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Researcher profile

Viola Priesemann

Viola Priesemann contributes to research discovery and scholarly infrastructure.

ResearcherAffiliation not importedOpen to collaborate
Neurons and CognitionPopulations and Evolutionphysics.soc-phcond-mat.dis-nnApplicationsComputation and Languagemath.DSMultiagent Systemsnlin.AO

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Published work

10 published item(s)

preprint2026arXiv

Conformity Generates Collective Misalignment in AI Agents Societies

Artificial intelligence safety research focuses on aligning individual language models with human values, yet deployed AI systems increasingly operate as interacting populations where social influence may override individual alignment. Here we show that populations of individually aligned AI agents can be driven into stable misaligned states through conformity dynamics. Simulating opinion dynamics across nine large language models and one hundred opinion pairs, we find that each agent's behavior is governed by two competing forces: a tendency to follow the majority and an intrinsic bias toward specific positions. Using tools from statistical physics, we derive a quantitative theory that predicts when populations become trapped in long-lived misaligned configurations, and identifies predictable tipping points where small numbers of adversarial agents can irreversibly shift population-level alignment even after manipulation ceases. These results demonstrate that individual-level alignment provides no guarantee of collective safety, calling for evaluation frameworks that account for emergent behavior in AI populations.

0 citations0 reviewsNo code linkedOpen access
preprint2023arXiv

Impact of the Euro 2020 championship on the spread of COVID-19

Large-scale events like the UEFA Euro~2020 football (soccer) championship offer a unique opportunity to quantify the impact of gatherings on the spread of COVID-19, as the number and dates of matches played by participating countries resembles a randomized study. Using Bayesian modeling and the gender imbalance in COVID-19 data, we attribute 840,000 (95% CI: [0.39M, 1.26M]) COVID-19 cases across 12 countries to the championship. The impact depends non-linearly on the initial incidence, the reproduction number $R$, and the number of matches played. The strongest effects are seen in Scotland and England, where as much as 10,000 primary cases per million inhabitants occur from championship-related gatherings. The average match-induced increase in $R$ was 0.46 [0.18, 0.75] on match days, but important matches caused an increase as large as +3. Altogether, our results provide quantitative insights that help judge and mitigate the impact of large-scale events on pandemic spread.

0 citations0 reviewsNo code linkedOpen access
preprint2023arXiv

Model-based assessment of sampling protocols for infectious disease genomic surveillance

Genomic surveillance of infectious diseases allows monitoring circulating and emerging variants and quantifying their epidemic potential. However, due to the high costs associated with genomic sequencing, only a limited number of samples can be analysed. Thus, it is critical to understand how sampling impacts the information generated. Here, we combine a compartmental model for the spread of COVID-19 (distinguishing several SARS-CoV-2 variants) with different sampling strategies to assess their impact on genomic surveillance. In particular, we compare adaptive sampling, i.e., dynamically reallocating resources between screening at points of entry and inside communities, and constant sampling, i.e., assigning fixed resources to the two locations. We show that adaptive sampling uncovers new variants up to five weeks earlier than constant sampling, significantly reducing detection delays and estimation errors. This advantage is most prominent at low sequencing rates. Although increasing the sequencing rate has a similar effect, the marginal benefits of doing so may not always justify the associated costs. Consequently, it is convenient for countries with comparatively few resources to operate at lower sequencing rates, thereby profiting the most from adaptive sampling. Finally, our methodology can be readily adapted to study undersampling in other dynamical systems.

0 citations0 reviewsNo code linkedOpen access
preprint2022arXiv

Autocorrelations from emergent bistability in homeostatic spiking neural networks on neuromorphic hardware

A unique feature of neuromorphic computing is that memory is an implicit part of processing through traces of past information in the system's collective dynamics. The extent of memory about past inputs is commonly quantified by the autocorrelation time of collective dynamics. Based on past experimental evidence, a potential explanation for the underlying autocorrelations are close-to-critical fluctuations. Here, we show for self-organized networks of excitatory and inhibitory leaky integrate-and-fire neurons that autocorrelations can originate from emergent bistability upon reducing external input strength. We identify the bistability as a fluctuation-induced stochastic switching between metastable active and quiescent states in the vicinity of a non-equilibrium phase transition. This bistability occurs for networks with fixed heterogeneous weights as a consequence of homeostatic self-organization during development. Specifically, in our experiments on neuromorphic hardware and in computer simulations, the emergent bistability gives rise to autocorrelation times exceeding 500 ms despite single-neuron timescales of only 20 ms. Our results provide the first verification of biologically compatible autocorrelation times in networks of leaky integrate-and-fire neurons, which here are not generated by close-to-critical fluctuations but by emergent bistability in homeostatically regulated networks. Our results thereby constitute a new, complementary mechanism for emergent autocorrelations in networks of spiking neurons, with implications for biological and artificial networks, and introduces the general paradigm of fluctuation-induced bistability for driven systems with absorbing states.

