Risk of childhood asthma following infant bronchiolitis during the respiratory syncytial virus season

James, Kristina; Gebretsadik, Tebeb; Escobar, Gabriel J.; Wu, Pingsheng; Carroll, Kecia N.; Li, Sherian Xu; Walsh, Eileen M.; Mitchel, Edward F.; Sloan, Chantel D.; Hartert, Tina V.

doi:10.1016/j.jaci.2013.01.009

Cited by 75 publications

(67 citation statements)

References 14 publications

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“…Prospective follow-up is needed to determine the long-term outcomes of children with EV-D68 infection. Due to the severity of infection and bronchospasm symptoms, we hypothesize that in young children, EV-D68 may subsequently be associated with the development of asthma, similar to other respiratory viruses [43].…”

Section: Discussionmentioning

confidence: 99%

Severe enterovirus 68 respiratory illness in children requiring intensive care management

Schuster¹,

Miller²,

Selvarangan³

et al. 2015

Journal of Clinical Virology

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Section: Discussionmentioning

confidence: 99%

Severe enterovirus 68 respiratory illness in children requiring intensive care management

Schuster¹,

Miller²,

Selvarangan³

et al. 2015

Journal of Clinical Virology

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“…In support of a causal role for allergic sensitization in asthma inception, a sequential relationship of allergic sensitization preceding virusinduced wheezing in preschool children has been identified (14). A "dosedependent" relationship between allergic sensitization and asthma has been identified, with greater degrees of allergic sensitization (increased numbers of allergens and increased level of allergen-specific IgE) conferring much greater risk for asthma inception and severe exacerbations (15,16 (17,18). Further, animal studies provide evidence for a mechanism through which RSV may cause asthma (19).…”

Section: Host and Environment Interactions In Asthma Inceptionmentioning

confidence: 99%

Asthma: NHLBI Workshop on the Primary Prevention of Chronic Lung Diseases

et al. 2014

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Asthma is a common disease with enormous public health costs, and its primary prevention is an ambitious and important goal. Understanding of how host and environmental factors interact to cause asthma is incomplete, but persistent questions about mechanisms should not stop clinical research efforts aimed at reducing the prevalence of childhood asthma. Achieving the goal of primary prevention of asthma will involve integrated and parallel sets of research activities in which mechanism-oriented studies of asthma inception proceed alongside clinical intervention studies to test biologically plausible prevention ideas. For example, continued research is needed, particularly in young children, to uncover biomarkers that identify asthma risk and provide potential targets of intervention, and to improve understanding of the role of microbial factors in asthma risk and disease initiation. In terms of clinical trials that could be initiated now or in the near future, we recommend three interventions for testing: (1) preventing asthma through prophylaxis against respiratory syncytial virus and human rhinovirus infections of the airway; (2) immune modulation, using prebiotics, probiotics, and bacterial lysates; and (3) prevention of allergen sensitization and allergic inflammation, using anti-IgE. These interventions should be tested while other, more universal prevention measures that may promote lung health are also investigated. These potential universal lung health measures include prevention of preterm delivery; reduced exposure of the fetus and young infant to environmental pollutants, including tobacco smoke; prevention of maternal and child obesity; and management of psychosocial stress.

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“…The prevalence of RV in infants with LRTI is approximately 20 to 30% (77). Although the odds of developing asthma after RV LRTI are higher in most studies than for RSV LRTI, RSV LRTI in the first year of life is significantly more common and therefore, if causal, may be responsible for a greater proportion of asthma that develops in children with RSV compared with RV (73,82,109). Thus, the phenotype of asthma after infant RSV LRTI accounts for up to 31% of early childhood asthma, with a population-attributable risk estimated at about 13% in several diverse populations (80,109).…”

Section: The Contribution Of Early-life Infection To Asthmamentioning

confidence: 99%

Toward Primary Prevention of Asthma. Reviewing the Evidence for Early-Life Respiratory Viral Infections as Modifiable Risk Factors to Prevent Childhood Asthma

Feldman

Moore

et al. 2015

Am J Respir Crit Care Med

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173

172

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A first step in primary disease prevention is identifying common, modifiable risk factors that contribute to a significant proportion of disease development. Infant respiratory viral infection and childhood asthma are the most common acute and chronic diseases of childhood, respectively. Common clinical features and links between these diseases have long been recognized, with early-life respiratory syncytial virus (RSV) and rhinovirus (RV) lower respiratory tract infections (LRTIs) being strongly associated with increased asthma risk. However, there has long been debate over the role of these respiratory viruses in asthma inception. In this article, we systematically review the evidence linking early-life RSV and RV LRTIs with asthma inception and whether they could therefore be targets for primary prevention efforts.

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Risk of childhood asthma following infant bronchiolitis during the respiratory syncytial virus season

Cited by 75 publications

References 14 publications

Severe enterovirus 68 respiratory illness in children requiring intensive care management

Severe enterovirus 68 respiratory illness in children requiring intensive care management

Asthma: NHLBI Workshop on the Primary Prevention of Chronic Lung Diseases

Toward Primary Prevention of Asthma. Reviewing the Evidence for Early-Life Respiratory Viral Infections as Modifiable Risk Factors to Prevent Childhood Asthma

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