The proclivity with which human alpha herpesviruses establish latent infections in neural ganglia is manifest by the presence of their viral genomes as multiple nonreplicating nuclear episomes.1 This penchant for residing in neurons presents a puzzling problem for these viruses. In particular they must negotiate a life-cycle in non-dividing cells that fail to express host proteins that are required for their replication or may even express proteins that result in a block to replication. While there is no obvious solution to this problem, replicate they do as evidenced by their ability to reactivate. A question that occurs is; what are these viruses doing while they lay in wait, to replicate, descend the axon and pronounce their appearance as overt local lesions? This is a problem that the laboratory has tried to address, with varied success, during the past 15 years.
|Title of host publication||From the Hallowed Halls of Herpesvirology|
|Subtitle of host publication||A Tribute to Bernard Roizman|
|Publisher||World Scientific Publishing Co.|
|Number of pages||35|
|State||Published - Jan 1 2012|