Molecular biology and clinical implication of hepatitis C virus

Abstract

Hepatitis C virus (HCV) was first described in 1989 as the putative viral agent of non-A non-B hepatitis. It is a member of the Flaviviridae family and has been recognized as the major causative agent of chronic liver disease, including chronic active hepatitis, cirrhosis and hepatocellular carcinoma. HCV is a positive RNA virus with a genome containing approximately 9500 nucleotides. It has an open reading frame that encodes a large polyprotein of about 3000 amino acids and is characterized by extensive genetic diversity. HCV has been classified into at least 6 major genotypes with many subtypes and circulates within an infected individual as a number of closely related but distinct variants known as quasispecies. This article reviews aspects of the molecular biology of HCV and their clinical implication.

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“…Our findings showed that nucleotide 35–100 is highly conserved between the three studied groups. The 5'UTR is highly conserved out of the HCV genomic organization [33]. …”

Factors Associated with the Prevalence of Hepatitis B among Volunteer Blood Donors at Jimma Blood Bank, South Ethiopia

“…According to the estimation of the World Health Organization (WHO), unsafe blood transfusions due to infection with the hepatitis B virus were 8–16 million [ 2 ]. Around 45,000 hepatitis B virus or hepatitis C virus illnesses are predicted to spread by infected transfusions in Sub-Saharan Africa each year, according to the World Health Organization [ 5 ]. Multiple studies in Ethiopia have found that the prevalence of HBV and HCV in blood donors ranges between 2.1% and 25.9% and 0.2% and 13.3%, respectively, according to the findings of [ 6 – 9 ].…”

The role of HCV proteins on treatment outcomes

“…HCV is a small enveloped virus with a positive single-stranded RNA genome containing approximately 9,600 nucleotides which encodes for a large polyprotein of about 3,000 amino acids. The polyprotein precursor is cleaved by the host and viral proteases into three structural proteins (core, E1, E2) and seven nonstructural proteins (p7, NS2, NS3, NS4A, NS4B, NS5A, NS5B) [ 1 , 2 ] (Fig. 1 ).…”

“…The polyprotein precursor is processed by both host and viral enzymes to release functional structural and non-structural proteins. HCV NS3/4A, HCV NS5A, and HCV NS5B are targets for antiviral agents [ 1 , 2 ] …”