= Solution
\b[Base composition changes both the initial <buoyant density> and the size of the BUdR-induced density increment.] The fraction-number axis runs toward lower density. The unlabelled viral peak lies at a lower fraction number than the corresponding host peak, consistent with viral <DNA> having a higher <GC content>. <BUdR> replaces <thymidine> in newly synthesized strands, so relatively AT-rich <DNA> incorporates more brominated <nucleoside> per unit length and undergoes a larger density increase.
Consequently the more AT-rich host <DNA> can overtake the viral <DNA> in the fully substituted class: the host fully heavy peak is slightly farther toward the dense end, although host unlabelled <DNA> was less dense. The hybrid peaks are intermediate. A useful qualitative model is $\rho_{LL}=\rho_0(g)$, $\rho_{LH}=\rho_0(g)+\Delta\rho(g)/2$ and $\rho_{HH}=\rho_0(g)+\Delta\rho(g)$, where $g$ is GC fraction, $\rho_0$ increases with $g$, and $\Delta\rho$ decreases as the <thymidine> fraction decreases. Unequal substitution efficiencies could contribute, but different replication mechanisms are unnecessary. These are equilibrium density positions, not molecular-length measurements.
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