There are two types of herpes simplex virus type 1 (HSV-1) vector systems in gene therapy, termed amplicon and recombinant virus1,2,3,4,5. The majority of tumor cells in these malignancies harbor latent KSHV episomes (20, 21, 23), and latent infection is thought to play a major role in the development of KSHV-associated neoplasms. We constructed and analysed fluorophore expression from a recombinant pseudorabies virus (PRV263) carrying a Brainbow cassette (Cre-conditional expression of different fluorophores). Autophagy-mediated degradation of the capsid will expose the viral DNA to Toll-like receptor 9 (TLR9) in endosomes. K-Rta was shown to interact with both C/EBPα binding motifs and the R response elements (RRE) within oriLyt. The plasmid containing Xba I F can be replaced by two smaller plasmids, one of which contains only the gene for the HSV-encoded DNA polymerase, and the other of which contains only the gene for the major DNA binding protein (ICP8). Kaposi’s sarcoma-associated herpesvirus (KSHV) is a cancer-causing agent in immunocompromised patients that establishes long-lasting infections in its hosts.
TopoIIβ plays an important role in LANA-dependent latent DNA replication, as addition of ellipticine, a selective inhibitor of TopoII, negatively regulated replication mediated by the TR. Our data suggest that LANA1 recruits ORCs to KSHV TRs for latent replication of the viral genome. Furthermore, to gain insight into possible common functions of PYHIN proteins, we constructed the interaction network for the entire family of proteins. It is one of the seven recognized human cancer causing viruses (Moore and Chang, 2010). Similar to IFI16, we found that IFIX interacts with and localizes at PML bodies. Therefore, we further characterized IFIX, demonstrating its function in restricting HSV-1 replication and its ability to bind to viral DNA to mount an immune response.