Su Ying-Hsiu, Zhang Xianchao, Aiamkitsumrit Benjamas, Tang Qiyi, Maul Gerd, Fraser Nigel W, Block Timothy M
Department of Microbiology and Immunology, College of Medicine, Drexel University, Doylestown, Pennsylvania 18901-2697, USA.
J Neurovirol. 2006 Oct;12(5):375-86. doi: 10.1080/13550280600975358.
Maintaining the viral genome intact following infection and prior to replication is critical to the virus life cycle. Here we report an analysis of the stability of herpes simplex virus type 1 (HSV-1) genomes, relative to host chromosomal DNA, in infected cells as a function of viral induced apoptosis. The results show that, in the absence of DNA replication, the input genomes of wild-type (KOS), and replication compromised ICP27 deleted (d27-1) virus are remarkably stable. Intracellular half-lives of their genomes exceeded 24 hours. In contrast, the half-life of replication incompetent ICP4 deleted (d120) viral genomes were significantly less (approximately 8 hours). Interestingly, it was also noted that in cells infected under conditions permissible for replication, viral DNA replication occurs, even in cells undergoing apoptosis. The possibility that the genome structure and replication compartment formation provide protection to the HSV-1 genome from degradation is discussed.
