# Dengue Viral Infection Induces Alteration of CD95 Expression in B Cell Subsets with Potential Involvement of Dengue Viral Non-Structural Protein 1

**Authors:** Siyu Wang, Premrutai Thitilertdecha, Ladawan Khowawisetsut, Theeraporn Maneesawat, Ampaiwan Chuansumrit, Kulkanya Chokephaibulkit, Kovit Pattanapanyasat, Nattawat Onlamoon

PMC · DOI: 10.3390/v17040541 · 2025-04-08

## TL;DR

Dengue virus infection changes B cell subsets and increases CD95 expression, possibly through the virus's NS1 protein.

## Contribution

The study identifies NS1's role in inducing CD95 expression in B cell subsets during dengue infection.

## Key findings

- Tissue memory and antibody-secreting B cells increase in dengue patients.
- CD95 expression rises in most B cell subsets during dengue infection.
- DENV NS1 protein induces CD95 expression and membrane changes in B cells.

## Abstract

Little is known about the regulation of B cell subpopulations in association with programmed cell death during dengue virus (DENV) infection. Therefore, blood samples from dengue-infected patients and healthy donors were obtained for B cell subset characterization and the analysis of pro-apoptotic CD95 expression in these cell subsets. The results showed that the activated memory (AM) subset in the patients remained unchanged compared to the healthy donors. In contrast, tissue memory (TM) and antibody-secreting cells (ASCs) were notably increased, whereas naïve cells and resting memory (RM) cells were considerably decreased. Although the ASCs maintained comparably high levels of CD95 expression in both groups, significantly increased percentages of CD95-expressing cells in the other B cell subsets were found in the patients. When B cells from the healthy donors were treated with DENV non-structural protein 1 (NS1), the results showed that the NS1 protein at 2 µg/mL could induce CD95 expression and the exposure of phosphatidylserine on the cell membrane in most B cell subsets, except for the RM. This study demonstrates that DENV infection could induce CD95 expression in both activated and resting B cell subsets in all patients. The results also suggest a potential mechanism of apoptotic regulation in B cell subsets through the increased CD95 expression caused by the interaction between the B cells and the NS1 protein.

## Linked entities

- **Proteins:** FAS (Fas cell surface death receptor), PTPN11 (protein tyrosine phosphatase non-receptor type 11)
- **Diseases:** dengue virus infection (MONDO:0005502)

## Full-text entities

- **Genes:** FAS (Fas cell surface death receptor) [NCBI Gene 355] {aka ALPS1A, APO-1, APT1, CD95, FAS1, FASTM}, PTPN11 (protein tyrosine phosphatase non-receptor type 11) [NCBI Gene 5781] {aka BPTP3, CFC, JMML, METCDS, NS1, PTP-1D}
- **Diseases:** Dengue Viral Infection (MESH:D014777), DENV infection (MESH:D003715)
- **Species:** Dengue virus (no rank) [taxon 12637], Homo sapiens (human, species) [taxon 9606]

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12031515/full.md

---
Source: https://tomesphere.com/paper/PMC12031515