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. 2014 Jul 23;9(7):e102821. doi: 10.1371/journal.pone.0102821

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© 2014 Schlesinger et al

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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Relative to Fig. 4, this increased pressure ( for all infections in the main phase diagram) has the overall effect of suppressing the immune response, allowing early escape and chronic infection to occur at lower pathogen mutation rates () and larger affinity ranges (). In addition, as shown in the insets, convergence to the approximate steady state of chronic infection occurs much more quickly under high homeostatic pressure (inset A), due to the damping effect of the homeostatic constraint on population oscillations. Inset B shows population densities for an infection with low homeostatic pressure from Fig. 4D; these display stronger, more sustained oscillations. Inset A and infection A have and sites. Inset B and its corresponding infection in Fig. 4D have , , and sites. All other parameter values are specified in Table 1.

Inline graphic — Relative to Fig. 4, this increased pressure ( for all infections in the main phase diagram) has the overall effect of suppressing the immune response, allowing early escape and chronic infection to occur at lower pathogen mutation rates () and larger affinity ranges (). In addition, as shown in the insets, convergence to the approximate steady state of chronic infection occurs much more quickly under high homeostatic pressure (inset A), due to the damping effect of the homeostatic constraint on population oscillations. Inset B shows population densities for an infection with low homeostatic pressure from Fig. 4D; these display stronger, more sustained oscillations. Inset A and infection A have and sites. Inset B and its corresponding infection in Fig. 4D have , , and sites. All other parameter values are specified in Table 1.