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A better understanding of the epidemiology and natural history of acute hepatitis C virus infection is vital for effective assessment of the impact of policies designed to reduce transmission
In the 16 years that have elapsed since the first report of identification of the hepatitis C virus (HCV), much has been learnt about the epidemiology, natural history, and consequences of chronic infection with this virus. Global estimates of 170 million infected individuals are widely quoted, with infection leading to cirrhosis, hepatocellular carcinoma, and consequent life threatening complications in 20–30% of infected individuals over a lifetime. Cofactors for disease progression, such as increased age at infection, male sex, and alcohol intake, have been described in multiple large scale studies. However, in marked contrast, there are major gaps in our understanding of the process of acute HCV infection, an event which must necessarily precede the development of chronic disease. There are no reliable or validated data on the incidence of acute infections, either at the national or global level. Precise behavioural and other risk factors for acquisition of acute infection are not well defined, even among injecting drug misusers, the largest “at risk” group of individuals, reflecting ignorance about possible routes and modes of transmission, and there are uncertainties about the percentage of acute infections which are spontaneously cleared, and the viral and host factors responsible for these fundamental differences in outcome.
Acute HCV infection is usually defined as the new occurrence of viraemia, at which stage serum from the patient is HCV RNA positive, anti-HCV negative. Seroconversion to anti-HCV positivity occurs after a variable period of time, known as the window period, which may last for six months or even longer, although most patients become antibody positive within three months of infection. A proportion of patients, variously estimated at approximately 20–40%, …
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