T helper type 2 bias and type 17 suppression in primary dengue virus infection in infants and young children

Trans R Soc Trop Med Hyg. 2013 Jul;107(7):411-9. doi: 10.1093/trstmh/trt044. Epub 2013 Jun 13.

Abstract

Background: The immune response to dengue virus (DENV) primary infection in infants and young children is not well characterized. In Northern Argentina, >90% of the population was DENV-naïve before the 2009 outbreak, allowing evaluation of age-dependent primary responses to infection.

Methods: We conducted a comparative study of the immune response to DENV in 27 infected infants, young children and their mothers. Lymphocyte T helper (Th) 1, Th2, Th17 and inflammatory responses were assayed in blood during the 2009 DENV-1 epidemic.

Results: The immune response to DENV-1 was significantly biased to Th2 in infected infants and young children, compared to infants with other febrile illnesses (for IL-4 p < 0.001) and to their infected mothers (for IL-4 p < 0.01). In addition, IL-17 suppression was observed in the memory response to DENV-1 in infected infants (p < 0.01 vs placebo).

Conclusion: Age-related differences in the primary response to DENV, characterized by an immature Th2 polarization and Th17 suppression in infants, should be studied further in order to expand our understanding of the mechanism of dengue pathogenesis.

Keywords: Dengue virus; Immune immaturity; Infant; Th2 polarization.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Antibodies, Neutralizing / blood
  • Antibodies, Viral / analysis
  • Argentina / epidemiology
  • Child, Preschool
  • Cytokines / immunology
  • Dengue / immunology*
  • Dengue Virus / immunology*
  • Epidemics
  • Female
  • Humans
  • Immunity, Cellular / immunology
  • Immunoglobulin G / blood
  • Infant
  • Infant, Newborn
  • Interleukin-17 / immunology*
  • Male
  • T-Lymphocytes, Helper-Inducer / immunology
  • Th2 Cells / immunology*

Substances

  • Antibodies, Neutralizing
  • Antibodies, Viral
  • Cytokines
  • Immunoglobulin G
  • Interleukin-17