Some herpesviruses, particularly lymphotropic viruses such as Marek's disease
virus (MDV) and human herpesvirus 6 (HHV-6), integrate their DNA into host
chromosomes. MDV and HHV-6, among other herpesviruses, harbor telomeric
repeats (TMRs) identical to host telomeres at either end of their linear
genomes. Using MDV as a natural virus-host model, we show that herpesvirus
TMRs facilitate viral genome integration into host telomeres and that
integration is important for establishment of latency and lymphoma formation.
Integration into host telomeres also aids in reactivation from the quiescent
state of infection. Our results and the presence of TMRs in many herpesviruses
suggest that integration mediated by viral TMRs is a conserved mechanism,
which ensures faithful virus genome maintenance in host cells during cell
division and allows efficient mobilization of dormant viral genomes. This
finding is of particular importance as reactivation is critical for virus
spread between susceptible individuals and is necessary for continued
herpesvirus evolution and survival
