HBoV infections have been commonly diagnosed by PCR of respiratory tract samples. Only a few serologic studies have been reported; these studies have addressed mainly epidemiologic issues (11) (12) (13) (14) (15) . However, Endo et al. documented seroconversions by immunofluorescent analysis in 4 HBoV PCR-positive patients (12) , and Lindner et al. detected IgM against HBoV by EIA in 12 patients, 10 of whom were viremic children (15) . In a study of 117 wheezing children, we showed by using immunoblotting and prokaryotically expressed HBoV VP2 capsid antigens that HBoV infections can be diagnosed serologically (11) . We also showed that the unique region in VP1 is far less immunogenic than the major virus capsid protein VP2. We have now expressed HBoV VP2 VLPs in insect cells for use in IgM and IgG EIAs that are superior to immunoblots in diagnostic performance. We diagnosed acute primary HBoV infections in 48 (19%) of 258 children with expiratory wheezing. Consistent with other reports, no crossreactivity between 2 human pathogenic parvoviruses (B19 and HBoV), was detected (11) (12) (13) 15) . Prevalence rates of immunity increased with age from 5% in infants to >64% in children 2-4 years of age and continued to increase until a maximum of 100% was reached in children 7 years of age. Seroprevalence among young adults was 96%. Furthermore, IgG levels of adults were as diverse as those of children ( Figure 2 ). These results contrast sharply with our previous immunoblot results with denatured VP2 antigen (11) , which showed decreased seropositivity among children >2 years of age. This difference is likely caused by a time-related conformational dependence of the antibody, similar to immunity to B19 virus (18, 20, 22, 23) . In other HBoV seroprevalence studies, similar rates were reported (12, 13, 15) , which validate the accuracy of our results.