Trigeminal ganglion DNA from mice latently infected with herpes simplex virus type 1 was analysed by restriction enzyme digestion, agarose gel electrophoresis and blot hybridization to P-labelled viral DNA. Viral DNA from parental virions and from virions obtained as a consequence of reactivation by ganglion neurectomy were similarly analysed. The HI restriction fragments of parental and reactivated virions were almost indistinguishable from each other, and several of the larger HI fragments of viral DNA were also found in latently infected ganglia at unaltered sizes. In contrast, fractionation of RI fragments of latently infected ganglion DNA by reverse phase column (RPC-5) chromatography, followed by gel electrophoresis and blot hybridization to a viral DNA probe from the S component terminal repetition, revealed the presence of several terminal fragments at discrete sizes ranging from 1 kb to 15 kb, quite unlike the 5.7 kb terminal RI K fragment of virion-derived DNA. These results indicate that structural changes occur in the viral genome concomitantly with the establishment of latency, such as may result from extensive gene rearrangement or integration into cellular DNA.


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