Virology and Immunology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Egypt Email : email@example.com
Several studies have addressed the possible role of hepatitis C virus genotype4 (HCV GT4) in apoptosis. However, this still not fully understood. In the current study a reconstructed clone of E1/E2 polyprotein region of the HCV GT4 was transfected into the Huh7 cell line and a human apoptotic PCR array of 84 genes was used to investigate its possible significance for apoptosis. Out of the 84 genes, only 35 showed significant differential expression, 12 genes being upregulated and 23 downregulated. The highestup regulated genes were APAF1 (apoptotic peptidaseactivating factor 1), BID (BH3 interacting domain death agonist) and BCL 10 (Bcell CLL/ lymphoma protein 10) with fold regulation of 33.2, 30.1 and 18.9, respectively. The most downregulated were FAS (TNF receptor super family), TNFRSF10B (tumor necrosis factor receptor superfamily member 10b) and FADD (FASassociated death domain) with fold regulation of 30.2, 27.7 and 14.9, respectively. These results suggest that the E1/E2 proteins may be involved in HCVinduced pathogenesis by modulating apoptosis through the induction of the intrinsic apoptosis pathway and disruption of the BCL2 gene family.