To follow the coevolution of resistance and infectivity of host and virus, 11 time points were selected on the basis of population size dynamics. For each time point, 10 algal clones were randomly isolated from previously plated populations on agar plates and regrown in BBM. Afterward, each host clone was exposed to virus populations from all time points. To determine the resistance or susceptibility of the algal clones toward the virus populations, their growth when exposed to virus (initial ratio of algal cells to virus particles: 0.01) was compared with the growth of the algal clone in the absence of the virus. Growth rates were calculated on the basis of optical density measurements (Tecan, Infinite M200PRO, 680 Männedorf, Switzerland) measured at time point 0 and after 72 hours. A host clone was deemed susceptible when the mean growth rate plus 2 SDs of four technical replicates in the presence of the virus was lower than mean growth rate minus 2 SDs of the control or when mean growth rate in the presence of the virus was negative. Resistance and infectivity ranges were calculated as the proportion of virus populations a host individual was resistant to and the proportion of host individuals a virus population could infect, across sampled time points. Growth rates of algal clones measured in the absence of virus were correlated to resistance range to estimate trade-offs between resistance and growth rates.

We defined phenotypic match and mismatch intervals based on resistance and infectivity evolution over time. Resistance evolution occurred when hosts from a given time point became resistant against virus from their past and contemporary time points (horizontal arrows in fig. S1). Infectivity evolution occurred when virus became able to infect previously resistant hosts, i.e., when contemporary virus or virus from the next time point could infect hosts, whereas the same hosts could not be infected by virus from past time points (vertical arrows in fig. S1). As we do not have continuous data, we marked these transitions between the different stages by arrows in the infection matrix. Note that we only took observations into account when the phenotype was maintained in the next time step. Because we were only interested in identifying when resistance and infectivity evolved, we marked transitions at the time point when a phenotype was first observed and did not take into account the frequency at this time point.

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