Relationship Between IFN-γ Genotypes and the Development of Otitis Media (OM) During Respiratory Syncytial Virus (RSV) Infection in Young Children

2007 ◽  
Vol 119 (1) ◽  
pp. S303
Author(s):  
J.M. Koehrsen ◽  
D.P. Skoner ◽  
D.A. Gentile ◽  
A. Patel ◽  
M. Varga ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Young Children ◽  
Otitis Media ◽  
Rsv Infection ◽  
Ifn Γ ◽  
Syncytial Virus

Detection of Genomic Sequences of Respiratory Syncytial Virus in Otitis Media with Effusion in Children

1992 ◽  
Vol 101 (10_suppl) ◽  
pp. 7-10 ◽  
Author(s):  
Yoshitaka Okamoto ◽  
Kazuo Kudo ◽  
Koji Shirotori ◽  
Misao Nakazawa ◽  
Eiko Ito ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Respiratory Syncytial Virus ◽  
Otitis Media ◽  
Otitis Media With Effusion ◽  
Chain Reaction ◽  
Nested Polymerase Chain Reaction ◽  
Rsv Infection ◽  
Polymerase Chain ◽  
Syncytial Virus ◽  
Viral Sequences

The reverse transcriptase—polymerase chain reaction and the nested polymerase chain reaction were used for detection of respiratory syncytial virus (RSV) sequences in middle ear effusions collected from children with otitis media. Sequences of RSV were detected in 21 of 34 samples tested. These samples were collected during and/or after natural outbreaks of RSV infection in the community. In those patients from whose nasopharynges RSV was isolated, the viral sequences were highly detectable (75%) in the effusions. These observations suggest RSV as an important factor in the pathogenesis of otitis media with effusion.

scholarly journals The Human Immune Response to Respiratory Syncytial Virus Infection

2017 ◽  
Vol 30 (2) ◽  
pp. 481-502 ◽  
Author(s):  
Clark D. Russell ◽  
Stefan A. Unger ◽  
Marc Walton ◽  
Jürgen Schwarze
Keyword(s):  
Immune Response ◽  
Respiratory Syncytial Virus ◽  
T Cell ◽  
T Cell Response ◽  
Rsv Infection ◽  
Human Immune Response ◽  
Ifn Γ ◽  
Human Immune ◽  
Syncytial Virus

SUMMARY Respiratory syncytial virus (RSV) is an important etiological agent of respiratory infections, particularly in children. Much information regarding the immune response to RSV comes from animal models and in vitro studies. Here, we provide a comprehensive description of the human immune response to RSV infection, based on a systematic literature review of research on infected humans. There is an initial strong neutrophil response to RSV infection in humans, which is positively correlated with disease severity and mediated by interleukin-8 (IL-8). Dendritic cells migrate to the lungs as the primary antigen-presenting cell. An initial systemic T-cell lymphopenia is followed by a pulmonary CD8+ T-cell response, mediating viral clearance. Humoral immunity to reinfection is incomplete, but RSV IgG and IgA are protective. B-cell-stimulating factors derived from airway epithelium play a major role in protective antibody generation. Gamma interferon (IFN-γ) has a strongly protective role, and a Th2-biased response may be deleterious. Other cytokines (particularly IL-17A), chemokines (particularly CCL-5 and CCL-3), and local innate immune factors (including cathelicidins and IFN-λ) contribute to pathogenesis. In summary, neutrophilic inflammation is incriminated as a harmful response, whereas CD8+ T cells and IFN-γ have protective roles. These may represent important therapeutic targets to modulate the immunopathogenesis of RSV infection.

scholarly journals Epidemiology of laboratory-confirmed respiratory syncytial virus infection in young children in England, 2010–2014: the importance of birth month

2016 ◽  
Vol 144 (10) ◽  
pp. 2049-2056 ◽  
Author(s):  
R. M. REEVES ◽  
P. HARDELID ◽  
R. GILBERT ◽  
J. ELLIS ◽  
H. ZHAO ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Young Children ◽  
Control Measures ◽  
Surveillance Systems ◽  
Logistic Regression Models ◽  
Birth Month ◽  
Laboratory Surveillance ◽  
Rsv Infection ◽  
Syncytial Virus ◽  
Positive Results

