ENTEROVIRUS-LINKED TYPE 1 DIABETES EXPOSED -MECHANISMS AND PREVENTION

Project Information

ENT1DEP

Grant agreement ID: 101137457

DOI

10.3030/101137457

EC signature date 7 December 2023

Start date 1 January 2024

End date 31 December 2027

Funded under

• Health

Total cost

€ 7 144 790,00

EU contribution

€ 7 144 790,00

Coordinated by

TAMPEREEN KORKEAKOULUSAATIO SR
Finland

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

Reporting period: 2024-01-01 to 2025-06-30

Summary of the context and overall objectives of the project

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.

Work performed from the beginning of the project to the end of the period covered by the report and main results achieved so far

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.

Progress beyond the state of the art and expected potential impact (including the socio-economic impact and the wider societal implications of the project so far)

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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