FIG 1.

Schematic and simulations of environmental and intrinsic models. Both models assume that the mechanism of RB/EB conversion is in response to signal concentration. High signal concentration prevents RB/EB conversion, and RB replication continues. As RBs replicate, the signal is consumed. Once the signal is depleted past a given threshold, RBs convert to IBs, which then convert to EBs. (A) Schematic of the environmental signal model. The RBs compete for a single pool of signal (S). (B) Schematic of the intrinsic model. Each RB contains its own signal, eliminating competition between RBs. (C) Simulations of the two models (environmental and intrinsic) using a multiplicity of infection (MOI) of 1 and an RB generation time of 2.27 h produced results that mimic the general kinetics of the chlamydial cycle and were indistinguishable from each other. (D) Simulations of RB doubling times of 1.13 h (half the measured RB doubling time) resulted in a reduced time to EB production, whereas 4.54 h (2× the measured RB doubling time) increased time to EB production. However, both models (environmental and intrinsic) produced the same outcome. (E) Simulations using an MOI of 10 predicted EB conversion to occur more rapidly in the environmental signal model but to remain unchanged in the intrinsic model. Similarly, simulations of the models using a time-delayed superinfection resulted in RB-to-EB conversion occurring more rapidly in the environmental model but remaining unchanged in the intrinsic model.