SUMMARYThe epidemiology of laboratory-confirmed respiratory syncytial virus (RSV) infections in young children has not recently been described in England, and is an essential step in identifying optimal target groups for future licensed RSV vaccines. We used two laboratory surveillance systems to examine the total number and number of positive RSV tests in children aged <5 years in England from 2010 to 2014. We derived odds ratios (ORs) with 95% confidence intervals (CIs) comparing children by birth month, using multivariable logistic regression models adjusted for age, season and sex. Forty-seven percent of RSV tests (29 851/63 827) and 57% (7405/13 034) of positive results in children aged <5 years were in infants aged <6 months. Moreover, 38% (4982/13 034) of positive results were in infants aged <3 months. Infants born in September, October and November had the highest odds of a positive RSV test during their first year of life compared to infants born in January (OR 2·1, 95% CI 1·7–2·7; OR 2·4, 95% CI 2·1–2·8; and OR 2·4, 95% CI 2·1–2·7, respectively). Our results highlight the importance of young age and birth month near the beginning of the RSV season to the risk of laboratory-confirmed RSV infection. Future control measures should consider protection for these groups.

Differences in respiratory syncytial virus and influenza infection in a house-dust-mite-induced asthma mouse model: consequences for steroid sensitivity

2013 ◽  
Vol 125 (12) ◽  
pp. 565-574 ◽  
Author(s):  
Hiroki Mori ◽  
Nicole S. Parker ◽  
Deborah Rodrigues ◽  
Kathryn Hulland ◽  
Deborah Chappell ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Virus Infection ◽  
Mouse Model ◽  
Influenza Infection ◽  
Prednisolone Treatment ◽  
Dust Mite ◽  
Rsv Infection ◽  
Ifn Γ ◽  
Syncytial Virus ◽  
Clinical Asthma

A significant number of clinical asthma exacerbations are triggered by viral infection. We aimed to characterize the effect of virus infection in an HDM (house dust mite) mouse model of asthma and assess the effect of oral corticosteroids. HDM alone significantly increased eosinophils, lymphocytes, neutrophils, macrophages and a number of cytokines in BAL (bronchoalveolar lavage), all of which were sensitive to treatment with prednisolone (with the exception of neutrophils). Virus infection also induced cell infiltration and cytokines. RSV (respiratory syncytial virus) infection in HDM-treated animals further increased all cell types in BAL (except eosinophils, which declined), but induced no further increase in HDM-elicited cytokines. However, while HDM-elicited TNF-α (tumour necrosis factor-α), IFN-γ (interferon-γ), IL (interleukin)-2, IL-5 and IL-10 were sensitive to prednisolone treatment, concomitant infection with RSV blocked the sensitivity towards steroid. In contrast, influenza infection in HDM- challenged animals resulted in increased BAL lymphocytes, neutrophils, IFN-γ, IL-1β, IL-4, IL-5, IL-10 and IL-12, but all were attenuated by prednisolone treatment. HDM also increased eNO (exhaled NO), which was further increased by concomitant virus infection. This increase was only partially attenuated by prednisolone. RSV infection alone increased BAL mucin. However, BAL mucin was increased in HDM animals with virus infection. Chronic HDM challenge in mice elicits a broad inflammatory response that shares many characteristics with clinical asthma. Concomitant influenza or RSV infection elicits differing inflammatory profiles that differ in their sensitivity towards steroids. This model may be suitable for the assessment of novel pharmacological interventions for asthmatic exacerbation.

Strategies for Reducing the Risk of Respiratory Syncytial Virus Infection in Infants and Young Children: A Canadian Nurses’ Perspective

2012 ◽  
Vol 31 (6) ◽  
pp. 357-368 ◽  
Author(s):  
Marianne Bracht ◽  
Debbie Basevitz ◽  
Marilyn Cranis ◽  
Rose Paulley ◽  
Bosco Paes
Keyword(s):  
Health Care ◽  
Respiratory Syncytial Virus ◽  
Young Children ◽  
Health Care Providers ◽  
Critical Role ◽  
Care Providers ◽  
Adverse Health Outcomes ◽  
Rsv Infection ◽  
Syncytial Virus ◽  
Infants And Young Children

Respiratory syncytial virus (RSV) infections are prevalent globally and can cause substantial morbidity in infants and young children. The virus is easily transmitted by direct hand-to-hand contact and can lead to serious respiratory disease and hospitalization, particularly in premature infants and children with certain medical conditions. Educating families with young children, especially those in remote rural regions, regarding the potential adverse health outcomes of RSV infection and measures to reduce the risk of transmitting or acquiring RSV has been a key focus of the health care system in Canada. Geographic, cultural, and socioeconomic factors present formidable challenges to the execution of this endeavor. Therefore, it is critical to develop and systematically implement effective educational programs for both families and health care providers. In Canada, nurses play a critical role in education and counseling. In this review, we share our perspectives and suggest empirical practices that may be applicable worldwide.

