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Objective: The relationship between Chlamydia pneumoniae (Cpn) infection and arterial measures of preclinical atherosclerosis has remained controversial. Because atherogenesis begins in early life, we examined whether carotid and aortic intima-media thickness (IMT) and brachial artery endothelial function are associated with Cpn seropositivity in children., Methods and Results: Cpn-specific IgG and IgA antibodies were assessed by enzyme immunoassay in 199 healthy children followed-up annually from 7 to 11 years of age. Carotid (cIMT) and aortic IMT (aIMT), and brachial artery flow-mediated dilatation (FMD) were measured in 137 of the 199 children at the age of 11 years using high-resolution ultrasound. Children with persistent IgG and/or IgA seropositivity to Cpn had significantly increased aIMT compared with seronegative children (IgG< or =45 and IgA< or =12 enzyme immunounits) or children with transient Cpn seropositivity (seronegative, 0.496 [0.054]; transient, 0.494 [0.061]; and persistent, 0.532 [0.086] mm; P<0.05 for trend). This trend was not explained by traditional atherosclerotic risk factors or pubertal stage. cIMT and FMD were not associated with Cpn seropositivity., Conclusions: Eleven-year-old children with persistent Cpn seropositivity show increased aIMT but not cIMT, suggesting that Cpn may affect the aortic wall, the site where the earliest atherosclerotic lesions are known to occur, in otherwise healthy children.

Objective: Chronic Chlamydia pneumoniae (Cpn), Helicobacter pylori (Hp), and herpes virus infections have been associated with atherogenic serum lipid profile and an excess of cardiovascular events in adults. Because mechanisms leading to atherosclerosis are active since early childhood, we examined whether Cpn, Hp, or cytomegalovirus (CMV) seropositivity relates to serum lipid, lipoprotein, or apolipoprotein concentrations in children. We also looked for factors increasing probability of Cpn seropositivity in children., Methods and Results: Cpn-specific IgG and IgA, as well as Hp-specific and CMV-specific IgG antibodies were assessed by enzyme immunoassay in 199 apparently healthy children, followed-up from 7 to 11 years of age. Serum lipid profiles were studied at the ages of 7, 9, and 11 years using standard methods. Neither seroconversion to Cpn IgG or IgA antibody positivity nor persistent seropositivity for Cpn, Hp, or CMV was associated with proatherogenic serum lipid values. Children with siblings were more likely to possess Cpn antibodies than children without siblings (IgG: OR, 5.24; 95% CI, 1.63 to 16.82; IgA: OR, 3.32; 95% CI, 1.15 to 9.57)., Conclusions: These data suggest that contrary to the observations in adults, Cpn, Hp, and CMV seropositivity in otherwise healthy children is not associated with disturbances in serum lipid profile.

Islet-like cell clusters (ICCs) prepared from human fetal pancreases were infected with mumps or coxsackie B3 virus. Double-labeled antibody technique showed that the viruses infected both insulin-secreting and other pancreatic cells and that secretion of immunoreactive insulin into the culture medium of the mumps virus-infected cells had already ceased on day 7. The mumps virus-infected ICC clusters produced virus for 14 days, and the mumps virus antigen was detected in the ICCs through the whole 22-day observation period. The coxsackie B3 virus-infected ICCs contained cells highly positive for viral antigen during the first 2 days after infection, and the infectious virus was detected in the culture medium for 22 days. This in vitro model indicates that mumps and coxsackie B3 viruses infect human fetal pancreatic endocrine cells and are able to alter beta-cell function. Coxsackie B3 virus infection in ICCs is lytical and seems to lead to rapid cell destruction, but long-lasting, restricted mumps virus infection in human fetal pancreatic ICCs offers an interesting model to study the effects of viral infection in the endocrine pancreas and beta cell.