Each bacterial phylum grows logistically toward a shared gut carrying capacity K, but the whole community is also gut virome — bacteriophages that infect and lyse their bacterial hosts. Real gut phage populations show frequency-dependent (kill-the-winner) predation: a lytic phage's own replication rate scales with how often it meets a susceptible host, so whichever phylum is currently most abundant gets hunted hardest.
dB_i/dt = r_i · B_i · (1 − S/K) − φ · (B_i / S)^n · B_i
S = Σ B_i (total bacterial population)
r_i (intrinsic growth rate of phylum i)
φ = predation strength (overall lytic pressure)
n = selectivity exponent (0 = density-independent kill, higher = sharper "hunt the winner")
H = − Σ p_i · ln(p_i), p_i = B_i / S (Shannon diversity)
- Predation strength — scales how much lytic pressure the virome exerts overall. At 0, phages have no effect and the fastest grower eventually excludes the rest.
- Kill-the-winner selectivity (n) — how sharply phage attack concentrates on the currently dominant phylum. At n = 0 predation is spread evenly by abundance only; increasing n turns it into targeted suppression of whoever is winning, which is what keeps diversity high in a real gut.
- Diet skew — a Western, high-sugar/low-fibre diet gives Firmicutes an intrinsic growth advantage; raise it to see how strong the phage response needs to be to stop that advantage collapsing the community into one phylum.
- Antibiotic pulse — wipes out most of every phylum at once (both susceptible bacteria and their resident phages lose their hosts), then lets you watch the community re-equilibrate under the current predation settings.
This mechanism is why the gut virome is now studied alongside the bacterial microbiome: bacteriophages are not just bystanders, they are an active regulatory layer that suppresses competitive exclusion and preserves the phylum-level diversity that keeps the ecosystem — and its host — resilient.