Evidence map›Paper›PMID 42607096›Full record

ArticlePLoS computational biology2026

The limitations of non-mechanistic methods for characterizing pathogen-pathogen interactions: A simulation study.

Sarah C Kramer, Sarah Pirikahu, Cana Kussmaul, Lulla Opatowski, Matthieu Domenech de Cellès

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Article in PLoS computational biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Sarah C KramerMax Planck Institute for Infection Biology, Infectious Disease Epidemiology Group, Berlin, Germany.ORCID 0000-0002-6177-2309
Sarah PirikahuMax Planck Institute for Infection Biology, Infectious Disease Epidemiology Group, Berlin, Germany.
Cana KussmaulMax Planck Institute for Infection Biology, Infectious Disease Epidemiology Group, Berlin, Germany.
Lulla OpatowskiInstitut Pasteur, Université Paris Cité, Epidemiology and Modelling of Antibiotic Evasion (EMAE) Unit, Paris, France.
Matthieu Domenech de CellèsMax Planck Institute for Infection Biology, Infectious Disease Epidemiology Group, Berlin, Germany.ORCID 0000-0002-9302-4858

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathogen-pathogen interactions occur when infection with one pathogen influences one's chance of infection or disease due to another. Increasingly, evidence suggests that interactions are a common feature of infectious disease epidemiology. However, due to both the nonlinearities and stochasticity inherent to infectious disease transmission, and the frequency of confounding (e.g., by shared seasonal forcing), simple, correlative methods for characterizing interactions may be prone to failure. Here, we perform a simulation study to evaluate several more complex non-mechanistic approaches for inferring causality from time series data: generalized additive models (GAMs), Granger causality, transfer entropy, and convergent cross-mapping (CCM). Specifically, we use a two-pathogen mechanistic transmission model, calibrated to produce dynamics resembling outbreaks of influenza and respiratory syncytial virus (RSV), to generate synthetic datasets with a range of values for interaction strength and duration. We then apply each method to all synthetic datasets. We find that Granger causality, transfer entropy, and CCM all fail to consistently infer whether data contain signal of an interaction; in particular, methods tend to incorrectly identify interactions where none are modeled (average sensitivity = 80.6%, 92.1%, 72.1%, respectively; average specificity = 31.0%, 33.3%, 33.1%). Furthermore, we find little to no association between point estimates from each method and true interaction strength. In contrast, GAMs infer the existence of interactions more accurately than the other methods (sensitivity = 85.2%, specificity = 72.5%), and consistently yield larger point estimates for stronger interactions. However, their practical utility is limited by an inability to evaluate interaction asymmetry (i.e., whether the effect of pathogen A on pathogen B is identical to that of B on A). Overall performance patterns were similar when methods were applied to two real-world datasets from Hong Kong and Canada. We conclude that accurately and comprehensively characterizing pathogen-pathogen interactions based on outbreak data remains a significant challenge. For this reason, it is critical that any proposed methods be rigorously evaluated before being used to draw conclusions about interactions.

Indexed as

Host-Pathogen InteractionsModels, BiologicalComputational BiologyComputer SimulationDisease OutbreaksHumansInfluenza, HumanRespiratory Syncytial Virus Infections

Identifiers

PMID42607096
PMCPMC13480661

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.