Saudi Journal of Gastroenterology
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ORIGINAL ARTICLE
Year : 2016  |  Volume : 22  |  Issue : 3  |  Page : 240-248

Hepatitis c virus genotype 4 replication in the hepatocellular carcinoma cell line HepG2/C3A


1 College of Medicine Research Center, King Saud University, Riyadh, Saudi Arabia; Department of Medical Microbiology and Immunology, College of Medicine, Menofia University, Egypt
2 College of Medicine Research Center, King Saud University, Riyadh, Saudi Arabia
3 College of Medicine Research Center, King Saud University; Department of Surgery, College of Medicine, King Saud University, Riyadh, Saudi Arabia

Correspondence Address:
Medhat K Shier
College of Medicine Research Center, King Saud University, PO Box 2925 (74), Riyadh - 11461, Saudi Arabia

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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1319-3767.182461

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Background/Aims: The lack of a reliable cell culture system allowing persistent in vitro hepatitis C virus (HCV) propagation is still restraining the search for novel antiviral strategies. HepG2 cells transfection with HCV allows for viral replication. However, the replication is weak presumably because of HepG2 lack of miRNA-122, which is essential for viral replication. Other agents such as polyethylene glycol (PEG) and dimethyl sulfoxide (DMSO) have been shown to increase the efficiency of infection with other viruses. This study included comparison of HCV genotype 4 5′UTR and core RNA levels and HCV core protein expression at different time intervals in the absence or presence of PEG and/or DMSO postinfection. Materials and Methods: We used serum with native HCV particles in infecting HepG2 cells in vitro. HCV replication was assessed by reverse transcriptase polymerase chain reaction for detection of HCV RNA and immunofluorescence and flow cytometry for detection of HCV core protein. Results: HCV 5′UTR and core RNA expression was evident at different time intervals after viral infection, especially after cells were treated with PEG. HCV core protein was also evident at different time intervals using both immunofluorescence and flow cytometry. PEG, not DMSO, has increased the HCV core protein expression in the treated cells, similar to its effect on viral RNA expression. Conclusions: These expression profiles suggest that the current model of cultured HepG2 cells allows the study of HCV genotype 4 replication and different stages of the viral life cycle.


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