Chromatin structure is strictly regulated during the cell cycle. DNA viruses 
occasionally disturb the spatial organization of the host cell chromatin due to 
formation of the viral DNA replication compartment. To examine chromatin 
behavior in baculovirus-infected cells, we constructed recombinant plasmids 
expressing fluorescent protein-tagged histone H4 molecules and visualized the 
intracellular localization of chromatin by their transient expression in live 
infected cells. Similar to other DNA viruses, the baculovirus Bombyx mori 
nucleopolyhedrovirus induced marginal relocation of chromatin within the nuclei 
of BmN cells, simultaneously with expansion of the viral DNA replication 
compartment, the virogenic stroma (VS). In the late stage of infection, however, 
the peristromal region (PR), another virus-induced subnuclear compartment, was 
also excluded from the chromatin-localizing area. Provided that late-gene 
products such as PR proteins (e.g., envelope proteins of the occlusion-derived 
virus) were expressed, blockage of viral DNA synthesis failed to inhibit 
chromatin relocation, despite abrogation of VS expansion. Instead, chromatin 
became marginalized concomitantly with PR expansion, suggesting that the PR 
contributes directly to chromatin replacement. In addition, chromatin was 
excluded from relatively large subnuclear structures that were induced in 
uninfected cells by cotransfection with four baculovirus genes, ie1, lef3, p143, 
and hr. Omission of any of the four genes, however, failed to result in 
formation of the large structures or chromatin exclusion. This correlation 
between compartmentalization and chromatin exclusion suggests the possibility 
that a chromatin-exclusive property of viral molecules, at least in part, 
supports nuclear compartmentalization of virus-infected cells.