Alteration in the simian virus 40 maturation pathway after butyrate-induced hyperacetylation of histones.

The role of histone acetylation in the replication and maturation pathways of simian virus 40 was assessed. Histones were hyperacetylated by briefly exposing infected cells to sodium butyrate. Viral DNA in cells exposed to butyrate was found to reenter replication to a greater extent and mature to the previrion form to a lesser extent than viral DNA in control cells. Previrions formed in the presence of butyrate had altered sedimentation properties. These data suggest that increased acetylation of histones is not the signal for removal of DNA from the pool of molecules available for replication. It appears, in fact, that hyperacetylation retards entry into and progression along the maturation pathway.