In the United States, the incidence of acute HCV infection has sharply decreased during the past decade, but its prevalence remains high.
According to US Centers for Disease Control and Prevention (CDC) estimates, 2.7-3.9 million people (most of whom were born from 1945 through 1965) in the United States have chronic hepatitis C which develops in approximately 75% of patients after acute a leading cause of morbidity and mortality, primarily through the development of liver fibrosis and cirrhosis; persons with chronic infection live an average of 2 decades less than healthy persons.
Genotypes 1a and 1b are prevalent in the United States, whereas in other countries, genotype 1a is less frequent.
Genotype details are as follows: Transfusion of blood contaminated with hepatitis C virus (HCV) was once a leading means of HCV transmission.
HCV genomic analysis by means of an arduous gene sequencing of many viruses has led to the division of HCV into six genotypes based on homology. Arabic numerals denote the genotype, and lower-case letters denote the subtypes for lesser homology within each genotype.
Molecular differences between genotypes are relatively large, and they have a difference of at least 30% at the nucleotide level.
Two regions of the E2 protein, designated hypervariable regions 1 and 2, have an extremely high rate of mutation, believed to result from selective pressure by virus-specific antibodies.
The envelope protein E2 also contains the binding site for CD-81, a tetraspanin receptor expressed on hepatocytes and B lymphocytes that acts as a receptor or coreceptor for HCV.
In most infected people, viremia persists and is accompanied by variable degrees of hepatic inflammation and fibrosis.
Findings from studies suggest that at least 50% of hepatocytes may be infected with HCV in patients with chronic hepatitis C.