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hepatitis C virus hepatitis

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Hepatitis C infection is a slowly progressive disease of the liver caused by the hepatitis C virus. It is a highly variable and unpredictable condition with effects of the infection varying from asymptomatic disease to liver failure or primary liver cancer (1).

Prior to 1991 hepatitis C virus was an important cause of post-transfusion hepatitis. It accounts for most cases of viral hepatitis previously designated as non-A, non-B viral hepatitis.

  • unlike hepatitis A and B, there is no vaccine for hepatitis C but infection is avoidable through strategies that reduce transmission.
  • HCV is a single stranded, enveloped RNA virus. It is structurally similar to the flaviviruses and is 30-38 nm in size has a genome of 9379-9481 base pairs.
  • the incubation period of 15-150 days which is broadly comparable to that of HBV.

The patient may be asymptomatic. About 10% develop jaundice. Fulminant hepatitis is rare. Patients who are HIV positive may have a rapidly progressive course.

Serum diagnosis is usually by detecting anti-HCV. HCV RNA may be detected by PCR 1-2 weeks after infection. PCR is a supersensitive technique but is not routinely available.

Hepatitis C virus is a highly variable agent and there are 6 recognised genotypes with numerous subtypes.

  • genotype 1 is the most common in the UK, accounting for about 40-50% of cases. Genotypes 2 and 3 contribute another 40-50%; and genotypes 4, 5 and 6 constitute the remainder, about 5%
  • antiviral treatment of hepatitis C, previously interferon-based, has become interferon-free, with resulting improvements in sustained virological response rates, safety, and tolerability and a shorter duration of treatment
  • available drugs for interferon-free antiviral treatment of hepatitis C include inhibitors of the RNA-dependent RNA polymerase, NS3/4A protease, and NS5A protein of the hepatitis C virus (HCV), and ribavirin
    • typically, two specific inhibitors are given in combination; the usual duration of treatment is 12 weeks
    • the antiviral drugs differ in their genotypic antiviral effectiveness and resistance barriers - appropriate drug(s) should be chosen in consideration of the patient’s hepatic and renal function and potential drug interactions
    • patients with hepatitis C, whatever their disease stage, can derive a sustained eradication of HCV from a combination of drugs with direct antiviral activity

In England, an estimated 89,000 people are chronically infected with hepatitis C (HCV)

  • in 2018 sentinel surveillance data suggests that, of all individuals testing positive for anti-HCV
    • 85% were tested for HCV RNA. Among persons who were HCV RNA tested after a positive anti-HCV test
    • 52% were RNA positive, of whom 42% had an HCV genotype recorded; 49% were genotype 1, with a further 43% genotype 3
  • Drug injection continues to be the most important documented risk factor for HCV infection in 2018, being cited as the risk in 93% of all laboratory reports where risk factors were disclosed
  • Of those participating in the Unlinked Anonymous Monitoring (UAM) Survey
    • proportion of people who inject drugs (PWID) who test HCV antibody (anti-HCV) positive has increased in recent years, from 45% in 2011 to 55% in 2018, however, chronic prevalence has remained relatively stable over this period (28% in 2018);
    • prevalence of cleared infection (anti-HCV positive, RNA-negative) has increased from 19% in 2011 to 27% in 2018

By 2018, the number of liver transplant registrations and transplants undertaken in those where post-HCV cirrhosis and hepatocellular carcinoma (HCC) is given as the indication for transplant, fell by 44% and 29% respectively when compared to pre-2015 levels, although both showed a rise over the previous year (by 19% and 13% respectively).

Deaths from HCV-related end stage liver disease (ESLD) and hepatocellular cancer (HCC) have been falling since 2014, with a decline of 20% by 2018 from the 2015 World Health Organization (WHO) baseline.

 

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Last edited 07/2020 and last reviewed 07/2020

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