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Hepatitis C 

Hepatitis C

Chapter:
Hepatitis C
Author(s):

Paul Klenerman

, K.J.M. Jeffery

, and J. Collier

DOI:
10.1093/med/9780199204854.003.070522_update_002

Update:

Genetic predictors of acute viral clearance and response to treatment.

Further information on directly acting antiviral agents (DAAs) and new drugs in development.

Updated on 31 May 2012. The previous version of this content can be found here.
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date: 30 March 2017

Hepatitis C virus (HCV) is an RNA virus that has evolved into multiple genotypes (1–6) and subtypes. Humans are the only known natural host. HCV replication is highly error-prone, hence within any one person the virus exists as a swarm of closely related variants, known as ‘quasispecies’.

Epidemiology—HCV is a major cause of liver disease worldwide, with 170 million people probably infected. Spread is parenteral and usually associated with needle use, most commonly by injection drug users in the West; mother-to-child transmission does occur but is infrequent, as is sexual spread. Before the screening of blood products was introduced, blood transfusion recipients and patients with haemophilia were also at risk, and outbreaks in some countries (e.g. Egypt) have been associated with mass vaccination and parenteral therapy programmes.

Clinical aspects—these are discussed in detail in Chapter 15.21.1, but HCV tends to become persistent in most of those infected, although around 25% clear the virus as a result of effective innate and adaptive immune responses at the time of acute infection. The clinical course is variable in those with persistent infection: most develop some degree of hepatic inflammation and fibrotic liver disease, with a fraction going on to develop cirrhosis, with an increased risk of hepatocellular carcinoma. Cofactors which predispose to progression include simultaneous HIV infection and drinking alcohol.

Treatment: now and in the future—treatment is currently a combination of pegylated interferon-α‎ and ribavirin with or without a protease inhibitor, with outcome dependent on viral genotype. Future therapies will include other compounds directed against specific viral gene products (direct acting antiviral compound, DAA) such as polymerase inhibitors, but the capacity of the virus to mutate and thus evade both drug therapy and immune responses may be a major barrier to universal virus eradication.

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