Publications by Year: 2026

Influenza A viruses (IAVs), particularly highly pathogenic avian influenza (HPAI) strains like H5N1 and H7N9, cause severe pneumonia and acute respiratory distress syndrome (ARDS) driven by dysregulated cytokine storms. A key mediator of this immunopathology is the excessive activation of the NLRP3 inflammasome, which governs the maturation of IL-1β. Galectin-3 (Gal3), a β-galactoside-binding lectin, is upregulated during infection; however, its specific regulatory role in coordinating NLRP3 inflammasome activation across distinct viral hemagglutinin (HA) subtypes remains to be elucidated. In this study, we demonstrate that Gal3 functions as a critical amplifier of influenza pathogenesis through a distinct dual-stage mechanism. Results from viral binding and internalization assays indicate that extracellular Gal3 promotes viral entry by interacting with viral HA, an effect that is strictly strain-dependent (H5N1 > H1N1 > H7N9). This enhanced entry consequently amplifies the initial signal for inflammasome activation. Intracellularly, Gal3 regulates the NLRP3 cascade by sustaining NF-κB activation (priming) to upregulate NLRP3 and pro-IL-1β transcription and acting as a facilitator to strengthen the NLRP3-ASC-pro-caspase-1 interaction, promoting ASC oligomerization (activation). Consistently, in vivo studies demonstrate that Gal3-deficient mice exhibit significantly improved survival, reduced weight loss, and attenuated pulmonary inflammation and IL-1β release following infection, with the most pronounced protective effects observed against H5N1. Collectively, these findings identify Gal3 as a potent host factor that orchestrates excessive inflammation by simultaneously facilitating viral entry and driving the assembly of the NLRP3 inflammasome, highlighting the Gal3-NLRP3 axis as a promising therapeutic target to mitigate severe influenza-induced lung injury.

Epstein-Barr virus (EBV) is a ubiquitous herpesvirus associated with a broad spectrum of malignancies and immune-mediated disorders, and growing evidence highlights the importance of host glycan-lectin interactions in shaping viral persistence and immune escape. Among these, galectins have emerged as key regulators of the EBV life cycle, influencing viral attachment, latency maintenance, lytic reactivation, and the remodeling of the tumor microenvironment. Galectin-1, -3, and -9 exhibit context-dependent functions that collectively modulate oncogenic signaling pathways, T‑cell exhaustion, regulatory T‑cell expansion, and innate immune sensing. Recent clinical studies further suggest that circulating galectins and galectin-enriched exosomes may serve as non-invasive biomarkers for disease progression and prognosis in EBV-associated malignancies. Despite these advances, major knowledge gaps remain regarding member-specific functions, compensatory galectin networks, and the spatiotemporal dynamics of galectin regulation during infection. Targeting the galectin-glycan axis therefore represents a promising frontier for host-directed antiviral and anticancer therapies, with the potential to disrupt viral latency, restore antiviral immunity, and improve clinical outcomes in EBV-driven diseases.

The recent mpox outbreaks in non-endemic countries highlight the urgent need for improved therapeutics and diagnostics. In this study, monoclonal antibodies (mAbs) targeting the mpox enveloped virion antigens A35 and B6 were transiently expressed in Nicotiana benthamiana using a geminiviral vector system. Following agroinfiltration, anti-A35 and anti-B6 mAbs accumulated to 27 µg/g fresh weight at 3 days and 260 µg/g at 7 days post-infiltration, respectively. SDS-PAGE and Western blot analyses confirmed the assembly of antibodies, and the purified antibodies bound to mpox-infected Vero cells. The neutralization assays demonstrated moderate reductions in viral infection under the tested conditions. Additionally, an electrochemical immunosensor demonstrated the ability of plant-produced antibodies to detect mpox virus through antigen-antibody binding induced current changes. These results support that the plant-based systems as rapid platforms for producing mpox-specific antibodies for diagnostics and antiviral research.

BACKGROUND: Taiwan, a region traditionally considered non-endemic for dengue, experienced an unexpected and large-scale outbreak in 2023. We investigated the multifactorial drivers of this outbreak, including cross-border viral importation, serotype cocirculation, vector ecology, and climate variability.

METHODS: We analyzed national dengue surveillance data (2013-2023), meteorological records, and Breteau Index (BI) values, alongside molecular serotyping and whole-genome sequencing of clinical isolates. Time-lagged Poisson regression was used to identify predictors of indigenous dengue transmission in Kaohsiung and Tainan. Full-genome comparisons were conducted between 2023 strains and historical epidemic isolates.

RESULTS: A total of 26 706 laboratory-confirmed cases were reported, primarily in Tainan (80.7%) and Kaohsiung (11.9%). Real-time RT-PCR identified cocirculating DENV-1 and DENV-2 strains. Phylogenetic analysis confirmed the 2023 DENV-1 and DENV-2 strains were genetically linked to contemporary strains from Southeast Asian countries. Whole-genome sequencing identified several nonsynonymous mutations in the NS2A, NS3, and NS5 regions when compared with historical outbreak isolates. Time-lagged regression showed that imported cases, precipitation, and the BI were associated with incidence in univariate models. In Kaohsiung, the best-fitting multivariable model included the BI, but temperature and precipitation were the independent predictors. In Tainan, precipitation and, at longer lags, imported cases were more influential, while the BI lost significance after adjustment.

CONCLUSIONS: The 2023 dengue outbreak in Taiwan was driven by a complex interplay between viral introductions, climatic conditions, and vector dynamics. The differing transmission drivers observed between cities highlight the need for region-specific vector surveillance, climate-informed early warning systems, and sustained genomic monitoring to prevent future re-emergence of dengue in this non-endemic setting.