽  
Mary Pat Meagher
Keyword(s):  
Respiratory Syncytial Virus ◽  
Viral Infections ◽  
Close Contact ◽  
Initial Infection ◽  
Staff Members ◽  
Rsv Infection ◽  
Syncytial Virus ◽  
Repeated Infections

We evaluated methods to control the spread of respiratory syncytial virus (RSV) on our infants' ward during a community outbreak of RSV infection. Methods included isolation and cohorting of infected infants, strict handwashing, use of gowns, and the cohorting of staff to the ill infants. Of 123 infants studied, 36 were admitted with RSV infections. Of the remaining 87 contact infants, eight (19%) acquired nosocomial RSV disease. Three of the eight developed pneumonia and one died. Of the 43 staff members, 24 (56%) became infected and 82% were symptomatic. Four acquired repeated infections within weeks of the initial infection. Studies a year previously had revealed that 45% of contact infants and 42% of the staff had acquired nosocomial RSV infections. Thus, the employed procedures appeared to have decreased the transmission of RSV to infants but not to the staff. Staff may continue to be infected by large droplets from close contact with ill infants or by self-inoculation of contaminated secretions.

scholarly journals Respiratory Syncytial Virus Infection Induces Chromatin Remodeling to Activate Growth Factor and Extracellular Matrix Secretion Pathways

Viruses ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 804 ◽  
Author(s):  
Xiaofang Xu ◽  
Dianhua Qiao ◽  
Morgan Mann ◽  
Roberto P. Garofalo ◽  
Allan R. Brasier
Keyword(s):  
Extracellular Matrix ◽  
Respiratory Syncytial Virus ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Expression Profiles ◽  
Open Chromatin ◽  
High Confidence ◽  
Chromatin Domains ◽  
Rsv Infection ◽  
Syncytial Virus

Lower respiratory tract infection (LRTI) with respiratory syncytial virus (RSV) is associated with reduced lung function through unclear mechanisms. In this study, we test the hypothesis that RSV infection induces genomic reprogramming of extracellular matrix remodeling pathways. For this purpose, we sought to identify transcriptionally active open chromatin domains using assay for transposase-accessible-next generation sequencing (ATAC-Seq) in highly differentiated lower airway epithelial cells. High confidence nucleosome-free regions were those predicted independently using two peak-calling algorithms. In uninfected cells, ~12,650 high-confidence open chromatin regions were identified. These mapped to ~8700 gene bodies, whose genes functionally controlled organelle synthesis and Th2 pathways (IL6, TSLP). These latter cytokines are preferentially secreted by RSV-infected bronchiolar cells and linked to mucous production, obstruction, and atopy. By contrast, in RSV infection, we identify ~1700 high confidence open chromatin domains formed in 1120 genes, primarily in introns. These induced chromatin modifications are associated with complex gene expression profiles controlling tyrosine kinase growth factor signaling and extracellular matrix (ECM) secretory pathways. Of these, RSV induces formation of nucleosome-free regions on TGFB1/JUNB//FN1/MMP9 genes and the rate limiting enzyme in the hexosamine biosynthetic pathway (HBP), Glutamine-Fructose-6-Phosphate Transaminase 2 (GFPT2). RSV-induced open chromatin domains are highly enriched in AP1 binding motifs and overlap experimentally determined JUN peaks in GEO ChIP-Seq data sets. Our results provide a topographical map of chromatin accessibility and suggest a growth factor and AP1-dependent mechanism for upregulation of the HBP and ECM remodeling in lower epithelial cells that may be linked to long-term airway remodeling.

scholarly journals Contribution of Resident Memory CD8+ T Cells to Protective Immunity Against Respiratory Syncytial Virus and Their Impact on Vaccine Design

Pathogens ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 147 ◽  
Author(s):  
Retamal-Díaz ◽  
Covián ◽  
Pacheco ◽  
Castiglione-Matamala ◽  
Bueno ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Respiratory Syncytial Virus ◽  
Viral Infections ◽  
Memory T Cells ◽  
Effector Memory ◽  
Memory Cells ◽  
Effective Immune Response ◽  
Syncytial Virus ◽  
Tract Infections

Worldwide, human respiratory syncytial virus (RSV) is the most common etiological agent for acute lower respiratory tract infections (ALRI). RSV-ALRI is the major cause of hospital admissions in young children, and it can cause in-hospital deaths in children younger than six months old. Therefore, RSV remains one of the pathogens deemed most important for the generation of a vaccine. On the other hand, the effectiveness of a vaccine depends on the development of immunological memory against the pathogenic agent of interest. This memory is achieved by long-lived memory T cells, based on the establishment of an effective immune response to viral infections when subsequent exposures to the pathogen take place. Memory T cells can be classified into three subsets according to their expression of lymphoid homing receptors: central memory cells (TCM), effector memory cells (TEM) and resident memory T cells (TRM). The latter subset consists of cells that are permanently found in non-lymphoid tissues and are capable of recognizing antigens and mounting an effective immune response at those sites. TRM cells activate both innate and adaptive immune responses, thus establishing a robust and rapid response characterized by the production of large amounts of effector molecules. TRM cells can also recognize antigenically unrelated pathogens and trigger an innate-like alarm with the recruitment of other immune cells. It is noteworthy that this rapid and effective immune response induced by TRM cells make these cells an interesting aim in the design of vaccination strategies in order to establish TRM cell populations to prevent respiratory infectious diseases. Here, we discuss the biogenesis of TRM cells, their contribution to the resolution of respiratory viral infections and the induction of TRM cells, which should be considered for the rational design of new vaccines against RSV.

scholarly journals Pathogenesis of Respiratory Syncytial Virus Infection in BALB/c Mice Differs Between Intratracheal and Intranasal Inoculation

Viruses ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 508 ◽  
Author(s):  
Elisabeth A. van Erp ◽  
Anke J. Lakerveld ◽  
H. Lie Mulder ◽  
Willem Luytjes ◽  
Gerben Ferwerda ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Animal Models ◽  
Antiviral Agents ◽  
Mouse Strains ◽  
Immunological Parameters ◽  
Intranasal Inoculation ◽  
Rsv Infection ◽  
Syncytial Virus ◽  
Tract Disease

Human respiratory syncytial virus (RSV) is a major cause of severe lower respiratory tract disease requiring hospitalization in infants. There are no market-approved vaccines or antiviral agents available, but a growing number of vaccines and therapeutics are in (pre)clinical stages of development. Reliable animal models are crucial to evaluate new vaccine concepts, but in vivo RSV research is hampered by the lack of well-characterized animal models that faithfully mimic the pathogenesis of RSV infection in humans. Mice are frequently used in RSV infection and vaccination studies. However, differences in the use of mouse strains, RSV subtypes, and methodology often lead to divergent study outcomes. To our knowledge, a comparison between different RSV inoculation methods in mice has not been described in the literature, even though multiple methods are being used across different studies. In this study, we evaluated various pathological and immunological parameters in BALB/c mice after intratracheal or intranasal inoculation with RSV-A2. Our study reveals that intranasal inoculation induces robust pathology and inflammation, whereas this is not the case for intratracheal inoculation. As immunopathology is an important characteristic of RSV disease in infants, these data suggest that in mice intranasal inoculation is a more appropriate method to study RSV infection than intratracheal inoculation. These findings will contribute to the rational experimental design of future in vivo RSV experiments.

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