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Harnessing Artificial Intelligence to Fight Infectious Diseases
Charlene Lancaster speaks with Cesar de la Fuente about using artificial intelligence to discover novel antibiotics from organisms and genetic sources spanning spiders, archaea, woolly mammoths, and humans.
Prosocial Learning and Motivation across the Lifespan
2024 BACN Early-Career Prize Lecture Many of our decisions affect other people. Our choices can decelerate climate change, stop the spread of infectious diseases, and directly help or harm others. Prosocial behaviours – decisions that help others – could contribute to reducing the impact of these challenges, yet their computational and neural mechanisms remain poorly understood. I will present recent work that examines prosocial motivation, how willing we are to incur costs to help others, prosocial learning, how we learn from the outcomes of our choices when they affect other people, and prosocial preferences, our self-reports of helping others. Throughout the talk, I will outline the possible computational and neural bases of these behaviours, and how they may differ from young adulthood to old age.
Mutation induced infection waves in diseases like COVID-19
After more than 4 million deaths worldwide, the ongoing vaccination to conquer the COVID-19 disease is now competing with the emergence of increasingly contagious mutations, repeatedly supplanting earlier strains. Following the near-absence of historical examples of the long-time evolution of infectious diseases under similar circumstances, models are crucial to exemplify possible scenarios. Accordingly, in the present work we systematically generalize the popular susceptible-infected-recovered model to account for mutations leading to repeatedly occurring new strains, which we coarse grain based on tools from statistical mechanics to derive a model predicting the most likely outcomes. The model predicts that mutations can induce a super exponential growth of infection numbers at early times, which self-amplify to giant infection waves which are caused by a positive feedback loop between infection numbers and mutations and lead to a simultaneous infection of the majority of the population. At later stages -- if vaccination progresses too slowly -- mutations can interrupt an ongoing decrease of infection numbers and can cause infection revivals which occur as single waves or even as whole wave trains featuring alternative periods of decreasing and increasing infection numbers. Our results might be useful for discussions regarding the importance of a release of vaccine-patents to reduce the risk of mutation-induced infection revivals but also to coordinate the release of measures following a downwards trend of infection numbers.
Impact evaluation for COVID-19 non-pharmaceutical interventions: what is (un)knowable?
COVID-19 non-pharmaceutical intervention (NPI) policies have been one of the most important and contentious decisions of our time. Beyond even the "normal" inherent difficulties in impact evaluation with observational data, COVID-19 NPI policy evaluation is complicated by additional challenges related to infectious disease dynamics and lags, lack of direct observation of key outcomes, and a multiplicity of interventions occurring on an accelerated time scale. Randomized controlled trials also suffer from what is feasible and ethical to randomize as well as the sheer scale, scope, time, and resources required for an NPI trial to be informative (or at least not misinformative). In this talk, Dr. Haber will discuss the challenges in generating useful evidence for COVID-19 NPIs, the landscape of the literature, and highlight key controversies in several high profile studies over the course of the pandemic. Chasing after unknowables poses major problems for the metascience/replicability movement, institutional research science, and decision makers. If the only choices for informing an important topic are "weak study design" vs "do nothing," when is "do nothing" the best choice?
SARC-CoV-2 modeling: What have we learned from this pandemic about how (not) to model disease spread?
The SARS-CoV-2 pandemic is awash in data, including daily, spatially-resolved COVID case data, virus sequence data, patients `omics data, and mobility data. Journals are now also awash in studies that make use of quantitative modeling approaches to gain insight into the geographic spread of SARS-CoV-2 and its temporal dynamics, as well as studies that predict the impact of control strategies on SARS-CoV-2 circulation. Some, but by no means all, of these studies are informed by the massive amounts of available data. Some, but by no means all, of these studies have been useful — in that their predictions revealed something beyond simple back of the envelope calculations. To summarize some of these findings, in this symposium, we will address questions such as: What do we want from models of disease spread? What can and should be predicted? Which data are the most useful for predictions? When do we need mechanistic models? What have we learned about how to model disease spread from unmet and/or conflicting predictions? The workshop speakers will explore these questions from different perspectives on what data need to be considered and how models can be evaluated. As at other TMLS workshops, each speaker will deliver a 10-minute talk with ample time set aside for moderated questions/discussion. We expect the talks to be provocative and bold, while respecting different perspectives.