= Solution
\b[The evidence supports NVNA1 as a sequence-specific organizer of viral <chromatin>, with possible additional roles in <nuclear retention> and <episome partitioning>.] Binding to the <origin of replication> and <DNA bridging> explain assembly at separated viral repeat arrays. Access to recognition sites in <nucleosomes> and weakening of histone–DNA association provide a plausible way to make an origin accessible to cellular replication machinery. The density-labelling result is consistent with a latent <genome> using a host-coordinated copying programme; it does not establish that NVNA1 is itself a <DNA polymerase> or <DNA helicase>.
Association with host chromosomal <DNA> could also retain <episomes> in the nucleus and help distribute them during <biological cell> division. Such tethering is a plausible maintenance function, but the experiments here do not directly visualize a physical bridge between an <episome> and a host <chromosome>. Binding at a vulnerable host repeat could instead be an incidental consequence of recognition specificity. The enrichment of host <chromosome> rearrangements supports a damage connection; it does not show that <chromosome breakage> is required for viral replication or that integration is part of the normal latent programme. <chromatin> opening and host-locus interference are mechanistic interpretations of the presented binding data, not proof of one obligatory replication pathway.
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