0 citations0 reviewsNo code linkedOpen access
preprint2022arXiv

Interplay between risk perception, behaviour, and COVID-19 spread

Pharmaceutical and non-pharmaceutical interventions (NPIs) have been crucial for controlling COVID-19. They are complemented by voluntary health-protective behaviour, building a complex interplay between risk perception, behaviour, and disease spread. We studied how voluntary health-protective behaviour and vaccination willingness impact the long-term dynamics. We analysed how different levels of mandatory NPIs determine how individuals use their leeway for voluntary actions. If mandatory NPIs are too weak, COVID-19 incidence will surge, implying high morbidity and mortality before individuals react; if they are too strong, one expects a rebound wave once restrictions are lifted, challenging the transition to endemicity. Conversely, moderate mandatory NPIs give individuals time and room to adapt their level of caution, mitigating disease spread effectively. When complemented with high vaccination rates, this also offers a robust way to limit the impacts of the Omicron variant of concern. Altogether, our work highlights the importance of appropriate mandatory NPIs to maximise the impact of individual voluntary actions in pandemic control.

0 citations0 reviewsNo code linkedOpen access
preprint2022arXiv

Intrinsic timescales of spiking activity in humans during wakefulness and sleep

Information processing in the brain requires integration of information over time. Such an integration can be achieved if signals are maintained in the network activity for the required period, as quantified by the intrinsic timescale. While short timescales are considered beneficial for fast responses to stimuli, long timescales facilitate information storage and integration. We quantified intrinsic timescales from spiking activity in the medial temporal lobe of humans. We found extended and highly diverse timescales ranging from tens to hundreds of milliseconds, though with no evidence for differences between subareas. Notably, however, timescales differed between sleep stages and were longest during slow wave sleep. This supports the hypothesis that intrinsic timescales are a central mechanism to tune networks to the requirements of different tasks and cognitive states.

0 citations0 reviewsNo code linkedOpen access
preprint2020arXiv

Characterizing spreading dynamics of subsampled systems with non-stationary external input

Many systems with propagation dynamics, such as spike propagation in neural networks and spreading of infectious diseases, can be approximated by autoregressive models. The estimation of model parameters can be complicated by the experimental limitation that one observes only a fraction of the system (subsampling) and potentially time-dependent parameters, leading to incorrect estimates. We show analytically how to overcome the subsampling bias when estimating the propagation rate for systems with certain non-stationary external input. This approach is readily applicable to trial-based experimental setups and seasonal fluctuations, as demonstrated on spike recordings from monkey prefrontal cortex and spreading of norovirus and measles.

0 citations0 reviewsNo code linkedOpen access
preprint2020arXiv

The challenges of containing SARS-CoV-2 via test-trace-and-isolate

Without a cure, vaccine, or proven long-term immunity against SARS-CoV-2, test-trace-and-isolate (TTI) strategies present a promising tool to contain its spread. For any TTI strategy, however, mitigation is challenged by pre- and asymptomatic transmission, TTI-avoiders, and undetected spreaders, who strongly contribute to hidden infection chains. Here, we studied a semi-analytical model and identified two tipping points between controlled and uncontrolled spread: (1) the behavior-driven reproduction number of the hidden chains becomes too large to be compensated by the TTI capabilities, and (2) the number of new infections exceeds the tracing capacity. Both trigger a self-accelerating spread. We investigated how these tipping points depend on challenges like limited cooperation, missing contacts, and imperfect isolation. Our model results suggest that TTI alone is insufficient to contain an otherwise unhindered spread of SARS-CoV-2, implying that complementary measures like social distancing and improved hygiene remain necessary.

0 citations0 reviewsNo code linkedOpen access
preprint2019arXiv

Description of spreading dynamics by microscopic network models and macroscopic branching processes can differ due to coalescence

Spreading processes are conventionally monitored on a macroscopic level by counting the number of incidences over time. The spreading process can then be modeled either on the microscopic level, assuming an underlying interaction network, or directly on the macroscopic level, assuming that microscopic contributions are negligible. The macroscopic characteristics of both descriptions are commonly assumed to be identical. In this work, we show that these characteristics of microscopic and macroscopic descriptions can be different due to coalescence, i.e., a node being activated at the same time by multiple sources. In particular, we consider a (microscopic) branching network (probabilistic cellular automaton) with annealed connectivity disorder, record the macroscopic activity, and then approximate this activity by a (macroscopic) branching process. In this framework, we analytically calculate the effect of coalescence on the collective dynamics. We show that coalescence leads to a universal non-linear scaling function for the conditional expectation value of successive network activity. This allows us to quantify the difference between the microscopic model parameter and established macroscopic estimates. To overcome this difference, we propose a non-linear estimator that correctly infers the model branching parameter for all system sizes.

0 citations0 reviewsNo code linkedOpen access
preprint2019arXiv

Tailored ensembles of neural networks optimize sensitivity to stimulus statistics

The dynamic range of stimulus processing in living organisms is much larger than a single neural network can explain. For a generic, tunable spiking network we derive that while the dynamic range is maximal at criticality, the interval of discriminable intensities is very similar for any network tuning due to coalescence. Compensating coalescence enables adaptation of discriminable intervals. Thus, we can tailor an ensemble of networks optimized to the distribution of stimulus intensities, e.g., extending the dynamic range arbitrarily. We discuss potential applications in machine learning.

0 citations0 reviewsNo code linkedOpen access