Published ahead of print on October 19, 2006, doi:10.1164/rccm.200603-435PP Am. J. Respir. Crit. Care Med., Volume 175, Number 2, January 2007, 108-119 A more recent version of this article appeared on January 15, 2007
Submitted on March 28, 2006 Bronchiolitis to Asthma:A Review and Call for Studies of Gene-Viral Interactions in Asthma CausationAnne Marie Singh1*,1 Department of Medicine, University of Wisconsin-Madison, Madison, WI, USA, 2 Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, TN, USA, 3 Department of Pediatrics, University of Wisconsin-Madison, Madison, WI, USA, 4 Department of Medicine, University of Wisconsin-Madison, Madison, WI, USA; Department of Pediatrics, University of Wisconsin-Madison, Madison, WI, USA, 5 Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA * To whom correspondence should be addressed. E-mail: am.singh{at}hosp.wisc.edu.
Viral infections are important causes of asthma exacerbations in children, and lower respiratory tract infections (LRTI), 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 following 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 following 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. Key words: asthma, bronchiolitis, genetics, RSV, RV
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