scholarly journals Chlorobenzoxime inhibits respiratory syncytial virus infection in neonatal rats via up-regulation of IFN-γ in dendritic cells

2020 ◽  
Vol 19 (2) ◽  
pp. 239-246
Author(s):  
Junzhao Li ◽  
Yonghai Zhang ◽  
Hongmei Qiao ◽  
Yingji Jin ◽  
Jianmin Wang ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Respiratory Syncytial Virus ◽  
Neonatal Rat ◽  
Interleukin 4 ◽  
Neonatal Rats ◽  
Alveolar Cells ◽  
Rsv Infection ◽  
Ifn Γ ◽  
Syncytial Virus

Purpose: To investigate the effect of chlorobenzoxime on respiratory syncytial virus (RSV) infection in vitro in lung alveolar cells and in vivo in neonatal rats, as well as the mechanism of action involved. Methods: RSV infection in neonatal rats was induced via intranasal administration of 2 x 106PFU viral particles. Reverse transcriptase-polymerase chain reaction (RT-PCR) and western blotting were used for determination of changes in interleukin expression. Results: RSV infection in BEAS-2B cells caused significant reduction in viability and marked alteration in morphological appearance (p < 0.05). Exposure of RSV-infected BEAS-2B cells to chlorobenzoxime prevented viability reduction and changes in morphology, and led to reductions in RSV-mediated increases in levels of interleukin-6 and interleukin-8. Moreover, RSV infection significantly enhanced ROS levels in BEAS-2B cells, when compared to control cells (p < 0.05). Chlorobenzoxime at a concentration of 30 μM completely suppressed RSV-mediated generation of ROS in BEAS-2B cells. In neonatal rats, RSV-induced upregulation of interleukin-4, interleukin-13 and TNF-α, were suppressed in bronchoalveolar lavage fluid (BALF) and lung tissues by chlorobenzoxime. Moreover, the RSVmediated reduction in IFN-γ was maximally blocked by chlorobenzoxime at a dose of 10 mg/mL. Chlorobenzoxime enhanced the proportion of IFN-γ -producing cells in neonatal rat BALF. Conclusion: Chlorobenzoxime exhibits antiviral against RSV infection in neonatal rats via increase in dendritic cell population, leading to inhibition of cytokine production. Therefore, chlorobenzoxime is a potential therapeutic agent for RSV infection. Keywords: Respiratory syncytial virus, Cytokines, Dendritic cells, Lung aveolar cells, Morphology, Interleukins

scholarly journals Cell-Specific Expression of RANTES, MCP-1, and MIP-1α by Lower Airway Epithelial Cells and Eosinophils Infected with Respiratory Syncytial Virus

1998 ◽  
Vol 72 (6) ◽  
pp. 4756-4764 ◽  
Author(s):  
Barbara Olszewska-Pazdrak ◽  
Antonella Casola ◽  
Tadahito Saito ◽  
Rafeul Alam ◽  
Sheila E. Crowe ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Epithelial Cells ◽  
Cellular Response ◽  
Airway Epithelial Cells ◽  
Lower Airway ◽  
Small Airways ◽  
Specific Expression ◽  
Rsv Infection ◽  
Ifn Γ ◽  
Syncytial Virus

ABSTRACT Respiratory syncytial virus (RSV) is the major cause of acute bronchiolitis in infancy, a syndrome characterized by wheezing, respiratory distress, and the pathologic findings of peribronchial mononuclear cell infiltration and release of inflammatory mediators by basophil and eosinophil leukocytes. Composition and activation of this cellular response are thought to rely on the discrete target cell selectivity of C-C chemokines. We demonstrate that infection in vitro of human epithelial cells of the lower respiratory tract by RSV induced dose- and time-dependent increases in mRNA and protein secretion for RANTES (regulated upon activation, normal T-cell expressed and presumably secreted), monocyte chemotactic protein-1 (MCP-1), and macrophage inflammatory protein-1α (MIP-1α). Production of MCP-1 and MIP-1α was selectively localized only in epithelial cells of the small airways and lung. Exposure of epithelial cells to gamma interferon (IFN-γ), in combination with RSV infection, induced a significant increase in RANTES production that was synergistic with respect to that obtained by RSV infection or IFN-γ treatment alone. Epithelial cell-derived chemokines exhibited a strong chemotactic activity for normal human blood eosinophils. Furthermore, eosinophils were susceptible to RSV and released RANTES and MIP-1α as a result of infection. Therefore, the inflammatory process in RSV-induced bronchiolitis appears to be triggered by the infection of epithelial cells and further amplified via mechanisms driven by IFN-γ and by the secretion of eosinophil chemokines.

