Quantitative and qualitative differences in anti-Envelope IgG-secreting cells distinguish subclinical and hospitalized dengue in a Cambodian pediatric cohort.

Authors

Amandine Trouchet, Sokchea Lay, Matteo Broketa, Pablo Canales-Herrerias, Angga Perima, Bruno Iannascoli, Sotheary Sann, Borita Heng, Sowath Ly, Veasna Duong, Gaël A Millot, Laura Walker, Patrick England, Giovanna Barba-Spaeth, Tineke Cantaert, Pierre Bruhns

Published in

PLoS pathogens. Volume 22. Issue 10. Pages e1014552. Oct 01, 2026. Epub Oct 01, 2026.

Abstract

Dengue virus (DENV) infection can result in outcomes ranging from subclinical disease to life-threatening illness, yet the antibody features mediating protection in humans remain poorly defined. Dengue virus envelope protein (E) forms homodimers on the virion surface and elicits both neutralizing and non-neutralizing antibodies from IgG-secreting cells (IgG-SC). How the developing antibody response at the monoclonal level contributes to protection is unknown. We profiled single IgG-SC responses in a Cambodian pediatric cohort by measuring affinity and serotype cross-reactivity of secreted antibodies from patients with subclinical or hospitalized dengue during acute DENV1 or DENV2 infection. Using droplet-based microfluidic imaging, we analyzed over 3,300 single IgG-SC. Hospitalized patients exhibited significantly lower numbers of IgG-SC, despite comparable IgG secretion rates and similar frequencies of DENV E-specific antibody-secreting cells relative to subclinical cases. In hospitalized patients, the affinity of IgG-SC for the DENV1 E-dimer was 3-fold lower compared to subclinical cases. Notably, antibodies recognizing quaternary epitopes-binding E-dimers but not monomers-were detected exclusively in subclinical cases, whereas hospitalized patients predominantly produced monomer-reactive antibodies. These findings suggest that dengue severity may be linked to the inefficient generation of sufficient numbers of high-affinity, broadly reactive antigen-specific IgG-SC during post-primary infection.

PMID:
42821608
Bibliographic data and abstract were imported from PubMed on 02 Oct 2026.

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