Human papillomaviruses establish a reservoir of infection in the epithelial basal layer. To do
this they limit their gene expression to avoid immune detection and modulate epithelial
homeostasis pathways to inhibit the timing of basal cell delamination and differentiation to
favour persistence. For low-risk Alpha papillomaviruses, which cause benign self-limiting
disease in immunocompetent individuals, it appears that cell competition at the lesion edge
restricts expansion. These lesions may be considered as self-regulating homeostatic …