Effect of Interferon and Ribavirin on hepatitis C virus

Abstract

Hepatitis C Virus (HCV) is a blood-borne infection that can lead to many liver diseases and hence leads to its failure [1]. The current treatment for HCV infection involves combination therapy of pegylated Interferon and Ribavirin [2]. Combination therapy induces long term response in almost 50% of the patients [2-3]. No alternative therapy exists to those patients who do not respond to the combination therapy [3]. Therefore, it is necessary to identify the markers of the disease that leads to its progression and also the factors which can result in the long term response of the drugs. Beside this the exposure to the drug should be minimised; it should not cause side effects and should be inexpensive. With the onset of therapy, the viral load declines in a biphasic or triphasic manner. A biphasic decay pattern is observed in those patients who respond to the therapy. In biphasic decay, there is a sharp decline initially and then decreases gradually until the infection is not detected. In certain patients there could be relapse of the infection after the therapy and in some cases there might not be any second phase decline, i.e. in non-responders. So these changing patterns of the viral load under therapy, holds clues for the HCV pathogenesis and outcomes of therapy.
So a mathematical model for the suppression of HCV in the presence of the potential drugs was developed. From experimental and theoretical kinetic data, we can work on how we can decrease the level of viral RNA (ribonucleic acid) in hepatocyte cells. Using the model, we can verify the estimates for the efficiency of the effect of potential drugs on replication of viral RNA and viral protein processing. We have written the code in FORTRAN; the code has been tested against the published result and a good match is found. The developed mathematical model may serve as a tool for the evaluation of the efficiency of potential drug on the HCV genome.