Comparison of the etiology of viral respiratory illnesses in inner-city and suburban infants

James E Gern, Tressa Pappas, Cynthia M Visness, Katy F Jaffee, Robert F Lemanske, Alkis Togias, Gordon R Bloomberg, William W Cruikshank, Carin Lamm, Marina Tuzova, Robert A Wood, Wai Ming Lee, James E Gern, Tressa Pappas, Cynthia M Visness, Katy F Jaffee, Robert F Lemanske, Alkis Togias, Gordon R Bloomberg, William W Cruikshank, Carin Lamm, Marina Tuzova, Robert A Wood, Wai Ming Lee

Abstract

Background: The risk of developing childhood asthma has been linked to the severity and etiology of viral respiratory illnesses in early childhood. Since inner-city infants have unique environmental exposures, we hypothesized that patterns of respiratory viral infections would also be distinct.

Methods: We compared the viral etiology of respiratory illnesses in 2 groups: a cohort of 515 infants from 4 inner-city areas and a cohort of 285 infants from mainly suburban Madison, Wisconsin. Nasal secretions were sampled during periods of respiratory illness and at 1 year of age and were analyzed for viral pathogens by multiplex polymerase chain reaction.

Results: Overall, inner-city infants had lower rates of viral detection. Considering specific viruses, sick urban infants had lower rates of detectable rhinovirus or respiratory syncytial virus infection and higher rates of adenovirus infection. Every urban site had a higher proportion of adenovirus-positive samples associated with illnesses (10%-21%), compared with Madison (6%).

Conclusions: These findings provide evidence that inner-city babies have different patterns of viral respiratory illnesses than babies who grow up in a more suburban location. These findings raise important questions about the etiology of virus-negative illnesses in urban infants and the possibility of long-term consequences of early life infections with adenovirus in this population.

Figures

Figure 1.
Figure 1.
Predictors for the frequency of respiratory illnesses in 515 Urban Environment and Childhood Asthma study participants. Abbreviation: IgE, immunoglobulin E.
Figure 2.
Figure 2.
Rates of virus detection in the Childhood Origins of Asthma (COAST) and Urban Environment and Childhood Asthma (URECA) studies, according to symptom severity (see Materials and Methods for a discussion of this metric). The graphs include data from 656 specimens from URECA participants and 823 from COAST participants and depict differences in virus detection rates, according to severity of illness, for all viruses (A; P < .001), human rhinovirus (HRV; B; P < .001), respiratory syncytial virus (RSV; C; P = .14), and multiple viruses (D; P = .05). P values indicate overall differences between viral detection in the URECA and COAST studies. Abbreviation: Mod, moderate.
Figure 3.
Figure 3.
Study-specific detection of adenovirus according to symptom severity. The graphs include data on 656 specimens from Urban Environment and Childhood Asthma (URECA) participants and 823 from Childhood Origins of Asthma (COAST) participants and illustrate the frequency of adenovirus infections in the COAST (A) and URECA (B) populations. There were significant population-related differences in the rates of adenovirus infections as a solitary pathogen when averaged across severity (P =.002) and of adenovirus detected together with at least 1 other viral infection (P < .001).
Figure 4.
Figure 4.
Site-specific rates of adenovirus detection during respiratory illnesses (symptom score, ≥5; see Materials and Methods for a discussion of this metric) in 295 samples from ill children in the Urban Environment and Childhood Asthma cohort and 586 samples from ill children in the Childhood Origins of Asthma cohort. Abbreviation: NYC, New York City.

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