Data from: ATRX promotes maintenance of herpes simplex virus heterochromatin during chromatin stress

The mechanisms by which mammalian cells recognize and epigenetically
restrict viral DNA are not well defined. We used herpes simplex virus with
bioorthogonally labeled genomes to detect host factors recruited to viral
DNA shortly after its nuclear entry and found that the cellular IFI16,
PML, and ATRX proteins colocalized with viral DNA by 15 min post
infection. HSV-1 infection of ATRX-depleted fibroblasts resulted in
elevated viral mRNA and accelerated viral DNA accumulation. Despite the
early association of ATRX with vDNA, we found that initial viral
heterochromatin formation is ATRX-independent. However, viral
heterochromatin stability required ATRX from 4-8 h post infection.
Inhibition of transcription blocked viral chromatin loss in ATRX-knockout
cells; thus, ATRX is uniquely required for heterochromatin maintenance
during chromatin stress. These results argue that the initial formation
and the subsequent maintenance of viral heterochromatin are separable
mechanisms, a concept that likely extrapolates to host cell chromatin and
viral latency.