Submitted to: Herpesvirus International Workshop
Publication Type: Abstract Only
Publication Acceptance Date: 7/11/2007
Publication Date: 7/11/2007
Citation: Heidari, M., Huebner, M., Silva, R.F. 2007. Global gene expression profiling of Marek's disease virus during cytolytic and latency infection [abstract]. Herpesvirus International Workshop. Paper No. 1.55.
Technical Abstract: Marek’s disease (MD), a lymphoproliferative disease of domestic chickens, is caused by an avian alpha-herpesvirus, Marek’s disease virus (MDV). MDV causes an early cytolytic infection in B cells followed by a latency infection in CD4+ T cells. The transcriptional analysis of a limited number of MDV genes has revealed differential gene expression pattern during different phases of viral infection. In the present study, a comprehensive comparative MDV gene expression profiling was conducted during cytolytic and latency infection using Affymetrix genechip chicken genome arrays. These arrays contain probes for all the known MDV genes and open reading frames. Two-weeks-old MD-susceptible chickens were inoculated with a very virulent plus MDV strain and spleen samples were collected 5 and 15 days post inoculation (cytolytic and latency, respectively) for RNA isolation and microarray analysis. The transcriptional activities of more that 85 genes were detected during the cytolytic infection. vIL8, a secreted CXC chemokine involved in early lytic replication and target cell attraction, lipase, a homologue of pancreatic lipases required for viral replication during lytic infection, gC, a secreted glycoprotein necessary for viral pathogenesis, UL49.5, a transmembrane protein associated with down-regulation of MHC I, and pp38, a phosphoprotein involved in early cytolytic infection and reactivation from latency, were among the genes detected with substantial transcriptional activities. Among the limited number of MDV genes probed during the latent infection, meq, a homologue of fos and jun oncogenes, a 23 KD nuclear protein, and R-LORF5, a splice variant of meq, were noticeably upregulated. These chicken arrays are valuable tools in understanding the molecular mechanism of MDV pathogenesis and host-pathogen interaction.