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12 Supplement


Recent results in three areas of HSV research have significantly extended and advanced certain topics discussed in Chapter 12. These include detailed genetic mapping of mutant tsC75, information which is critical to one model of HSV replication; construction of virus with secondary sites for segment inversion; and the detailed analysis of the tk locus.

One proposed model of HSV replication (p.681) requires some sort of terminal-repair process that involves the copying of an internal repeated region. A key experimental datum in favor of this model was the report that the mutation tsC75 maps within the a sequence, which is at present in four copies per genome. Recent fine-structure mapping (Dixon and Schaffer 1980; Preston et al., pers. comm.) suggests that the mapping of tsC75 is anomalous and that it may very well map outside the a region. If this is true, then other models, not directly requiring “gene conversion” to absolute sequence identity, may be valid.

The mechanism of segment inversion may involve site-specific events (e.g., recombination) that depend on the nucleotide sequences located at the joint between the L and S components of the genome. In a recent test of this hypothesis (J. R. Smiley, pers. comm.), a mutant virus was constructed that contained an additional copy of the joint region inserted into the tk locus at 0.3 map units. Such viruses were viable, but segregated genomes with massive deletions between the joint sequence at 0.3 map units and the normal one at 0.82 map units. These deletions are...

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