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Published on: December 10, 2013
Bronchiolitis to asthma: a review and call for studies of gene-virus interactions in asthma causation
Anne Marie Singh1, Paul E Moore, James E Gern
1Department of Medicine, University of Wisconsin-Madison, Madison, WI 53792, USA. am.singh@hosp.wisc.edu
Insights
Viral infections like RSV and RV can cause severe respiratory illness in infants, increasing their risk for childhood asthma. Understanding host and virus factors is key to preventing asthma development after these infections.
Area of Science:
- Pediatric respiratory infections
- Asthma pathogenesis
- Viral immunology
Background:
- Viral lower respiratory tract infections (LRTIs), including bronchiolitis caused by respiratory syncytial virus (RSV) and rhinovirus (RV), are common in infants.
- Infants hospitalized for bronchiolitis have a higher risk of developing recurrent wheezing and childhood asthma.
- Previous research primarily focused on RSV, but other viruses like RV may also play a role in post-bronchiolitis asthma development.
Purpose of the Study:
- To investigate the relationship between viral bronchiolitis and subsequent asthma development.
- To explore the roles of host genetic factors and virus-specific properties in determining bronchiolitis severity and asthma risk.
- To clarify whether viral LRTIs cause asthma or if pre-existing asthma susceptibility leads to severe LRTI.
Main Methods:
- Review of recent studies on viral bronchiolitis and asthma incidence.
- Analysis of host (genetic) and virus (environmental) factors influencing LRTI severity.
- Evaluation of genetic susceptibility loci associated with asthma after viral bronchiolitis.
Main Results:
- The contribution of various respiratory viruses, including RV, to asthma development after bronchiolitis is under investigation.
- Genetic susceptibility and virus-specific properties are emerging as important determinants of bronchiolitis severity and asthma risk.
- The interplay between host genetics and viral infections in the context of asthma is a critical area requiring further research.
Conclusions:
- Clarifying the roles of host and viral factors in severe LRTIs is essential for understanding asthma causation.
- Identifying at-risk infants may allow for interventions to prevent or delay asthma development.
- Further research is needed to elucidate the causal pathways between viral bronchiolitis and childhood asthma.
Abstract:
Viral infections are important causes of asthma exacerbations in children, and lower respiratory tract infections (LRTIs), caused by viruses such as respiratory syncytial virus (RSV) and rhinovirus (RV), are a leading cause of bronchiolitis in infants. Infants hospitalized with bronchiolitis are at significantly increased risk for both recurrent wheezing and childhood asthma. To date, studies addressing the incidence of asthma after bronchiolitis severe enough to warrant hospitalization have focused almost exclusively on RSV, but a number of recent studies suggest that other respiratory pathogens, including RV, may contribute as well. It is not known whether viral bronchiolitis directly contributes to asthma causation or simply identifies infants at risk for subsequent wheezing, as from an atopic predisposition or preexisting abnormal lung function. Alternatively, the properties of the infecting virus may be important. Thus, many possible determinants exist that may contribute to the severity of bronchiolitis and the subsequent development of asthma. One such determinant is the potential involvement of genetic susceptibility loci to asthma after viral bronchiolitis, a critical area that is just beginning to be evaluated. By clarifying the roles of both host- (genetic) and virus- (environment) specific factors that contribute to the frequency and severity of viral LRTI, it may be possible to determine if severe LRTIs cause asthma, or if asthma susceptibility predisposes patients to severe LRTI in response to viral infection. Characterizing these relationships offers the potential of identifying at-risk hosts in whom preventing or delaying infection could alter the phenotypic expression of asthma.
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