Abstract
Hepatitis C virus is a major cause of chronic liver diseases which can lead to permanent liver damage, hepatocellular carcinoma and death. The presently available treatment with interferon plus ribavirin, has limited benefits due to adverse side effects such as anemia, depression and "flu-like" symptoms. Needless to mention, the effectiveness of interferon therapy is predominantly, if not exclusively, limited to virus type 3a and 3b whereas in Europe and North America the majority of viral type is 1a and 2a. Due to the limited efficiency of current therapy, RNA interference (RNAi) a novel regulatory and powerful silencing approach for molecular therapeutics through a sequence-specific RNA degradation process represents an alternative option. Several reports have indicated the efficiency and specificity of synthetic and vector based siRNAs inhibiting HCV replication. In the present review, we focused that combination of siRNAs against virus and host genes will be a better option to treat HCV
Highlights
Hepatitis C virus (HCV) infection is a serious global health problem that affects 180 million people worldwide and 10 million people in Pakistan [1]
An analysis of combined RNA interference (RNAi) and IFN treatment of HCV replicons in cell culture using lentivirus-delivered shRNAs has been performed and results indicated that IFN-a enhance gene silencing, and inhibition of HCV replication [48]
HCV causes acute and chronic hepatitis which eventually lead to permanent liver damage hepatocellular carcinoma and death
Summary
HCV infection is a serious global health problem that affects 180 million people worldwide and 10 million people in Pakistan [1]. An analysis of combined RNAi and IFN treatment of HCV replicons in cell culture using lentivirus-delivered shRNAs has been performed and results indicated that IFN-a enhance gene silencing, and inhibition of HCV replication [48] This underscores the possibility of combination therapies of siRNAs and IFN against HCV. The efficiency of silencing lamin A/C expression was similar either in presence or absence of replicating HCV RNAs. Hepatitis B and C viruses are not cytopathic, but triggers hepatitis when activate immune cells expressing FasL, infiltrating the liver, where infection up regulates the death receptor Fas on hepatocytes, making them major targets for immune cells and might provide an effective immune modulating therapy to avoid chronic liver cell damage [59]. Targeting multiple sites of the HCV genome and host factors involved in HCV replication are a realistic and valid approach aimed at preventing the virus from developing resistance
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