Simulated population dynamics of epithelial cells, immune effectors and free viruses in the case of HPV infections.

Wart-like epithelial dynamics in a wart-associated HPV infection (A) and a slow growing high-risk (HR) HPV infection that spontaneously regresses (B). The black shading shows the proportion of infected cells in each layer. (C) Dynamics of virus load (black) and the density of immune effectors (gray) for wart-associated HPV (dashed line) and HR-HPV (full line) infections. Immune cells start to proliferate upon infection but their number remains below −2 log for several months. (D) Simulated scenario where the infection is inoculated with few cells and the microabrasion repairs quickly: this results in both wart-associated and HR types causing asymptomatic infections. Here, the model predicts that infections with HR types have more infected cells, due to their higher proliferative properties, but wart-associated types produce more virions (i, ii, iii), and both infections can last for years, if stochasticity or the innate response do not clear them (i, ii). Parameter values are default (Tables 1 and 3) and infection models are 3. Infection rates of both wart-associated and HR HPVs are identical (β = 10−10) and all infections begin with 10 infected basal cells. In (D) the infection rate, β, decays to zero in 10 days (b = −0.5) to mimic tissue repair (see section A.3 in S1 Text for details).