Biology subjects

Pieters, R.

Publications and source records attributed to Pieters, R..

2 recordsLinked to original sources

bioRxiv2026

Loss of hemagglutination ability by H3N2 influenza A virus, subclade K.

Seasonal human H3N2 influenza viruses, subclade K (J.2.4.1), have been the predominant influenza A viruses in the Northern hemisphere influenza season of 2025/2026. Since 2024, the vaccine virus A/Darwin/6/21 has emerged in different antigenic variants. Antigenic changes are frequently caused by amino acid substitutions near the hemagglutinin (HA) receptor-binding pocket, which can also affect receptor binding properties, such as hemagglutination. Hemagglutination is crucial for assessing antigenicity using the hemagglutination inhibition (HAI) assay, and a loss of binding to turkey erythrocytes could significantly hamper this process. In this study, we explored how substitutions in or around the HA receptor-binding site affect binding to glycans at the molecular level. We employed ELISA, glycan array, flow cytometry, hemagglutination assays, and tissue staining. Substitutions at positions 140, 192, and 223 establish clade J viruses that emerged in 2024. Computational analysis of HA in complex with an elongated glycan reveals that mutation F192 forms a CH-Pi interaction to stabilize the binding. Based on this background, substitutions in antigenic sites A and B within subclade K viruses exhibit a binding preference for elongated glycans, which are not displayed on turkey erythrocytes. Conversely, our previously established glyco-remodeled erythrocytes are efficiently bound by these subclade K H3N2 viruses and could support influenza surveillance and vaccine development.

microbiology↗

bioRxiv2025

Microplastics cross the murine intestine and induce inflammatory cell death after phagocytosis by human monocytes and neutrophils

Microplastics are contaminating the environment but also our food and drinking products. In a crucial study, microplastics have been detected in circulating human blood, urging the investigation of the effects of microplastics on human health. Here we aimed to determine the distribution of microplastics after oral exposure in mice and their interactions with and effects on mouse and human innate immune cells. We established that both 1 and 10m polystyrene (PS) particles penetrated the intestinal epithelium after oral administration and could be detected in blood and liver of mice after ten days of oral administration. Using intravital microscopy we captured the in vivo phagocytosis of 1m PS by mouse neutrophils in the liver. Pristine PS were barely phagocytosed by primary human phagocytes, however, 1 and 10{micro}m PS pre-incubated with plasma were readily phagocytosed by human neutrophils and monocytes. Plasma-coated 1 and 10m PS both increased human neutrophil and monocyte cell death but only after phagocytosis. Importantly, neutrophil cell death occurred a few hours after phagocytosing a single coated 10{micro}m PS while PS of 1{micro}m needed to be administered at a ratio of 27 particles per cell to induce significant neutrophil cell death. Neutrophil cell death upon microplastic exposure was characterized by extracellular DNA, which together with other released DAMPs can potentially trigger inflammation. Our findings suggest that microplastics could negatively impact the immune system and human health.

immunology↗