Lower anti-echovirus antibody responses in children presenting to hospital with asthma exacerbations

J Iwasaki1, L Y Chai1, S-K Khoo1,2

  • 1Telethon Kids Institute, The University of Western Australia, Perth, WA, Australia.

Insights

Asthmatic children have lower antibody responses to gut-associated echoviruses but higher responses to respiratory rhinoviruses, suggesting a link between enterovirus immunity and asthma development. This indicates enteric infections may reduce asthma risk.

Area of Science:

  • Immunology
  • Virology
  • Pediatrics

Background:

  • Rhinoviruses (Enterovirus genus) induce high anticapsid antibodies in asthmatics.
  • Gut-trophic echoviruses show diminished neutralizing antibodies in asthmatics.
  • Enterovirus genus infections present differential antibody responses in asthmatics.

Purpose of the Study:

  • Assess antibody titres to echovirus 30 and poliovirus 1 VP1 antigens in asthmatic and non-asthmatic children.
  • Investigate the relationship between antibody titres and asthma status.
  • Examine correlations with total IgE levels and other immune responses.

Main Methods:

  • Produced recombinant VP1 capsid antigens for echovirus 30 and Sabin poliovirus 1.
  • Quantitated IgG1 antibody binding in plasma from asthmatic (n=45) and non-asthmatic (n=29) children.
  • Utilized immunoassays with immunoabsorptions to ensure specificity.

Main Results:

  • Asthmatic children had significantly lower IgG1 antibody titres to echovirus 30 (P < 0.05).
  • Echovirus 30 antibody titres inversely correlated with total IgE levels (r = -0.262; P < 0.05).
  • No significant differences in antibody titres to Sabin poliovirus 1 were observed between groups.

Conclusions:

  • Lower echovirus antibody titres in asthmatics, coupled with heightened rhinovirus response, suggest a dichotomy in enterovirus immunity and asthma risk.
  • Respiratory enterovirus infection may increase asthma probability, while enteric infections might lower the risk.
  • Supports the role of intestinal infections in allergic respiratory disease development.
Abstract

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