Hepatitis C is caused by an RNA virus that is often parenterally transmitted. It sometimes causes typical symptoms of viral hepatitis, including anorexia, malaise, and jaundice but may be asymptomatic. Fulminant hepatitis and death rarely occur. Chronic hepatitis develops in about 75% and can lead to cirrhosis and rarely hepatocellular carcinoma. Diagnosis is by serologic testing. Treatment is supportive. No vaccine is available.
(See also Causes of Hepatitis, Overview of Acute Hepatitis, and Chronic Hepatitis C.)
In the US, almost 3000 cases of acute hepatitis C infection were reported in 2016. However, because many cases are not recognized or not reported, the Centers for Disease Control and Prevention (CDC) estimates that the actual number of new infections was over 41,000 in 2016 (1).
Hepatitis C virus (HCV) is a single-stranded RNA flavivirus that causes acute viral hepatitis and is a common cause of chronic viral hepatitis. Six major HCV subtypes exist with varying amino acid sequences (genotypes); these subtypes vary geographically and in virulence and response to therapy. HCV can also alter its amino acid pattern over time in an infected person, producing quasispecies.
HCV infection sometimes occurs simultaneously with specific systemic disorders, including the following:
Essential mixed cryoglobulinemia
Porphyria cutanea tarda (about 60 to 80% of porphyria patients have HCV infection, but only a few patients infected with HCV develop porphyria)
Glomerulonephritis
The mechanisms are uncertain.
Up to 20% of patients with alcoholic liver disease harbor HCV. The reasons for this high association are unclear because concomitant alcohol and drug use accounts for only a portion of cases. In these patients, HCV and alcohol act synergistically to worsen liver inflammation and fibrosis.
