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ABSTRACT Microbial communities are complex ecological systems of organisms that evolve in time, with new variants created, while others disappear. Understanding how species interact within communities can help us shed light into the mechanisms that drive ecosystem processes. We studied systems with serial propagation, where the community is kept alive by taking a subsample at regular intervals and replating it in fresh medium. The data that are usually collected consist of the % of the population for each of the species, at several time points. In order to utilize this type of data, we formulated a system of equations (based on the generalized Lotka–Volterra model) and derived conditions of species noninteraction. This was possible to achieve by reformulating the problem as a problem of finding feasibility domains, which can be solved by a number of efficient algorithms. This methodology provides a cost‐effective way to investigate interactions in microbial communities. 

Human immunodeficiency virus (HIV-1) replicates in the secondary lymphoid tissues, which are characterized by complex compartmental structures. While cytotoxic T lymphocytes (CTL) readily access infected cells in the extrafollicular compartments, they do not home to follicular compartments, which thus represent an immune-privileged site. Using mathematical models, previous work has shown that this compartmental tissue structure can delay the emergence of CTL escape mutants. Here, we show computationally that the compartmental structure can have an impact on the evolution of advantageous mutants that are not related to CTL recognition: (i) compartmental structure can influence the fixation probability of an advantageous mutant, with weakened selection occurring if CTL responses are of intermediate strength; (ii) compartmental structure is predicted to reduce the rate of mutant generation, which becomes more pronounced for stronger CTL responses; and (iii) compartmental structure is predicted to slow down the overall rate of mutant invasion, with the effect becoming more pronounced for stronger CTL responses. Altogether, this work shows thatin vivovirus evolution proceeds slower in models with compartmental structure compared with models that assume equivalent virus load in the absence of compartmental structure, especially for strong CTL-mediated virus control. This has implications for understanding the rate of disease progression.