Cross sectional retrospective study of prevalence of atopy among Italian military students with antibodies against hepatitis a virus

Abstract

Objective: To investigate the working hypothesis that common infections occurring early in life prevent atopy. Design: Cross sectional, retrospective study of young Italian men with results for hepatitis A serology and atopy. Setting: Air force school for military students in

Asthma and atopy – the price of affluence?

“…In 1996, an inverse association between measles infection and atopy, defined by SPTs, was shown in a cohort of young adults in Guinea-Bissau (59), and in the next year, a similar inverse relationship between hepatitis A infection in childhood and occurrence of atopy, defined by SPTs and serum IgE antibodies, was found among Italian military cadets (60). Further, Japanese school children who responded positively to tuberculin, were found to have lower serum levels of total IgE and Th2 cytokines [interleukin (IL)-4, IL-10, IL-13], higher serum levels of IFN-c, and showed lower prevalence of atopy and asthma than children with a negative tuberculin test result (61).…”

“…The re-emergence of interest in microorganisms, not as initiators or inciters of asthma, but as protectors against atopic diseases, began finally after the publication of the three pioneer studies on the inverse association between childhood infections and the subsequent development of asthma and atopy (59)(60)(61).…”

Infections preventing atopy: facts and new questions

“…It is still not possible to answer this question, because the relations observed so far affected only the immune response to common airborne allergens in children or young adults (5)(6)(7).…”

Human TIM-1 Associates with the TCR Complex and Up-Regulates T Cell Activation Signals

“…Thus, the TAPR locus and TIM-1 have been linked to the development of atopic disease in both inbred mouse strains and in diverse human populations. The association of TIM-1 genetic variation with HAV seropositivity was particularly interesting, as rates of HAV infection and asthma have been inversely correlated (8), and TIM-1 has been identified as a receptor for HAV in primates (9). A recent analysis of human TIM-1 sequences identified a very high level of divergence in the mucin domain of TIM-1, suggesting that the gene was indeed subject to balancing selective pressure, as might be expected of a gene involved in both viral infectivity and disease susceptibility (10).…”