scholarly journals Characterization of Respiratory Syncytial Virus M- and M2-Specific CD4 T Cells in a Murine Model

2009 ◽  
Vol 83 (10) ◽  
pp. 4934-4941 ◽  
Author(s):  
Jie Liu ◽  
Tracy J. Ruckwardt ◽  
Man Chen ◽  
Teresa R. Johnson ◽  
Barney S. Graham
Keyword(s):  
T Cells ◽  
Respiratory Syncytial Virus ◽  
T Cell ◽  
Cd4 T Cells ◽  
Cd4 T Cell ◽  
Cell Responses ◽  
Rsv Infection ◽  
Ifn Γ ◽  
Syncytial Virus

ABSTRACT CD4 T cells have been shown to play an important role in the immunity and immunopathogenesis of respiratory syncytial virus (RSV) infection. We identified two novel CD4 T-cell epitopes in the RSV M and M2 proteins with core sequences M213-223 (FKYIKPQSQFI) and M227-37 (YFEWPPHALLV). Peptides containing the epitopes stimulated RSV-specific CD4 T cells to produce gamma interferon (IFN-γ), interleukin 2 (IL-2), and other Th1- and Th2-type cytokines in an I-Ab-restricted pattern. Construction of fluorochrome-conjugated peptide-I-Ab class II tetramers revealed RSV M- and M2-specific CD4 T-cell responses in RSV-infected mice in a hierarchical pattern. Peptide-activated CD4 T cells from lungs were more activated and differentiated, and had greater IFN-γ expression, than CD4 T cells from the spleen, which, in contrast, produced greater levels of IL-2. In addition, M209-223 peptide-activated CD4 T cells reduced IFN-γ and IL-2 production in M- and M2-specific CD8 T-cell responses to Db-M187-195 and Kd-M282-90 peptides more than M225-39 peptide-stimulated CD4 T cells. This correlated with the fact that I-Ab-M209-223 tetramer-positive cells responding to primary RSV infection had a much higher frequency of FoxP3 expression than I-Ab-M226-39 tetramer-positive CD4 T cells, suggesting that the M-specific CD4 T-cell response has greater regulatory function. Characterization of epitope-specific CD4 T cells by novel fluorochrome-conjugated peptide-I-Ab tetramers allows detailed analysis of their roles in RSV pathogenesis and immunity.

DNA encoding the attachment (G) or fusion (F) protein of respiratory syncytial virus induces protection in the absence of pulmonary inflammation

2000 ◽  
Vol 81 (10) ◽  
pp. 2519-2523 ◽  
Author(s):  
Gary P. Bembridge ◽  
Nuria Rodriguez ◽  
Regina Garcia-Beato ◽  
Carolyn Nicolson ◽  
Jose A. Melero ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Antibody Response ◽  
G Protein ◽  
Pulmonary Inflammation ◽  
Recombinant Vaccinia Virus ◽  
Dna Encoding ◽  
Th2 Response ◽  
Rsv Infection ◽  
Ifn Γ ◽  
Syncytial Virus

Significant protection against respiratory syncytial virus (RSV) infection was induced in mice vaccinated intramuscularly (i.m.) with DNA encoding the F or G protein of RSV. The amounts of IgG1 of IgG2a antibodies in mice immunized with DNA-G alone were similar. However, the antibody response in mice co-immunized with DNA-G and DNA encoding IL-4 (DNA-IL-4) was strongly biased towards IgG1. In contrast, the antibody response in mice co-immunized with DNA-G and DNA-IL-2, -IL-12 or-IFN-γ was biased towards IgG2a. Mice vaccinated with DNA-F either alone or in combination with DNA encoding cytokines developed a predominant RSV-specific IgG2a response, which was most pronounced in mice co-immunized with DNA-F and DNA-IL-12 or -IFN-γ. Vaccinated mice developed only a slightly enhanced pulmonary inflammatory response following RSV challenge. More significantly, and in contrast to mice scarified with recombinant vaccinia virus expressing the G protein, mice vaccinated i.m. with DNA-G did not develop pulmonary eosinophilia, even when the immune response was biased towards a Th2 response by co-administration of DNA-IL-4.

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