HealthDay News — Infants living in inner-city areas have different patterns of viral respiratory illness during the first year of life compared with babies living in suburban locations, which may help explain why they’re more likely to develop asthma, results from a prospective study suggest.

Infants with respiratory illnesses that resided in cities were more likely to be infected with adenoviruses (4.8% vs. 0.7%, P<0.001) than their suburban counterparts. In contrast, rhinoviruses — the most frequent cause of self-limited colds — were more prevalent among sick suburban infants (36% versus 24.1%, P<0.001), James E. Gern, MD, of the University of Wisconsin in Madison, and colleagues reported in the Journal of Infectious Diseases.

Adenoviruses are commonly accompanied by persistent respiratory symptoms, along with gastroenteritis and ocular infections, the researchers noted.

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“Adenovirus is of particular interest relative to long-term outcomes because acute infections can lead to viral shedding for weeks or months,” Gern and colleagues wrote. “Since both the immune system and the lungs are rapidly developing in infancy, chronic infections could influence these developmental processes, leading to long-term changes in lung and/or immune function.”

In an attempt to better understand the viral etiology of respiratory illnesses and how exposure to certain triggers — infectious, allergic, or environmental — contribute to asthma, the researchers compared findings from two birth cohort studies.

They analyzed specimens from participants in the Urban Environment and Childhood Asthma (URECA) study collected from 2005 to 2008, which included 515 infants from New York, Baltimore, St. Louis and Boston who had at least one parent with allergies or asthma.

The second study, the Childhood Origins of Asthma (COAST) study, involved specimens from 285 infants who lived in suburban Madison, Wis., and also had a parent with allergies or asthma. Specimens were collected from 1998 to 2001. Nasal secretions were sampled at age 1 year and during periods of respiratory illness, and parents were asked to fill out routine questionnaires about respiratory ailments every three months during the child’s first year

The researchers found significant differences among the two cohorts. In the URECA study, mothers were younger and had less education, the majority of participants had a household income lower than $15,000 and passive smoke exposure was more prevalent. More participants in the URECA study were black or Hispanic, and just one-quarter of infants were breastfed until age 3 months.

Among the urban cohort, several factors correlated with a greater number of respiratory illness. These included: other children in the home (r=0.20, P<0.001), mouse protein dust found in the child’s bedroom (r = 0.11, P=0.016), and eczema (r=0.10, P=0.03).

Exposure to secondhand smoke, dogs, cats or dust mites did not correlate with respiratory illness, the researchers found.

In the COAST group, infection with multiple viruses was more common than in the URECA group (25.3% vs. 18%, P=0.02), as was infection with respiratory syncytial virus (9.7% vs. 6.1%, P=0.07).

Infants from the URECA study had lower rates of viral detection overall (67.5% vs. 89.2%, P<0.001), possibly because respiratory illness in urban areas is more likely caused by bacterial infections or environmental triggers, the researchers noted.

Urban infants had higher rates of adenovirus infection, with a higher proportion of adenovirus-positive samples linked with illness at all four URECA study sites (10% to 21%) compared with Madison (6%). Among urban children with confirmed adenovirus, 80% had the virus detected on more than one occasion, with viral sequencing confirming infections were chronic rather than caused by different strains.

The study strengthens the hypothesis that interaction between viral respiratory infections and allergic inflammation play a role in asthma, Peter Heymann, MD, and Thomas A.E. Platts-Mills, MD, both of the University of Virginia in Charlottesville, wrote in an accompanying editorial.

“To what extent other environmental exposures can modulate this process will be easier to judge from these [cohorts] and other prospective studies, followed by intervention studies in the future,” they added.


  1. Gern J et al. J Infect Dis. 2012: doi: 10.1093/infdis/jis504.
  2. Heymann P, Platts-Mills T. J Infect Dis. 2012; doi:10.1093/infdis/jis507.