ArticleJournal of virology2026
Molecular and biophysical requirements for B cell receptor-dependent enhancement of dengue virus infection.
Article in Journal of virology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Dengue virus (DENV) is the causative agent of dengue, a mosquito-borne disease that represents a significant and growing public health burden around the world. A unique pathophysiological feature of dengue is immune-mediated enhancement, wherein preexisting immunity elicited by a primary infection can enhance the severity of a subsequent infection by a heterologous DENV serotype. A leading mechanistic explanation for this phenomenon is antibody-dependent enhancement (ADE), where sub-neutralizing concentrations of DENV-specific IgG antibodies facilitate the entry of DENV into FcγR-expressing cells. Accordingly, this model posits that phagocytic mononuclear cells are the primary reservoir of DENV. However, multiple independent groups have shown that B cells are the largest reservoir of virally infected cells in circulation during acute dengue, representing a disconnect in our understanding of immune-mediated DENV tropism. In response to this persistent knowledge gap, our team has previously identified a novel mechanism of immune-mediated enhancement we have termed B cell receptor (BCR)-dependent enhancement (BDE) of DENV infection. In this study, we show that DENV infection of DENV-reactive B cells is highly sensitive to BCR/DENV envelope (E) protein interactions. DENV entry into this subset of B cells is dynamin-mediated, requires proximal BCR signaling, and involves localization to late endosomes. Finally, we show that immortalized DENV-reactive B cells are productively infected by live DENV, capable of supporting active viral replication of all four serotypes. We propose that BDE provides an additional layer of pathogen-specific immune-mediated infection risk that complements existing models of ADE and offers additional insight into potential mechanisms of DENV immunopathogenesis.IMPORTANCEThis study provides mechanistic insight into the process of B cell receptor (BCR)-dependent enhancement of dengue virus (DENV) infection. Immune-mediated enhancement of infection is a cornerstone of dengue immunopathogenesis and is most often attributed to antibody-dependent enhancement (ADE). BCR-dependent enhancement of DENV infection is an alternative and complementary mechanism for immune-mediated enhancement that addresses several persistent knowledge gaps in the dengue field and may offer mechanistic insight into why some people progress to severe dengue after infection.
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