Fig. 3.

Disease Regression and the Immune Control of Papillomavirus Infections. Current thinking suggests that immune detection involves dendritic cells that despite papillomavirus immune-evasion strategies, will eventually become primed to PV-specific antigens (A) and present these to naïve T-cells in the local lymph node. Subsequent T-cell activation and T-cell infiltration is thought to suppress viral gene expression, leaving infected basal cells which already express viral gene products at low levels (B). Immune control and long-term immune surveillance is dependent on memory T-cells and on the balance of ongoing stimulation by viral antigens, and the suppression of viral gene expression following T-cell recognition (C). It is anticipated that this balance of immune control and viral gene expression may support low level virus particle production. (D) Removal of immunesurveillance allows viral gene expression to go unregulated, leading to the redetection of infection as viral copy number increases. Images based on data outlined in Refs. [19,22,56,57].