ENTEROVIRUS-LINKED TYPE 1 DIABETES EXPOSED -MECHANISMS AND PREVENTION

Información del proyecto

ENT1DEP

Identificador del acuerdo de subvención: 101137457

DOI

10.3030/101137457

Fecha de la firma de la CE 7 Diciembre 2023

Fecha de inicio 1 Enero 2024

Fecha de finalización 31 Diciembre 2027

Financiado con arreglo a

• Health

Coste total

€ 7 144 790,00

Aportación de la UE

€ 7 144 790,00

Coordinado por

TAMPEREEN KORKEAKOULUSAATIO SR
Finland

Periodic Reporting for period 1 - ENT1DEP (ENTEROVIRUS-LINKED TYPE 1 DIABETES EXPOSED -MECHANISMS AND PREVENTION)

Período documentado: 2024-01-01 hasta 2025-06-30

Resumen del contexto y de los objetivos generales del proyecto

Type 1 diabetes (T1D) is a chronic autoimmune disease with rising incidence, causing lifelong health burden and significant healthcare costs. Growing evidence indicates that certain virus infections, particularly enteroviruses (EVs), can trigger T1D in genetically susceptible individuals by damaging insulin-producing beta-cells. ENT1DEP addresses this critical unmet need by investigating the causal links between EV infections and T1D, aiming to enable early identification, preventive interventions, and the development of effective vaccines.

ENT1DEP combines epidemiology, virology, immunology, and translational research to generate robust evidence for preventing T1D. The project aims to: 1) determine the mechanisms by which EVs trigger autoimmune responses, 2) develop predictive biomarkers and AI-based models to identify children at high risk, and 3) evaluate vaccine and antiviral strategies in human trials and preclinical models. By linking infectious triggers to this chronic disease, ENT1DEP offers a paradigm shift from disease management to prevention, with potential long-term societal, economic, and public health benefits.

Trabajo realizado desde el comienzo del proyecto hasta el final del período abarcado por el informe y los principales resultados hasta la fecha

During the first project period, ENT1DEP established collaborative networks, optimized technologies, exchanged methodologies and successfully started the work. The key scientific achievements include:

• Demonstrating that stem-cell-derived pancreatic beta cells have a weaker innate immune response than alpha cells, providing mechanistic insight into why EV infections can precipitate T1D.
• Generating initial data from vaccine trials that help distinguish vaccine-induced immune responses from natural infection, informing future diagnostic assays.
• Developing AI-based prediction models and biomarker panels for early identification of high-risk children, providing tools for precision prevention.

In addition, the project has mapped approaches for risk identification and baseline disease progression, laying the groundwork for evaluating cost-effective preventive strategies, including vaccination. Coordinated efforts have maximized resource efficiency, while structured stakeholder engagement and ethical monitoring have strengthened public trust.

Avances que van más allá del estado de la técnica e impacto potencial esperado (incluida la repercusión socioeconómica y las implicaciones sociales más amplias del proyecto hasta la fecha)

ENT1DEP advances knowledge in several areas:

• Establishing mechanistic links between EV infections and T1D offers the first strong evidence of causality and opens the door for prevention.
• Innovative biomarkers, AI-based risk models, and early-phase vaccine and antiviral drug data provide tools for early intervention and precision prevention.
• Epidemiological and health-economic analyses highlight the potential for cost savings and reduced disease burden through targeted preventive strategies.

Further research and supportive frameworks are needed to enable broader implementation: regulatory approval pathways for vaccines, standardization of predictive tools, and integration of prevention into public health systems.

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