E1/E2 of Hepatitis C Virus Genotype-4 and Apoptosis

  • Zekri, Abdel-Rahman N (Virology and Immunology Unit, Cancer Biology Department, National Cancer Institute, Cairo University) ;
  • Sobhy, Esraa (Virology and Immunology Unit, Cancer Biology Department, National Cancer Institute, Cairo University) ;
  • Hussein, Nehal (Virology and Immunology Unit, Cancer Biology Department, National Cancer Institute, Cairo University) ;
  • Ahmed, Ola S (Virology and Immunology Unit, Cancer Biology Department, National Cancer Institute, Cairo University) ;
  • Hussein, Amira (Virology and Immunology Unit, Cancer Biology Department, National Cancer Institute, Cairo University) ;
  • Shoman, Sahar (Faculty of Science, Microbiology Department, Ain Shams University) ;
  • Soliman, Amira H (Department of Clinical Pathology, National Cancer Institute, Cairo University) ;
  • El-Din, Hanaa M Alam (Virology and Immunology Unit, Cancer Biology Department, National Cancer Institute, Cairo University)
  • Published : 2016.07.01


Several studies have addressed the possible role of hepatitis C virus genotype-4 (HCV GT4) in apoptosis. However, this still not fully understood. In the current study a re-constructed 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 up-regulated and 23 down-regulated. The highest-up regulated genes were APAF1 (apoptotic peptidase-activating factor 1), BID (BH3 interacting domain death agonist) and BCL 10 (B-cell CLL/lymphoma protein 10) with fold regulation of 33.2, 30.1 and 18.9, respectively. The most down-regulated were FAS (TNF receptor super family), TNFRSF10B (tumor necrosis factor receptor super-family member 10b) and FADD (FAS-associated 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 HCV-induced pathogenesis by modulating apoptosis through the induction of the intrinsic apoptosis pathway and disruption of the BCL2 gene family.


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