Digital twins (DTs) in precision medicine are increasingly viable, propelled by extensive data collection and advancements in artificial intelligence (AI), alongside traditional biomedical methodologies. We argue that including mechanistic simulations that produce behavior based on explicitly defined biological hypotheses and multiscale mechanisms is beneficial. It enables the exploration of diverse therapeutic strategies and supports dynamic clinical decision-making through insights from network science, quantitative biology, and digital medicine.

In the field of heritage science, especially applied to buildings and artefacts made by organic hygroscopic materials, analyzing the microclimate has always been of extreme importance. In particular, in many cases, the knowledge of the outdoor/indoor microclimate may support the decision process in conservation and preservation matters of historic buildings. This knowledge is often gained by implementing long and time-consuming monitoring campaigns that allow collecting atmospheric and climatic data. Sometimes the collected time series may be corrupted, incomplete and/or subjected to the sensors' errors because of the remoteness of the historic building location, the natural aging of the sensor or the lack of a continuous check of the data downloading process. For this reason, in this work, an innovative approach about reconstructing the indoor microclimate into heritage buildings, just knowing the outdoor one, is proposed. This methodology is based on using machine learning tools known as variational auto encoders (VAEs), that are able to reconstruct time series and/or to fill data gaps. The proposed approach is implemented using data collected in Ringebu Stave Church, a Norwegian medieval wooden heritage building. Reconstructing a realistic time series, for the vast majority of the year period, of the natural internal climate of the Church has been successfully implemented. The novelty of this work is discussed in the framework of the existing literature. The work explores the potentials of machine learning tools compared to traditional ones, providing a method that is able to reliably fill missing data in time series.

Background: Climate change, urbanization, and global mobility increase the risk of emerging infectious diseases with pandemic potential. There is a need for rapid methods that can assess their long-term effects on human health. In silico approaches are particularly suited to study processes that may manifest years later, under the assumption that perturbed biomolecular interactions underlie these outcomes. Here we focus on viral oncogenicity—the ability of viruses to increase cancer risk—which accounts for about 15% of global cancer cases. Methods: We characterize viruses through multilayer representations of protein–protein interaction (PPI) networks reconstructed from the human interactome. Statistical analyses of topological features, combined with interpretable machine learning models, are used to distinguish oncogenic from non-oncogenic viruses and to identify proteins with potential central role in these processes. Results: Our analysis reveals clear statistical differences between the network properties of oncogenic and non-oncogenic viruses. Furthermore, the machine learning approach enables classification of virus–host interaction networks and identification of relevant subsets of proteins associated with oncogenesis. Functional enrichment analysis highlights mechanisms related to viral oncogenicity, including chromatin structure and other processes linked to cancer development. Conclusions: This framework enables virus classification and highlights mechanisms underlying viral oncogenicity, providing a foundation for investigating long-term health effects of emerging pathogens.

Climate change, increasing urbanization and global human mobility have increased the risk of emergent infectious diseases and the risk for their pandemic potential. Consequently, there is a pressing need for methods that can provide rapid insights about the potential enduring effects on the human hosts. In-silico methods can be more suitable than in-vitro and in-vivo methods to identify effects potentially manifesting after a long time, under the hypothesis that the underlying causes can be ascribed to perturbed biomolecular processes. Here we focus on oncogenicity, i.e., the risk of developing cancer subsequent to a viral infection, a phenomenon estimated to account for approximately 15 of global cancer prevalence. We characterize viruses in terms of their oncogenic potential by analyzing a multilayer representation of protein-protein interaction networks reconstructed from the human interactome. Our framework facilitates classification and allows us to identify sub-sets of proteins involved in oncogenesis, highlighting the mechanisms underpinning viral oncogenicity, including factors like chromatin structure. Our framework serves as a foundational resource for medical research, paving the way for the study of other potential long-term effects associated with emerging viruses.

Genomic instability is a major driver of tumor evolution, promoting diversification and adaptation while simultaneously increasing the accumulation of deleterious alterations. How tumor populations balance these opposing effects remains poorly understood. Here, we introduce a computational framework that explicitly represents diploid genomes, functional gene classes, point mutations, and chromosome-segregation errors in spatially constrained and well-mixed tumor populations. We identify a viability boundary separating sustained tumor expansion from instability-induced population collapse. Within the viable regime, mutation and selection generate a stable distribution of genomic-instability classes that is accurately captured by an analytical replicator--mutator description. Near the viability boundary, tumor dynamics exhibit prolonged extinction transients and strong sensitivity to stochastic fluctuations, with important differences between solid and liquid architectures. Chromosomal alterations further modify growth by creating transient benefits through increased gene dosage and genetic redundancy, while ultimately increasing genomic fragility. Finally, simulated interventions show that eliminating low-instability subpopulations or increasing the global mutational burden can displace tumors beyond their viability boundary and trigger irreversible collapse. These results identify genome instability as both an evolutionary advantage and an intrinsic vulnerability, providing a quantitative framework for developing therapies that exploit the limits of tumor evolution.