Hitchhiking on host chromatin: how papillomaviruses persist

Persistent viruses need mechanisms to protect their genomes from cellular defenses and to ensure that they are efficiently propagated to daughter host cells. One mechanism by which papillomaviruses achieve this is through the association of viral genomes with host chromatin, mediated by the viral E2 tethering protein. Association of viral DNA with regions of active host chromatin ensures that the virus remains transcriptionally active and is not relegated to repressed heterochromatin. In addition, viral genomes are tethered to specific regions of host mitotic chromosomes to efficiently partition their DNA to daughter cells. Vegetative viral DNA replication also initiates at specific regions of host chromatin, where the viral E1 and E2 proteins initiate a DNA damage response that recruits cellular DNA damage and repair proteins to viral replication foci for efficient viral DNA synthesis. Thus, these small viruses have capitalized on interactions with chromatin to efficiently target their genomes to beneficial regions of the host nucleus. This article is part of a Special Issue entitled: Chromatin in time and space.

► Papillomaviruses develop a long term, persistent relationship with their host. ► The papillomavirus life cycle is tightly linked to keratinocyte differentiation. ► Papillomaviruses must overcome intrinsic cellular defenses to establish an efficient infection. ► Papillomaviruses retain their genomes in infected cells by tethering them to host chromatin. ► Papillomaviruses utilize the cellular DNA damage response for their own replication.