Respiratory Syncytial Virus and Childhood Asthma

2000 ◽  
Vol 14 (2) ◽  
pp. 91-92 ◽  
Author(s):  
John T. McBride
2020 ◽  
Author(s):  
Richard Thwaites ◽  
Jonathan Coutts ◽  
John Fullarton ◽  
ElizaBeth Grubb ◽  
Carole Morris ◽  
...  

2008 ◽  
Vol 21 (3) ◽  
pp. 495-504 ◽  
Author(s):  
Shyam S. Mohapatra ◽  
Sandhya Boyapalle

SUMMARY Virtually all children experience respiratory syncytial virus (RSV) infection at least once during the first 2 years of life, but only a few develop bronchiolitis and more severe disease requiring hospitalization, usually in the first 6 months of life. Children who recover from RSV-induced bronchiolitis are at increased risk for the development of recurrent wheeze and asthma in later childhood. Recent studies suggest that there is an association between RSV-induced bronchiolitis and asthma within the first decade of life but that this association is not significant after age 13. Despite the considerable progress made in our understanding of several aspects of respiratory viral infections, further work needs to be done to clarify the molecular mechanisms of early interactions between virus and host cell and the role of host gene products in the infection process. This review provides a critical appraisal of the literature in epidemiology and experimental research which links RSV infection to asthma. Studies to date demonstrate that there is a significant association between RSV infection and childhood asthma and that preventing severe primary RSV infections can decrease the risk of childhood asthma.


2017 ◽  
Vol 139 (1) ◽  
pp. 66-71.e3 ◽  
Author(s):  
Kecia N. Carroll ◽  
Tebeb Gebretsadik ◽  
Gabriel J. Escobar ◽  
Pingsheng Wu ◽  
Sherian Xu Li ◽  
...  

Thorax ◽  
2020 ◽  
Vol 75 (9) ◽  
pp. 725-734
Author(s):  
Ching-Hui Tsai ◽  
Ann Chen Wu ◽  
Bor-Luen Chiang ◽  
Yao-Hsu Yang ◽  
Shih-Pin Hung ◽  
...  

BackgroundRespiratory syncytial virus (RSV) is associated with childhood asthma. Nevertheless, not all children exposed to RSV develop asthma symptoms, possibly because genes modulate the effects of RSV on asthma exacerbations.ObjectiveThe purpose of this study was to identify genes that modulate the effect of RSV latent infection on asthma exacerbations.MethodsWe performed a meta-analysis to investigate differentially expressed genes (DEGs) of RSV infection from Gene Expression Omnibus datasets. Expression quantitative trait loci (eQTL) methods were applied to select single nucleotide polymorphisms (SNPs) that were associated with DEGs. Gene-based analysis was used to identify SNPs that were significantly associated with asthma exacerbations in the Taiwanese Consortium of Childhood Asthma Study (TCCAS), and validation was attempted in an independent cohort, the Childhood Asthma Management Program (CAMP). Gene–RSV interaction analyses were performed to investigate the association between the interaction of SNPs and RSV latent infection on asthma exacerbations.ResultsA total of 352 significant DEGs were found by meta-analysis of RSV-related genes. We used 38 123 SNPs related to DEGs to investigate the genetic main effects on asthma exacerbations. We found that eight RSV-related genes (GADD45A, GYPB, MS4A3, NFE2, RNASE3, EPB41L3, CEACAM6 and CEACAM3) were significantly associated with asthma exacerbations in TCCAS and also validated in CAMP. In TCCAS, rs7251960 (CEACAM3) significantly modulated the effect of RSV latent infection on asthma exacerbations (false-discovery rate <0.05). The rs7251960 variant was associated with CEACAM3 mRNA expression in lung tissue (p for trend=1.2×10−7). CEACAM3 mRNA was reduced in nasal mucosa from subjects with asthma exacerbations in two independent datasets.Conclusionsrs7251960 is an eQTL for CEACAM3, and CEACAM3 mRNA expression is reduced in subjects experiencing asthma exacerbations. CEACAM3 may be a modulator of RSV latent infection on asthma exacerbations.


2007 ◽  
Vol 26 (8) ◽  
pp. 733-739 ◽  
Author(s):  
Eduardo G. P??rez-Yarza ◽  
Antonio Moreno ◽  
Pablo L??zaro ◽  
Asunci??n Mej??as ◽  
Octavio Ramilo

2013 ◽  
Vol 132 (1) ◽  
pp. 227-229 ◽  
Author(s):  
Kristina M. James ◽  
Tebeb Gebretsadik ◽  
Gabriel J. Escobar ◽  
Pingsheng Wu ◽  
Kecia N. Carroll ◽  
...  

Viruses ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 505 ◽  
Author(s):  
Carrie-Anne Malinczak ◽  
Nicholas W. Lukacs ◽  
Wendy Fonseca

Respiratory syncytial virus (RSV) is often the first clinically relevant pathogen encountered in life, with nearly all children infected by two years of age. Many studies have also linked early-life severe respiratory viral infection with more pathogenic immune responses later in life that lead to pulmonary diseases like childhood asthma. This phenomenon is thought to occur through long-term immune system alterations following early-life respiratory viral infection and may include local responses such as unresolved inflammation and/or direct structural or developmental modifications within the lung. Furthermore, systemic responses that could impact the bone marrow progenitors may be a significant cause of long-term alterations, through inflammatory mediators and shifts in metabolic profiles. Among these alterations may be changes in transcriptional and epigenetic programs that drive persistent modifications throughout life, leaving the immune system poised toward pathogenic responses upon secondary insult. This review will focus on early-life severe RSV infection and long-term alterations. Understanding these mechanisms will not only lead to better treatment options to limit initial RSV infection severity but also protect against the development of childhood asthma linked to severe respiratory viral infections.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yoshihiko Raita ◽  
Marcos Pérez-Losada ◽  
Robert J. Freishtat ◽  
Brennan Harmon ◽  
Jonathan M. Mansbach ◽  
...  

AbstractRespiratory syncytial virus (RSV) bronchiolitis is not only the leading cause of hospitalization in U.S. infants, but also a major risk factor for asthma development. While emerging evidence suggests clinical heterogeneity within RSV bronchiolitis, little is known about its biologically-distinct endotypes. Here, we integrated clinical, virus, airway microbiome (species-level), transcriptome, and metabolome data of 221 infants hospitalized with RSV bronchiolitis in a multicentre prospective cohort study. We identified four biologically- and clinically-meaningful endotypes: A) clinicalclassicmicrobiomeM. nonliquefaciensinflammationIFN-intermediate, B) clinicalatopicmicrobiomeS. pneumoniae/M. catarrhalisinflammationIFN-high, C) clinicalseveremicrobiomemixedinflammationIFN-low, and D) clinicalnon-atopicmicrobiomeM.catarrhalisinflammationIL-6. Particularly, compared with endotype A infants, endotype B infants—who are characterized by a high proportion of IgE sensitization and rhinovirus coinfection, S. pneumoniae/M. catarrhalis codominance, and high IFN-α and -γ response—had a significantly higher risk for developing asthma (9% vs. 38%; OR, 6.00: 95%CI, 2.08–21.9; P = 0.002). Our findings provide an evidence base for the early identification of high-risk children during a critical period of airway development.


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