= Solution
\b[NVNA1 could contribute to <cancer> by increasing the chance of host <chromosome> damage and heritable rearrangements.] Persistent occupancy of a <chromosomal fragile site> could obstruct replication or normal <chromatin> reassembly. Incompletely replicated or damaged <DNA> can break, mis-segregate and be repaired into deletions, <gene fusions> or <copy-number alterations>. Particular surviving rearrangements might remove a <tumour suppressor gene> or deregulate an <oncogene>, after which <clonal selection> could expand that lineage. A viral <protein> can therefore promote <genomic instability> without the viral <genome> having to integrate at every breakpoint.
The tumour-sequencing association is consistent with this mechanism but does not establish causality by itself. <tumour> type, pre-existing instability, infection detection sensitivity and cellular composition can confound an NV-positive/NV-negative comparison. The induction experiment strengthens the case that NVNA1 can damage the locus, while its high doses limit direct estimation of risk during ordinary <viral latency>. Very common infection is compatible with rare <cancer> because susceptible <biological cell> types, expression fluctuations, time and cooperating alterations all matter. A documented biological analogue links EBNA1 occupancy of a <chromosome> 11 repeat cluster to <chromosome breakage> and rearrangement.<Chromosomal fragile site breakage by EBV-encoded EBNA1 at clustered repeats by Julia Su Zhou Li and others>[Figures 3–4 and tumour-genome analysis: locus damage and chromosome 11 structural variants]{ref}
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