Authors:
Iwasaki J, Chai LY, Khoo SK, Bizzintino J, Laing IA, Le Souëf PN, Thomas WR, Hales BJ,
Authors notes:
Clin Exp Allergy. 2015;45(10):1523-30.
Keywords:
Asthma, Children, Echovirus, Enteroviruses, IgG1 antibody, Poliovirus, Rhinovirus, VP1
Abstract:
Background: Rhinoviruses from the Enterovirus genus cause frequent infections and induce remarkably high titres of anticapsid antigen antibodies in asthmatics, while the prevalence of neutralising antibodies to the gut-trophic echoviruses from the same genus is diminished.
Objective: To assess the absolute and specific antibody titres to VP1 antigens of the gut-trophic enteroviruses, echovirus 30 and Sabin 1 poliovirus, in asthmatic and non-asthmatic children.
Methods: Recombinant polypeptides representing the VP1 capsid antigens of echovirus 30 and Sabin poliovirus 1 were produced.
Their ability to bind IgG1 antibodies from the plasma of asthmatic and non-asthmatic children were quantitated by immunoassays that incorporated immunoabsorptions to remove cross-reactivity.
Results: The IgG1 antibody titres and prevalence of antibody binding to echovirus 30 were significantly lower for asthmatic children compared to controls and inversely correlated with total IgE levels for the whole study population.
There was no difference in the prevalence and titre between groups to the VP1 antigen of Sabin poliovirus.
Anti-tetanus toxoid titres measured for comparison did not correlate with anti-echovirus or poliovirus, but correlated with anti-rhinovirus titres in controls but not asthmatics, where the titres were higher for the asthmatic group.
Conclusions and Clinical Relevance: The associations of lower antibody titres of asthmatic children to echovirus reported here and those of our previous findings of a heightened response to rhinovirus suggest a dichotomy where respiratory enterovirus infection/immunity increases the probability of developing asthma and enteric infections lower the risk.
This provides further support for the concept of intestinal infection playing a key role in the development of allergic respiratory disease.