5 research outputs found

    Effect of varying the initial densities of susceptible cells.

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    Plots show: (A, D) the predicted resistance type fractions, (B, E) cell counts, and (C, F) phage counts, with (A-C) the same initial phage dose (V = 106) or (D-F) when the initial dose of viruses was diluted to keep the same initial multiplicity of infection of 0.1. Amount of starting inoculum: 10% (K/10), 1% (K/100), 0.1% (K/1,000), 0.01% (K/10,000) of total final volume. Other parameter values: r = 1, m = 0, mv = 0, a = 10−8, B = 100, cR = 0.01, τ = 0.01, μ = 10−4, A = 5 10−4, L = 10−3. Panels (A-C) are also shown in Fig 2, alongside the experimental results (Fig 2D–2F). Data are available at https://doi.org/10.5281/zenodo.8193506. (TIF)</p

    Transitory dynamics of bacteria and viruses across time.

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    The plots show the dynamics for 3 transfers (20 hours between each transfer, indicated by a vertical grey line), including (A) density of S cells (susceptible, blue line), (B) density of V (viruses, black line), (C) densities of the different types of resistant cells (R (surface mutation, green line), C (CRISPR immune, red line), and D (both resistances, brown line), (D) frequencies of R, C, and D cells (dashed lines with same colours as in panel C), and (E) dynamics of linkage disequilibrium between the resistance loci across time. Linkage disequilibrium between the resistance loci is measured as: LD = fSfD−fRfC. Parameter values: r = 1, m = 0, mv = 0, a = 10−8, B = 100, cR = 0.01, τ = 0.01, μ = 10−4, A = 5 10−4, L = 10−3, K = 108, and (initial) V = 104. (TIF)</p

    Schematic representation of the model.

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    Naive and uninfected hosts (S hosts) reproduce at rate rS. Upon infection by the phages, they release a burst size B of new viral particles. Two distinct types of resistance may emerge: surface modification (R hosts) or CRISPR resistance (C hosts). R hosts reproduce at a rate , where cR measures the cost of resistance. C hosts reproduce at a rate , where τ measures the toxicity induced by CRISPR immunity when resistant cells are exposed to the virus. D hosts reproduce at a rate because even though they have both types of resistance, they only express the cost of constitutive resistance because they are never infected by phages. Cells acquire surface modification at rate μ (this rate is constant) and acquire CRISPR resistance at rate AaV (this rate varies with the exposition to viral particles).</p

    Emergence of phage resistance over time.

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    Frequency of the different bacterial resistance types (S (sensitive, white bars), C (CRISPR immune, blue), R (surface mutants, orange), or D (both CRISPR and surface mutants, red)) through time (3 days) and for different values of the initial doses of free viruses (V) and the carrying capacity (K). All the simulations started with an initial density of susceptible cells at K/100. Other parameter values: r = 1, m = 0, mv = 0, a = 10−8, B = 100, cR = 0.01, τ = 0.01, μ = 10−4, A = 5 10−4, L = 10−3. (TIF)</p
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